Loesche 之Dental Caries: A Treatable Infection書中共有21個章節，扣掉空白頁及referrance的部分約有495頁
參與醫師共9名，平均每人約負責63頁
（1）P.1~P.69 中間（Diet as a Nutrient source的標題以上）
（2）P69中間～P.134 下面 （caries scoring in animals標題以上）
( 3 ) P.134 ~P.201中間（The white spot lesion以上）
( 4 ) P.201~P.267中間（fissure surface caries以上）
（5）P.267~P.335中間（professional cleaning of the teeth以上）
（6）P.335~P.401 中間（Switzerland以上）
（7）P.401～P.467 (table 19.12)
( 8 )P.467~P.538
分配如下：
（1）瓊慧
（2）慶麟
( 3 ) 懿萱
( 4 ) 婉伶
（5）怡均
（6）容伊
（7）如軒學姐
( 8 ) 欣儒學姐
( 9 ) 盈盈負責圖說與表格的部分
2010年2月20日 星期六
第16章 P351
INTRODUCTION
The increase in dental caries prevalence among people ingesting moderate to high sucrose-containing diets is related to the bioavailability of sucrose to the plaque flora. Certain plaque organisms such as S. mutans and lactobacilli are able to exploit this bioavailability and progress from being supplemental members of the plaque flora to becoming indigenous members of this flora (See "Host-Parasite Interactions" in Chap. 4). The ascent of these organisms to numerical prominence in the plaque in most instances is synonymous with the transformation of the plaque from a noncariogenic plaque to a cariogenic plaque. An obvious treatment stratagem would be to prevent the emergence of these organisms. As this emergence appears to be sucrose dependent, then tactics which reduce sucrose bioavailability should be effective preventive and therapeutic measures. This treatment strategy was recognized and clinically verified some forty years ago. However, because of l) the difficulty in changing dietary habits, 2) the desirable characteristics of sucrose as a calorie source, 3) the obvious marketability of sucrose-containing products, 4) the safety regulations concerning foods, and 5) the hedonistic appeal of sucrose in food products, the control of dental caries by sucrose restriction has not been successful in clinical dentistry, except in rare instances. In this chapter we shall examine caries control measures based upon dietary approaches.
簡介
對於喜愛中等到高蔗糖含量的飲食會造成蛀牙的增加，這和蔗糖對於牙菌斑群的生物利用度有關。特定的牙菌斑微生物例如S. mutans和lactobacilli可利用這生物利用度，將牙菌斑群的supplemental members轉變成indigenous members (可見第四章的宿主-寄主交互作用)。在大部分例子中追溯這些微生物到站牙菌斑裡的大多數，是和將從非蛀牙的牙菌斑轉換成蛀牙牙菌斑是相同的。最直接的治療方法就是阻止這些微生物的出現。而這些微生物的出現看起來是和蔗糖有關，所以策略是要降低蔗糖的生物利用度且應具有有效之預防及治療較果。這治療政策應被認定和臨床上認定已四十年了。然而，因為1) 改善飲食習慣上困難 2) 蔗糖的理想特質被作為卡洛里的來源 3) 在市面上顯著的含蔗糖物質 4)食物之安全管理規定 5)快樂主義者易被食物裡的蔗糖所吸引，然而限制蔗糖攝取去控制蛀牙，除了少數例子外在牙科臨床上尚未成功。這這個章節我們會依據飲食來檢視控制蛀牙方法。
DIETARY COUNSELING
Dietary counseling to prevent and/or control any chronic disease such as dental caries, obesity, cardiovascular disease and diabetes, among others, has not been remarkably effective. The situation with dental caries is complicated by the youthful age of the patient and the ambiguous messages which the patient has already received concerning the "banned" sugar-containing items. He knows from personal experience that the high sucrose- containing products not only look good but are quite pleasant tasting. He may have been rewarded with such a sucrose item for good behavior or performance during the early formative years of his life. In fact, the sucrose eating pattern may have been acquired by (imposed on) the infant from the mother's sweet preferences (See Table 16-5). The older youngster perceives that sucrose is an energy food and certainly satisfying after exertion. The dentist's efforts to counteract all of these positive and immediate feelings concerning sugar with a distant threat of a toothache are essentially irrelevant to the patient. For at least these reasons, dietary counseling as a means of preventing decay in the average patient is not likely to be successful. Dietary counseling can be of therapeutic value, however, when the patient has clearly misused sucrose-containing foods and presents with a rampant caries situation
飲食諮詢
飲食諮詢去預防或是控制任何慢性疾病，例如蛀牙、肥胖、心臟血管疾病和糖尿病，對於這些並無明顯的有效性。蛀牙會因病人年幼的年紀而複雜化，還有病人已被輸入接受禁止吃含糖食物的含糊訊息。小朋友以個人經驗知道高糖分食物不僅外觀好看，而且有很好的口感。在年幼時有可能因行為或是表現良好因而接到含蔗糖的食物。事實上，蔗糖攝取形式可能是受母親喜愛吃甜食上所影響(見表16-5)。較年長的小朋友認為蔗糖是補給能量的來源並且會得到滿足感。而醫師所努力倡導，卻和吃甜食所得的正向快感背道而馳，而會蛀牙的威脅對病人無立即性的威脅。
因為上述這些原因，在一般病人身上，以飲食諮詢做為預防蛀牙是不太可成功的。飲食諮詢是有治療的價值，然而，當病人錯誤吃含蔗糖的食物，並表現出猛爆性蛀牙的情況。
Misuse of Food
Malnutrition is most often conceptualized to situations of under-nutrition. However, in modern industrialized societies malnutrition is more appropriately assigned to situations of over-nutrition. Thus we have health problems that relate to excesses of calorie intake, alcohol intake, sodium intake, fat intake and sucrose intake. Excessive sucrose intake has been linked to obesity, to cardiovascular disease and to mental disorders, but in no instance is the evidence for linkage as conclusive as in the relationship between dental caries and sucrose intake. (See "Nutritional Factors" in Chap. 11).
錯誤的飲食
錯誤的營養常被誤以為是營養不足。然而在現在這工業化社會錯誤的營養是指營養過剩。因此可能會因有攝取過多卡路里、酒精、鈉、脂肪和蔗糖，因而有健康的問題。過多蔗糖攝取會造成肥胖，心血管疾病和心理上缺失，然而這些關聯並不是絕對的，不像蛀牙和蔗糖攝取的關係(見11章的營養因素)
Yet even in regard to dental caries, the sucrose has to be misused. This misuse relates, 1) to the rapid replacement of traditional foods by high sucrose-containing foods, 2) to the increased frequency with which high sucrose-containing snack foods are eaten between meals, and 3) to the excessive indulgence in these snack foods for primarily hedonistic purposes. These misuses while not condoned by the food industry appear in certain instances to be encouraged by advertising practices.
即使會造成蛀牙，蔗糖依然被濫用。這樣濫用是因為1)用含高蔗糖食物來快速取代傳統食物，2)增加餐與餐之間吃高蔗糖含量的頻率，3) 為了當快樂主義者，過度沉溺於甜食中。這樣的濫用不會被食物公司所赦免反而還會用廣告來促銷。
Man evolved protective mechanisms against plaque acid production on the tooth surfaces that were within the context of food being consumed at a restricted frequency. Natural foods contain mostly macromolecular nutrients that are not rapidly degraded or solubilized in the oral cavity. The microbial acids that are formed as these nutrients pass through the oral cavity are diluted in the saliva, neutralized by salivary buffers and cleared from the mouth by swallowing. The efficacy of this protective system is verified by the low caries incidence of people who consume low-sucrose diets. These mechanisms can be overwhelmed when sucrose becomes the predominant nutrient in the food item. Thus the explosive epidemic of caries among nonindustrialized people who switched from natural foods to high-sucrose foods. (See "Nutritional Factors" in Chap. 11). This substitution is counterindicated in terms of dental health and would constitute a form of food misuse.
在食物上為了去對抗牙菌斑所產的酸，所發展出的保護機制是要去限制的頻率。天然食物含有大部分的大分子營養物，這樣才不會在口腔裡快速被分解或溶解。當這些營養物被唾液稀釋，並經過口腔被唾液中緩衝劑中和，並經吞嚥由口中清除。這個保護機制的效率可被吃低蔗糖食物的低蛀牙率族群所認同。而這些機制會隨蔗糖成為食物裡主要的營養物而被湮滅。在非工業性國家裡的人們，將天然食物轉成高蔗糖食物時，會有爆炸性蛀牙的發生(可見11章的營養因素)。這樣的取代危害到牙齒的健康並且造成食物上的濫用。
The Vipeholm study indicated that when high levels of sucrose were consumed at meal times, the caries incidence increased only slightly (Table 11-10). Accordingly, the argument can be made that sucrose when added to foods or when consumed with foods is not particularly cariogenic. This suggests that non-sucrose foods contain factors or elicit factors which minimize the access of sucrose to the plaque flora. Studies have shown that certain foods prevent or overcome the pH drop in plaque associated with exposure to sucrose (See "Foods Which Reduce Plaque Acid Production" in this chapter). These findings tend in some quarters to allay some of the concern associated with the industrial addition of sucrose to many food items that are consumed at mealtimes.
在Vipeholm的研究裡指出當在吃飯時間時吃含高蔗糖食物，其蛀牙發生率只有些微增加(表11-10)。 因此爭議點可以說當蔗糖添加在食物裡或是當我們所吃的食物不會特別容易引起蛀牙的發生。這建議非蔗糖性食物可包含或引起將低蔗糖接觸到牙菌斑群。研究指出當蔗糖暴露在牙菌斑時，在特定食物下可阻止酸鹼值的下降。這樣的發現使食品公司建議將這些含蔗糖的產品和吃飯時一起食用。
Sucrose-containing foods are so attractive and relatively inexpensive that they have evolved into a peculiarly unique modern food entity called a snack food. Snack foods apparently are devoid of food protective factors and as they are designed and promoted for frequent consumption, they are particularly cariogenic. Their acceptance in the American market is well documented by the multiplicity of such products. Desserts would comprise one class of high-sucrose foods that traditionally were consumed at the conclusion of a meal. In this location their potential cariogenicity could be muted by the salivary flow elicited by the mastication of the meal. In recent years desserts and other snack-type foods have been increasingly consumed between meals (Table 16-1). This temporal shift has transformed desserts into decidedly cariogenic food items and represents an example of food misuse.
含有蔗糖食物非常吸引人且又不貴，他們演進成現代的點心食物。現在的點心通常都缺乏保護因子並被設計成可經常攝取，這些都非常容易蛀牙的。這樣的食物因為其多樣性廣泛地被美國市場接受。甜點應該在餐點的最後才上。如此的安排才可以讓咀嚼食物的唾液中和這易蛀牙的特性。在這近幾年甜食和其他種類的零食食物在餐與餐之間攝取的頻率大大增加(表16-1)。這樣的轉變將甜食轉變成易蛀牙的食物，這也是食物錯誤使用的例子之一。
Snack foods are misused when a parent or other authority figure conditions, pacifies or rewards youngsters for any type of compliant behavior with the gift of a high-sucrose product. The milk-bottle baby syndrome represents a flagrant example of such. Children who are sent to bed with a bottle containing a high-sucrose beverage or with a high-sucrose snack often develop rampant caries. Some of this sucrose during its transit time in the mouth is sequestered by the plaque organisms forming both acids and polysaccharide polymers. Saliva flow decreases during sleep and actually appears to cease when the individual is in deep sleep. On the tooth surface the plaque organisms degrade the reserve polysaccharides, forming acid. This acid in the absence of saliva accumulates in the plaque causing the pH to fall to levels where the tooth mineral is solubilized. Under these conditions the plaque levels and proportions of S. mutans increase significantly. In this fashion bedtime ingestion of high-sucrose foods becomes particularly cariogenic. The situation is analogous to rampant caries secondary to xerostomia only in this instance, the xerostomia is physiologic due to sleep.
零食會誤用通常和用高蔗糖含量的食品來讚賞小朋友良好的行為有關。而乳牙的奶瓶性蛀牙即是很好的例子。小朋友若睡前喝高蔗糖含量的飲料或是點心通常會造成猛爆性蛀牙。在這段時間裡蔗糖在口內被牙菌斑物質分解成酸和polysaccharide polymers.唾液流量會在睡覺時減少或是在沉睡時停止分泌。在牙齒表面的牙菌斑微生物分解polysaccharide成酸性物質。這些酸性物質使酸鹼值往下降，使牙齒礦物質變成可溶解。在這樣形況下牙菌斑和S. mutans的量都上升。所以在睡前吃高蔗糖含量的食物會特別容易蛀牙。這樣的形況就像口乾症容易引起蛀牙，唯一不同的是口乾症是因睡覺所造成之生理性。
Sucrose has highly desirable taste characteristics, which accounts for its widespread ingestion by the public. In certain usages, such as the between-meal eating of candies, the sucrose consumption appears to be mainly for hedonistic purposes. Any overindulgence in high-sucrose foods for nonnutritional purposes usually predisposes to a rampant caries situation. This type of sucrose misuse can be identified by a diet history and corrective dietary therapy such as sucrose restriction and/or the appropriate usage of sucrose substitutes can be initiated (See Chap. 17).
蔗糖因有很好口感的特質，所以才可以廣為大眾所接受。在餐與餐之間吃甜食最主要是因為可得到快樂。任何過度沉溺於高蔗糖食物而不是以營養為主通常會造成猛冒蛀牙。這樣如此的濫用蔗糖可以從限制蔗糖或是適當地用蔗糖開始 (見17章)
The increase in dental caries prevalence among people ingesting moderate to high sucrose-containing diets is related to the bioavailability of sucrose to the plaque flora. Certain plaque organisms such as S. mutans and lactobacilli are able to exploit this bioavailability and progress from being supplemental members of the plaque flora to becoming indigenous members of this flora (See "Host-Parasite Interactions" in Chap. 4). The ascent of these organisms to numerical prominence in the plaque in most instances is synonymous with the transformation of the plaque from a noncariogenic plaque to a cariogenic plaque. An obvious treatment stratagem would be to prevent the emergence of these organisms. As this emergence appears to be sucrose dependent, then tactics which reduce sucrose bioavailability should be effective preventive and therapeutic measures. This treatment strategy was recognized and clinically verified some forty years ago. However, because of l) the difficulty in changing dietary habits, 2) the desirable characteristics of sucrose as a calorie source, 3) the obvious marketability of sucrose-containing products, 4) the safety regulations concerning foods, and 5) the hedonistic appeal of sucrose in food products, the control of dental caries by sucrose restriction has not been successful in clinical dentistry, except in rare instances. In this chapter we shall examine caries control measures based upon dietary approaches.
簡介
對於喜愛中等到高蔗糖含量的飲食會造成蛀牙的增加，這和蔗糖對於牙菌斑群的生物利用度有關。特定的牙菌斑微生物例如S. mutans和lactobacilli可利用這生物利用度，將牙菌斑群的supplemental members轉變成indigenous members (可見第四章的宿主-寄主交互作用)。在大部分例子中追溯這些微生物到站牙菌斑裡的大多數，是和將從非蛀牙的牙菌斑轉換成蛀牙牙菌斑是相同的。最直接的治療方法就是阻止這些微生物的出現。而這些微生物的出現看起來是和蔗糖有關，所以策略是要降低蔗糖的生物利用度且應具有有效之預防及治療較果。這治療政策應被認定和臨床上認定已四十年了。然而，因為1) 改善飲食習慣上困難 2) 蔗糖的理想特質被作為卡洛里的來源 3) 在市面上顯著的含蔗糖物質 4)食物之安全管理規定 5)快樂主義者易被食物裡的蔗糖所吸引，然而限制蔗糖攝取去控制蛀牙，除了少數例子外在牙科臨床上尚未成功。這這個章節我們會依據飲食來檢視控制蛀牙方法。
DIETARY COUNSELING
Dietary counseling to prevent and/or control any chronic disease such as dental caries, obesity, cardiovascular disease and diabetes, among others, has not been remarkably effective. The situation with dental caries is complicated by the youthful age of the patient and the ambiguous messages which the patient has already received concerning the "banned" sugar-containing items. He knows from personal experience that the high sucrose- containing products not only look good but are quite pleasant tasting. He may have been rewarded with such a sucrose item for good behavior or performance during the early formative years of his life. In fact, the sucrose eating pattern may have been acquired by (imposed on) the infant from the mother's sweet preferences (See Table 16-5). The older youngster perceives that sucrose is an energy food and certainly satisfying after exertion. The dentist's efforts to counteract all of these positive and immediate feelings concerning sugar with a distant threat of a toothache are essentially irrelevant to the patient. For at least these reasons, dietary counseling as a means of preventing decay in the average patient is not likely to be successful. Dietary counseling can be of therapeutic value, however, when the patient has clearly misused sucrose-containing foods and presents with a rampant caries situation
飲食諮詢
飲食諮詢去預防或是控制任何慢性疾病，例如蛀牙、肥胖、心臟血管疾病和糖尿病，對於這些並無明顯的有效性。蛀牙會因病人年幼的年紀而複雜化，還有病人已被輸入接受禁止吃含糖食物的含糊訊息。小朋友以個人經驗知道高糖分食物不僅外觀好看，而且有很好的口感。在年幼時有可能因行為或是表現良好因而接到含蔗糖的食物。事實上，蔗糖攝取形式可能是受母親喜愛吃甜食上所影響(見表16-5)。較年長的小朋友認為蔗糖是補給能量的來源並且會得到滿足感。而醫師所努力倡導，卻和吃甜食所得的正向快感背道而馳，而會蛀牙的威脅對病人無立即性的威脅。
因為上述這些原因，在一般病人身上，以飲食諮詢做為預防蛀牙是不太可成功的。飲食諮詢是有治療的價值，然而，當病人錯誤吃含蔗糖的食物，並表現出猛爆性蛀牙的情況。
Misuse of Food
Malnutrition is most often conceptualized to situations of under-nutrition. However, in modern industrialized societies malnutrition is more appropriately assigned to situations of over-nutrition. Thus we have health problems that relate to excesses of calorie intake, alcohol intake, sodium intake, fat intake and sucrose intake. Excessive sucrose intake has been linked to obesity, to cardiovascular disease and to mental disorders, but in no instance is the evidence for linkage as conclusive as in the relationship between dental caries and sucrose intake. (See "Nutritional Factors" in Chap. 11).
錯誤的飲食
錯誤的營養常被誤以為是營養不足。然而在現在這工業化社會錯誤的營養是指營養過剩。因此可能會因有攝取過多卡路里、酒精、鈉、脂肪和蔗糖，因而有健康的問題。過多蔗糖攝取會造成肥胖，心血管疾病和心理上缺失，然而這些關聯並不是絕對的，不像蛀牙和蔗糖攝取的關係(見11章的營養因素)
Yet even in regard to dental caries, the sucrose has to be misused. This misuse relates, 1) to the rapid replacement of traditional foods by high sucrose-containing foods, 2) to the increased frequency with which high sucrose-containing snack foods are eaten between meals, and 3) to the excessive indulgence in these snack foods for primarily hedonistic purposes. These misuses while not condoned by the food industry appear in certain instances to be encouraged by advertising practices.
即使會造成蛀牙，蔗糖依然被濫用。這樣濫用是因為1)用含高蔗糖食物來快速取代傳統食物，2)增加餐與餐之間吃高蔗糖含量的頻率，3) 為了當快樂主義者，過度沉溺於甜食中。這樣的濫用不會被食物公司所赦免反而還會用廣告來促銷。
Man evolved protective mechanisms against plaque acid production on the tooth surfaces that were within the context of food being consumed at a restricted frequency. Natural foods contain mostly macromolecular nutrients that are not rapidly degraded or solubilized in the oral cavity. The microbial acids that are formed as these nutrients pass through the oral cavity are diluted in the saliva, neutralized by salivary buffers and cleared from the mouth by swallowing. The efficacy of this protective system is verified by the low caries incidence of people who consume low-sucrose diets. These mechanisms can be overwhelmed when sucrose becomes the predominant nutrient in the food item. Thus the explosive epidemic of caries among nonindustrialized people who switched from natural foods to high-sucrose foods. (See "Nutritional Factors" in Chap. 11). This substitution is counterindicated in terms of dental health and would constitute a form of food misuse.
在食物上為了去對抗牙菌斑所產的酸，所發展出的保護機制是要去限制的頻率。天然食物含有大部分的大分子營養物，這樣才不會在口腔裡快速被分解或溶解。當這些營養物被唾液稀釋，並經過口腔被唾液中緩衝劑中和，並經吞嚥由口中清除。這個保護機制的效率可被吃低蔗糖食物的低蛀牙率族群所認同。而這些機制會隨蔗糖成為食物裡主要的營養物而被湮滅。在非工業性國家裡的人們，將天然食物轉成高蔗糖食物時，會有爆炸性蛀牙的發生(可見11章的營養因素)。這樣的取代危害到牙齒的健康並且造成食物上的濫用。
The Vipeholm study indicated that when high levels of sucrose were consumed at meal times, the caries incidence increased only slightly (Table 11-10). Accordingly, the argument can be made that sucrose when added to foods or when consumed with foods is not particularly cariogenic. This suggests that non-sucrose foods contain factors or elicit factors which minimize the access of sucrose to the plaque flora. Studies have shown that certain foods prevent or overcome the pH drop in plaque associated with exposure to sucrose (See "Foods Which Reduce Plaque Acid Production" in this chapter). These findings tend in some quarters to allay some of the concern associated with the industrial addition of sucrose to many food items that are consumed at mealtimes.
在Vipeholm的研究裡指出當在吃飯時間時吃含高蔗糖食物，其蛀牙發生率只有些微增加(表11-10)。 因此爭議點可以說當蔗糖添加在食物裡或是當我們所吃的食物不會特別容易引起蛀牙的發生。這建議非蔗糖性食物可包含或引起將低蔗糖接觸到牙菌斑群。研究指出當蔗糖暴露在牙菌斑時，在特定食物下可阻止酸鹼值的下降。這樣的發現使食品公司建議將這些含蔗糖的產品和吃飯時一起食用。
Sucrose-containing foods are so attractive and relatively inexpensive that they have evolved into a peculiarly unique modern food entity called a snack food. Snack foods apparently are devoid of food protective factors and as they are designed and promoted for frequent consumption, they are particularly cariogenic. Their acceptance in the American market is well documented by the multiplicity of such products. Desserts would comprise one class of high-sucrose foods that traditionally were consumed at the conclusion of a meal. In this location their potential cariogenicity could be muted by the salivary flow elicited by the mastication of the meal. In recent years desserts and other snack-type foods have been increasingly consumed between meals (Table 16-1). This temporal shift has transformed desserts into decidedly cariogenic food items and represents an example of food misuse.
含有蔗糖食物非常吸引人且又不貴，他們演進成現代的點心食物。現在的點心通常都缺乏保護因子並被設計成可經常攝取，這些都非常容易蛀牙的。這樣的食物因為其多樣性廣泛地被美國市場接受。甜點應該在餐點的最後才上。如此的安排才可以讓咀嚼食物的唾液中和這易蛀牙的特性。在這近幾年甜食和其他種類的零食食物在餐與餐之間攝取的頻率大大增加(表16-1)。這樣的轉變將甜食轉變成易蛀牙的食物，這也是食物錯誤使用的例子之一。
Snack foods are misused when a parent or other authority figure conditions, pacifies or rewards youngsters for any type of compliant behavior with the gift of a high-sucrose product. The milk-bottle baby syndrome represents a flagrant example of such. Children who are sent to bed with a bottle containing a high-sucrose beverage or with a high-sucrose snack often develop rampant caries. Some of this sucrose during its transit time in the mouth is sequestered by the plaque organisms forming both acids and polysaccharide polymers. Saliva flow decreases during sleep and actually appears to cease when the individual is in deep sleep. On the tooth surface the plaque organisms degrade the reserve polysaccharides, forming acid. This acid in the absence of saliva accumulates in the plaque causing the pH to fall to levels where the tooth mineral is solubilized. Under these conditions the plaque levels and proportions of S. mutans increase significantly. In this fashion bedtime ingestion of high-sucrose foods becomes particularly cariogenic. The situation is analogous to rampant caries secondary to xerostomia only in this instance, the xerostomia is physiologic due to sleep.
零食會誤用通常和用高蔗糖含量的食品來讚賞小朋友良好的行為有關。而乳牙的奶瓶性蛀牙即是很好的例子。小朋友若睡前喝高蔗糖含量的飲料或是點心通常會造成猛爆性蛀牙。在這段時間裡蔗糖在口內被牙菌斑物質分解成酸和polysaccharide polymers.唾液流量會在睡覺時減少或是在沉睡時停止分泌。在牙齒表面的牙菌斑微生物分解polysaccharide成酸性物質。這些酸性物質使酸鹼值往下降，使牙齒礦物質變成可溶解。在這樣形況下牙菌斑和S. mutans的量都上升。所以在睡前吃高蔗糖含量的食物會特別容易蛀牙。這樣的形況就像口乾症容易引起蛀牙，唯一不同的是口乾症是因睡覺所造成之生理性。
Sucrose has highly desirable taste characteristics, which accounts for its widespread ingestion by the public. In certain usages, such as the between-meal eating of candies, the sucrose consumption appears to be mainly for hedonistic purposes. Any overindulgence in high-sucrose foods for nonnutritional purposes usually predisposes to a rampant caries situation. This type of sucrose misuse can be identified by a diet history and corrective dietary therapy such as sucrose restriction and/or the appropriate usage of sucrose substitutes can be initiated (See Chap. 17).
蔗糖因有很好口感的特質，所以才可以廣為大眾所接受。在餐與餐之間吃甜食最主要是因為可得到快樂。任何過度沉溺於高蔗糖食物而不是以營養為主通常會造成猛冒蛀牙。這樣如此的濫用蔗糖可以從限制蔗糖或是適當地用蔗糖開始 (見17章)
第15章 P335-349
PROFESSIONAL CLEANING OF THE TEETH
Preventive treatment by the dentist in the United States consists, at least as is reported for income purposes (Table 13- 8), primarily of annual or biannual tooth cleanings administered by the hygienist. As this procedure, when given to children, is often followed by topical application of fluorides, the caries preventive efficacy of the mechanical component cannot be assessed. However, one may deduce that an annual cleaning in the absence of fluoride will not be a particularly effective preventive caries procedure. In particular, there is the potential to select in the recolonization process for organisms buried within pits, fissures and other inaccessible anatomic sites. This has been beautifully demonstrated by means of scanning electron photomicrographs taken at various intervals following a dental cleaning. In Figure 15-1A a tooth surface containing a crack is shown immediately after a dental prophylaxis. No bacteria are observed on the flat tooth surfaces nor on the visible walls of the crack. However, four hours later a line of dense microbial growth is observed along the entire length of the crack (Fig. 15-1B). The appearance of the growth indicates that the bacteria left behind in the crack had quickly recolonized the vicinity of the crack and had established dominance in that site. If these bacteria contained S. mutans, then a cariogenic plaque was selected for. If these bacteria contained noncariogenic organisms, then a noncariogenic plaque would occupy this caries-prone site and could serve to exclude cariogenic organisms from the niche. The identity of the recolonizing bacteria thus would be decisive in determining the eventual caries outcome of the site. If the professionally administered mechanical debriding procedures are repeated at two or three-week intervals and are supplemented with a fluoride paste as was done in the Karlstad studies (Fig. 13-3, Table 13-11), there is the possibility that the fluoride could sterilize or greatly reduce the number of organisms left behind in pits, fissures and cracks. In this event, recolonization of these retentive sites would come from organisms in the saliva and would lead to a repopulation of these caries-prone sites with noncariogenic organisms, as was illustrated in Figure 14-1. If this is so, then fluoride was essential for the efficacy of these Swedish studies.
專業潔牙
對美國的牙醫師而言，預防治療是建議一年有一次到兩次的專業潔牙，這樣潔牙動作是讓衛教師來執行，有報導部分是基於收入的因素。這樣的專業潔牙到最後都會給與局部塗氟，用這種機械方法來預防蛀牙的效率是不可被評估的。然而，可能會有人說這樣專業潔牙若不給以氟，不會被視為一有效的預防蛀牙方法。特別來說，藏在溝縫裡或是其他不可接觸的地方，對於細菌而言是有潛力可以去選擇再次聚集的過程。這可以經由在潔牙時不同階段所拍攝的微電子照片美麗地呈現出來。如圖15-1，牙齒經過專業潔牙後可看出有一個裂縫，在平滑表面或是裂縫的強壁上都未發現任何細菌。然而經過四小時後，在整條縫隙處可見密集地細菌成長，可見圖15-1 B。被藏在縫隙裡的細菌很快地又再次聚集成菌落，並且成為此處的主要菌落者。若這些細菌包含S. mutans，則這些形成的菌落會是易蛀牙的細菌。若這些細菌包含的是非蛀牙性細菌，則非蛀牙細菌則會佔滿這容易蛀牙的地方，並排除那些易蛀牙的細菌。所以再次聚集細菌的種類會是決定這地方是否蛀牙重要因素。在Karlstand 所做的研究，每兩到三個禮拜所做的專業機械性潔牙並佐用氟膏，研究顯示氟可以消毒或是大量地減少在溝縫、或裂痕裡的細菌。在這個事件裡，重新聚集在這些地方的細菌是從唾液中來的，在這些容易引起蛀牙的地方重新聚集非蛀牙的細菌，像圖14-1所示。若真如這個所說，對於這些瑞典研究所顯示，氟是最重要的。
A Danish group consisting of Poulsen, Agerbaek, Melsen, Glavind and their colleagues have conducted a series of clinical experiments in which the various components of the Karlstad regimen have been isolated and individually studied. They observed that oral hygiene instructions and dietary and bacteriological information had no effect on caries reduction (Table 15-2). In a separate study they evaluated the effect that frequent toothcleaning using a nonfluoridated paste would have on caries increment. Seven-year-old children were stratified according to the presence or absence of smooth-surface lesions and then children within each of the two strata were randomly assigned to an experimental and a control group. The experimental group was given careful professional cleaning of the teeth every second week during the two years of the study. Both groups received biweekly 0.2 percent sodium fluoride rinses and were given complete restorative dental treatment before the baseline examinations and another course of treatment at six-month intervals.
有一群丹麥研究員包含Poulsen, Agerbaek, Melsen, Glavind和其他成員進行了以Karlstad研究裡不同的因素應被隔離或是個別研究進行的一系列實驗。他們發現口腔衛教、飲食還有細菌的資訊對於降低蛀牙是不會有幫助(表15-2)。在另一個實驗中他們評估經常用不含氟的牙膏刷牙對於蛀牙的增加率。一群七歲的小朋友以有無平滑面的蛀牙病炤來分層，所以當小朋友有在兩層以下的就被平均分配到實驗組和控制組。在這兩年的實驗中，實驗組每兩個禮拜就給予專業潔牙一次。這兩組每兩個禮拜都給予0.2%鈉化氟的漱口水。而且在實驗開始前所有蛀牙都有填補，且每六個禮拜會定期檢查。
After one year the experimental group averaged one less decayed permanent surface than the control group, and after two years the experimental group had 1.7 fewer decayed surfaces (Table 15-6). This difference was low compared to the reduction of 5.5 surfaces observed after two years in the seven to eight-year-old children treated by the Karlstad regimen (Fig. 13-3). These findings indicate that repeated professional cleaning with a nonfluoridated paste decreased caries incidence, but that the treatment effect is only about 30 to 40 percent of that which was obtained when a fluoridated paste and motivational programs were also used. Motivational programs by themselves were without a noticeable treatment effect (Table 15-2), whereas topical fluorides alone yielded about a 70 percent reduction (See Table 18-8). This would suggest that the dramatic success of the Swedish studies had both a fluoride and a mechanical component. The fluoride most likely, via its antimicrobial and remineralizing actions, enhanced the ability of the mechanical debriding procedures to change the plaque flora from a cariogenic to a nondisease-associated flora (See "Fluoride" in Chap. 18).
經過一年後，實驗組在恆牙上蛀洞的面比起控制組平均少一面。過兩年後，實驗組則少1.7面(見表15-6)。這樣的差距比起Karlstad研究裡，觀察七到八歲的小朋友共兩年，降低5.5面的蛀牙所得的數據是些微的(圖13-3)。這樣觀察的結果是指使用不含氟的牙膏反覆潔牙是會降低蛀牙發生率。但是有用含氟牙膏和提高行動力下，其治療較率只有百分之三十到四十。提高行動力並不會有影響不同的治療結果(表15-2)；然而局部圖氟給予百分之七十的蛀牙降低率(表18-8)。這樣結果表示在瑞典研究裡用氟和機械性方法造成引人注目的成功，這是因為氟藉由抵抗微生物再礦化的作用，進而增加機械性移除的程序，並將這群菌落由蛀牙細菌改變成不會造成細菌的組合。
SEALANTS
The occlusal fissures are the most caries-prone sites in the dentition (Table 11-1). The bacteria contained therein subside into a micro-environment which is virtually inaccessible to mechanical debriding procedures (Figure 15-2). In the 1920s Hyatt recommended eradication of fissures by replacing them with Class I amalgam restorations, and Bodecker advocated reshaping of the fissure morphology to produce wide, non-retentive, self-cleaning grooves. In the latter procedure, called a prophylactic odontotomy, there was the problem that the extreme depths of some fissures would lead to dentinal exposures during the reshaping process. Neither procedure was subsequently adapted because of its invasive nature and its cost effectiveness relative to the placement of a dental restoration only after caries had developed. However, these procedures conceptualized a valid treatment strategy in preventive dentistry, namely the recontouring of the fissure anatomy, that was to become a reality in the 1970s with the introduction of plastic sealants. Only now the recontouring was achieved by an onlay of an adhesive resin which occluded the natural fissures so as to provide, in plastic, the same wide, non-retentive grooves that Bodecker recommended.
溝隙封填劑
在牙齒表面的縫隙是最容易蛀牙的地方(表11-1)。藏在溝縫裡的細菌是不可經由機械性移除的過程而被清除(圖15-2)。在1920年代，Hyatt建議以Class I 汞齊填補的方式來移除溝縫。Bodecker則提倡將溝縫的形狀重新塑形成較寬、無故持性，可以自行清潔的溝縫。在Bodecker的發法裡，又稱作預防性修行齒質，若有個極深的溝縫經過重新塑形後有可能會造成牙本質的暴露，這會造成問題。不管這些步驟是因為其侵略性的特質，或是在蛀牙發生後放上牙科填補材料之成本效益的考量。然而，這些步驟將在預防醫學有效的治療方法概念化，重新塑形溝縫，在1970年代開始有溝隙封填劑的引進。只有在現，用有黏性的樹脂做為一嵌體，封閉溝縫來重新塑形。
The technical knowledge of polymer chemistry which led to the development of the cyanoacrylates, polyurethanes and bisphenol A-glycidyl methacrylates (bis-GMA) plastics for clinical usage in dentistry are beyond the scope of this monograph. Suffice it to say that complex problems dealing with the binding of the resin to the inorganic tooth structure, control of setting time and exclusion of an aqueous environment have been solved to the extent that two generations of bis-GMA sealants have been evaluated clinically and been found to significantly reduce decay on fissure surfaces. The ability of these resins to reduce decay was initially demonstrated by Buonocore in a study in which a single application of bis-GMA was applied to one member of a contralateral pair of either permanent or primary teeth. The teeth were carefully dried and after pretreatment with a phosphoric acid etching solution, the adhesive was painted onto the fissure and then its polymerization was activated by means of an ultraviolet light. After either one or two years in vivo, the sealant was removed and the caries status of the underlying surface was determined and compared to the unsealed control teeth.
In plastic由Bodecker所介紹同樣較寬、無故持性的溝縫。
在化學上聚合物的知識增加，進而發明了氰基丙烯酸酯、聚氨酯和雙酚甲烷甘油基甲基丙烯酸酯(bis-GMA)塑膠，這些在牙科臨床上的運用遠超過此篇所討論的範圍。已有足夠能力去處理將樹脂黏到無機牙齒的表面，控制行成時間，並排除含水的環境，隨著這些問題的克服以有兩代的bis-GMA溝隙封填劑已在臨床運用評估過，且成功地降低溝縫的蛀牙。這些樹酯可降低蛀牙的發生，最先被Buonocore在研究中發現，將bis-GMA塗一次在任一恆牙或乳牙上。牙齒很小心被吹乾，接著用磷酸酸蝕，再塗上adhesive，接著用紫外光聚合。經過在人體一年或兩年的時間，溝隙封填劑被移除，來評估其下面的蛀牙，並和未封閉的牙齒來比較。
In the permanent teeth the adhesive was retained on all surfaces after one year and on 87 percent after two years (Table 15-7). The adhesive was not as well retained on the primary teeth. This was attributed to the prismless enamel layer found on these teeth which apparently did not dissolve upon acid etching, thereby preventing the formation of interprismatic voids which could be occupied by the resin. After two years only one sealant-treated permanent tooth had become carious, whereas 68 of 113 or 60 percent of the control teeth had become carious (Table 15-7). Over the same time period two sealant-treated primary teeth had become carious compared to 15 control teeth (Table 15-7).
在經一年後黏著劑仍全部保存在所有的恆牙牙齒表面上，經兩年後剩百分之87(表18-7)。黏著劑也沒有完全保存在乳牙表面上。這是因為牙齒上的無錐狀體的牙釉質，在酸蝕時沒有被溶解，如此就無法和樹脂形成錐體間的裂縫(interprismatic voids)。經兩年後只有一顆購隙封填劑處理的恆牙有蛀洞，然而在控制組中，113個牙齒中有68顆，或是百分之六十有蛀牙(表15-7)。經過相同的時間，有兩顆放有溝隙封填劑的牙齒有蛀牙，而控制組則是15顆。
Reductions in dental decay of this magnitude are impressive and have ushered in an era where preventive treatment of occlusal fissure decay is a distinct reality. However, other investigators have not achieved the same degree of success with sealants and have raised important practical questions concerning the retention of the sealant and the cost benefit of a procedure that requires exacting clinical conditions in regard to the dryness of the operating field, and which may need to be repeated several times during the caries-prone years of the patient. The great success of the Ypsilanti study in reducing occlusal fissure decay probably was related to the repeated applications of the sealant as needed (Table 13-12), but this vigilance contributed appreciably to the cost of the study.
溝隙封填劑這樣大量地降低蛀牙是令人印像深刻的，並帶領我們進入溝隙封填劑可以有效預防咬合面的蛀牙時代。然而其他的研究結果並不能完全達到這樣一般的成功率，並且還有許多實際的問題，如有關溝隙封填劑的故持力，還有在臨床操作上為了要保持有個乾燥的工作區域所需的成本效益，或是對於高蛀牙率的牙齒會需要重複治療。在Ypsilanti研究裡，在降低咬合面溝縫的蛀牙有很高的成功率，是因為能重複地放置溝隙封填劑(表13-12)，但這樣會影響到整個實驗的花費。
Some have raised questions concerning leakage along the sealant-enamel margin that could lead to decay beneath the sealant, as well as questions concerning the survival of the bacteria that were left beneath the sealant during placement. It would also be of interest to know whether the absence of a retentive surface had any effect on the ability of S. mutans to successfully colonize the occlusal surface. These bacteriological issues will comprise the remaining sections of this chapter.
有關溝隙封填劑和牙本質的交界可能會產生裂縫，並可能會在封填劑下產生蛀牙，或是在放溝隙封填劑時藏在底下細菌的存活率，這些問題都有被注意到。對於缺乏故持性的表面，會影響到S. mutans是否會成功聚集在咬合面上，是很有趣的一點。有關於細菌這方面的爭議在這章節剩餘的部分會繼續討論。
Bacterial Leakage Beneath Sealants
In-vitro tests employing extracted teeth demonstrated minimal if any leakage of water-soluble dyes or radioactive compounds between the resin-enamel junction. These results indicated that the resin bound so intimately to the enamel surface that it effectively "sealed" off the underlying fissure surface from the oral environment. When this "seal" was challenged in vitro with a bacterial system however, bacteria had no difficulty in penetrating methyl-2-cyanoacrylate or bis-GMA sealants.
在溝隙封填劑下細菌的滲透
一個在口外的實驗，用水溶性的染料或具放射性化合物去測試拔下來的牙齒在樹脂牙釉質交界處是否有任何裂縫。這結果說明樹脂可以和牙釉質非常緊密的黏合，所以這樣可以緊密地將溝縫和口外環境隔絕起來。在體外實驗時，這個封閉性面對細菌系統是很具挑戰性的，然而細菌對於穿透甲基二氰基丙烯酸酯或bis-GMA溝隙封填劑沒有困難的。
Extracted molars were prepared so as to have an open connection between the occlusal fissure and the root apex. The occlusal end was then closed by the placing of a cyanoacrylate sealant. The teeth were embedded in plastic petri dishes in such a way that their crown surfaces were bathed in a medium inoculated with either S. mutans or F. nucleatum (acidogenic and nonacidogenic organisms, respectively), while their roots extended into a second petri dish containing sterile medium. Growth occurred in the sterile medium in 47 of 48 teeth, indicating that the sealant posed no barrier to bacterial penetration. This model because of the gravity drop between the fluid levels bathing the crowns and the roots introduced an unrealistic sink condition that would exploit any defects in the adequacy of the sealant-enamel bond.
有一實驗把拔下來的臼齒用來做在咬合溝縫上和牙根尖的一開放連結。在咬合面放上氰基丙烯酸酯的溝隙封填劑。並將牙齒浸泡在有蓋培養皿裡，且牙冠的部分是泡在含有S. mutans 或F. nucleatum的容易裡(分別是酸性和非酸性的細菌)。而牙根的部份則是浸泡在第二層的培養皿中，期中包含無菌的培養液。而在無菌培養皿裡48個有47個發現有生長，這結果指出溝隙封填劑並不能阻止細菌的穿透。因為在牙冠和牙根間培養液有受重力影響，這樣不像現實的下沉現象會發現溝細封填劑和牙釉質黏合的任何缺陷。
The system was modified by obturating the apices of the extracted teeth with epoxy resin so as to minimize the influence of hydrostatic pressures. Sterile endodontic paper points were aseptically placed in the pulp canals, covered with a cotton pellet and followed by the placement of a bis-GMA sealant. The teeth were placed, as before, in a medium inoculated with S. mutans and F. nucleatum. Forty two of 68 paper points were contaminated with the test organisms indicating that the tested adhesive resins were not sealants in the literal sense. However, the fact that in 26 teeth the paper points were sterile suggested that the sealants, while not a perfect barrier to bacterial penetration, were indeed a formidable barrier.
這系統藉由用樹脂來阻塞拔下來牙齒的根間孔，這樣是用來降低流體淨力的壓力。將消毒過的指針無菌地放入根管內，用棉花覆蓋起來，接著放入bis-GMA溝隙封填劑。接著將牙齒放在像之前一樣的培養液裡。68隻指針裡有42隻受到測試的細菌所感染，這表示受測試的樹脂並不是如實的溝係封填劑。然而實際上26隻消毒的指針指出溝隙封填劑對於細菌並不是一個完美的阻隔，但的確也可算上一傑出的阻隔。
Subsequent studies were performed in vivo using noncarious primary teeth that were within months of exfoliation. A narrow preparation, 3 mm long, 1 mm wide and 2 mm deep was made in the central groove of the occlusal surface and filled with sterile paper points in 23 teeth and with paper points saturated with the patient's saliva in 21 teeth. All experimental points were sandwiched between two sterile paper points to avoid direct contact with the sealant. The experimental teeth were extracted at four to 16-week intervals after application of the sealant. The teeth were disinfected, carefully entered from the pulp chamber and the experimental points aseptically removed and cultured. Nine of 19 points in which the point had been initially sterile and in which the sealant had been retained were still sterile at the conclusion of the experiment (Table 15-8). The average CFU count for the ten contaminated points was 11,600, but this count reflected primarily the contribution of one point with a count of 92,000 CFUs. From this data it would appear that bacterial leakage can occur in about half the teeth but that the amount of leakage is low judging from the magnitude of the bacterial recoveries. If the fluid which seeps in has the same bacterial density as saliva, i.e., 10,000,000 CFU/ml, then the cumulative volume which could account for 11,000 CFUs is only 0.1 ml.
接下來的實驗是在人體內進行，是利用在幾個月內脫落下未蛀的乳牙。在咬合面的中央溝上做出一狹長的修行，3釐米長，1釐米寬，2釐米深，在23顆牙齒上修行的窩洞內放消毒過的指針，在21顆牙齒上則用沾滿病人的口水指針。在實驗組裡的指針是放在兩個消毒過指針的中間，去避免和溝係封填劑接觸。而實驗組裡的牙齒是在放溝係封填劑後四到十六週後再拔除。而拔下來牙齒被消毒過，小心地從牙髓腔進入，而實驗的指針小心低被取出並培養細菌。十九個一開始就被消毒過的指針，其中有九個其溝隙封填劑仍維持在上面，在實驗結尾後仍是維持無菌的(表15-8)。十個受污染指針的平均菌落數是11,600 CFU，這樣的數據反映出每個指針上大約有92,000 CFU。從這資料裡可得知約一半的牙齒其細菌會滲透，但從細菌中重新再覆蓋的觀點來看，這樣滲透的量是很低的。若滲透進來的液體和唾液裡細菌的有相同的密度，換言之每毫升有10,000,000 CFU，則累積的量可以達到僅0.1毫升就有11,000 CFU。
It is possible that somewhat larger volumes than 0.1 ml penetrated the sealant-enamel interface, but that the amount of nutrients available for bacterial growth was so low that some bacterial cells could not survive, let alone grow. This was suggested by the second experiment in which 18 paper points were inserted after they had been purposely contaminated with saliva to the extent that they contained about 733,000 CFUs (Table 15-8). When these points were examined after being in vivo beneath the sealant for 30 to 73 days, nine points showed a decrease in bacterial counts and two of these were sterile. This would indicate that the available nutrients were barely able to sustain the size of the initial inoculum.
對於稍微大於0.1毫升是可能滲入溝隙封填劑和牙釉質的交界面，但是對於剩餘可供細菌生長的養分是很低的，有時低到有些細菌細胞不可生存，更別說生長了。這一點可被第二個實驗證實，當18個指針被口水故意污染再放入，內含有733000 CFU。當這些指針在放入口中後，在溝係封填劑下30到73天，九個指針在細菌量上有減少，有兩個仍是無菌。這顯示出剩餘的養分幾乎可以維持一開始接種的量。
These bacterial studies demonstrate that some leakage occurred in about half the sealant-treated teeth, but that the magnitude was so low as to make questionable its biological significance. This incidence of leakage is probably no more than occurs with any dental restorative material. However, the question has been raised as to whether if incipient lesions were present, would this leakage sustain further bacterial growth and enlargement of the lesion. The answer appears to be no, as will be discussed in the next section.
這些細菌的研究顯示出部分的滲漏是發生在約一半有放溝隙封填劑的牙齒。但所改變的量是非常低，在生物重要性上是一個疑問。這樣的滲漏可能是不會發生在任何填補的材料上。然而，不知是否出初期蛀牙是否存在是一問題，是否滲露是否會讓更多的細菌生長，並將病炤擴大。這答案是否定的，會在下個部份來討論。
Survival of Bacteria Beneath the Sealant
In the previous study (Table 15-8) a small Class I cavity preparation was filled with contaminated paper points prior to being covered by an occlusal sealant. The topography of the cavity preparation bore little resemblance to the fissure surface and while the bacterial levels tended to decrease, this could have been an artifact due to the inability of paper points to provide the same nutritive support as the enamel. These objections have been eliminated by studies in which carious teeth were covered with a sealant, and by a study which used a modification of the artificial fissure model (See "Fissure Colonization" in Chap. 6). In this latter investigation, Theilade et al. removed blocks of enamel containing the occlusal fissure from unerupted third molars and inserted them into specially-prepared recesses in occlusal amalgam fillings. The molar fissures were allowed to become colonized by the oral flora and then some were sealed with an adhesive resin. Immediately thereafter both the sealed and unsealed molar fissures were removed and cultured. The viable anaerobic count in the sealed teeth was reduced about 50-fold compared to the unsealed teeth. This killing effect was attributed to the 50 percent phosphoric acid solution used to condition the enamel surface. The ultraviolet light used for sealant polymerization probably had no antibacterial effect because penetration was unlikely beyond the thickness of the sealant. Thus the procedures used to apply the sealant will exert a marked antibacterial action upon the organisms embedded in the fissure.
在溝隙封填劑下細菌的存活
在前一個實驗裡(15-8)，Class I 窩洞裡在放溝隙封填劑前放入受污染的指針。而修行的窩洞和溝縫是很相似的，而當細菌量是傾向降低的，這有可能會是加工的因素，因為指針不能像牙釉質一樣供應相同的營養。而這樣的缺點以被本實驗中有放溝隙封填劑給消除，還有另一實驗中用人造溝縫的模型(可見第六章”溝縫處的菌落”)。在後者的實驗中，Theiland 等學者移除未萌發的第三大臼齒上部份牙釉質包含咬合面的溝縫，將他們放入在咬合面上汞齊填補處特製的一個地方。而臼齒的溝縫有口內細菌的聚集，有部分牙齒是用樹脂將溝縫封閉起來。在封閉或是沒封閉的臼齒被立刻移除且被培養。在封閉牙齒上無菌細菌的數量是未封閉牙齒降低的50倍。而用於將溝係封填劑聚合的紫外光可能是沒有抑菌的效用，因為紫外光的穿透力是不可能透過溝縫的厚度。因此這樣放溝隙封填劑的步驟會對於藏在溝縫裡的細菌有很大抑制的效用。
The studies involving the placement of sealants over carious lesions demonstrated a definite decline in bacterial viabilities over time that would be independent of the acid etch procedure. Handelman et al. in two separate studies showed that both an ultraviolet polymerizing and an autopolymerizing bis-GMA sealant caused about a 1000-fold reduction in bacterial counts per mg of carious dentin (Table 15-9). The study involving the autopolymerizing sealant Delton“ extended only one month and included unsealed control teeth that had or had not been acid etched. The acid etch reduced the bacterial counts four-fold, but the sealant decreased the counts 35-fold after one to two weeks, and 925-fold after one month. When the ultraviolet polymerized sealant was used, the counts decreased 20-fold after one to two weeks, l95-fold after six months and about 1900-fold after 24 months (Table 15-9). The longer the sealant remained in place the lower the bacterial counts became. The bacterial density of 600 bacteria per mg of dentin observed after 24 months was extremely low, being approximately one millionth the bacterial density found in plaque. The amount of metabolic activity that this small level of bacteria could muster would be minuscule compared to plaque and would be more comparable to that of sterile tissue. Thus it was no surprise that the clinical appearance of this formerly carious dentin was dry and leathery, resembling the texture of an arrested carious lesion.
在蛀牙上放溝係封填劑表現出細菌量上的下降，這和酸蝕的步驟是獨立的。Handelman等人在兩個不同的實驗中顯示出用紫外光聚合或是自行聚合的bis-GMA溝係封填劑，造成在蛀牙牙本質的每毫克細菌量約減少一千倍(表15-9)。這實驗包含自行聚合的溝係封填劑Delton，只維持了一個月，並包含那些有或是沒有被酸蝕的未封閉牙齒。而酸蝕降低四倍的細菌量。而溝隙封填劑經一到兩個禮拜會降低細菌量35倍，而過一個月後會降低925倍的細菌量。當使用紫外光聚合的溝係封填劑時，經一到兩個禮拜會降低細菌量20倍，而過六個月後會降低細菌量195倍，過兩年後則將低1900倍(表15-9)。當封閉劑停留在牙齒上月久，則得到的細菌數越低。在經兩年後牙本質的細菌密度是每毫克600隻，這是非常低，大約是在聚落裡所得細菌量的百萬分之一。這樣微小的細菌和聚落的細菌量比較起來是渺小的，而這樣的量是比較能和無菌的細菌量做比較。而且臨床上這些之前形成的蛀牙是乾燥且向皮革般的，和那已停止的蛀牙病炤的質地是相似的。
The arrest of dentinal decay after being covered with a sealant was shown by Going et al. Teeth that were clinically carious or suspected to be carious had been sealed in 1972 with a single application of an ultraviolet polymerized bis-GMA sealant. In 1977 the carious and bacteriological status of these fissures was evaluated. The fissure site was carefully encircled by drilling and then an islet of tooth structure containing the fissure plus associated dentin was fractured off, weighed and immediately cultured. The remaining dentinal surface was examined for caries status Of 30 occlusal sites judged in 1972 to be either carious (18 sites) or suspected to be carious (12 sites), only four were deemed to be carious in 1977 (Table 15-10). Of 21 control sites judged in 1972 to be either carious (7 sites) or caries free (14 sites), all were carious in 1977 (Table 15-10). Thus the sealant had arrested caries in 87 percent of the previously carious surfaces, at the same time that the control teeth in the same mouth were developing new decay.
由Going等人有研究用溝係封填劑去覆蓋以停止的牙本質蛀牙。這些牙齒在臨床上評估為蛀牙或是疑似蛀牙，在1972年時，單次用紫外線聚合的bis-GMA溝係封填劑將牙齒封閉起來。等到1977年再去評估這些牙齒溝縫裡蛀牙及細菌分布的情況。在溝縫處用鑽針將含有溝縫和牙本質的齒質小心地分切割來，秤重並立即培養細菌。檢查剩餘齒質的蛀牙狀況。在1972年有放溝係封填劑的30顆牙齒，其中被認定18顆被任定為有蛀牙，12顆為疑似蛀牙。到1977回診時只有四顆有蛀牙 (Table 15-10)。在1972年沒放溝隙封填劑的21顆牙齒，其中被認定7顆被任定為有蛀牙，14顆為無蛀牙。到1977回診時全部都有蛀牙 (Table 15-10)。因此溝隙封填劑可以抑制８７％的咬合面蛀牙，而同個時間在對照組上卻是有蛀牙在發生。
The bacteriological findings confirmed the clinical diagnosis. In 9 of 18 teeth judged to be carious in 1972, no bacteria could be cultivated in 1977. Six of 12 teeth suspected of being carious in 1972, were also found to be sterile in 1977 (Table 15-10). No sterile teeth were found among the unsealed teeth. The 14 actively carious teeth in the control group in 1977 had significantly more bacteria per mg of dentin than any of the other groups, including the four carious teeth in the sealant group (Table 15-10). This suggested that while these four teeth were still considered to be carious, they could well be in a transition stage on their way to caries arrest.
從細菌分布上也證實其臨床診斷。在1972年18顆被認定為蛀牙的牙齒，其中9顆到1977年未有細菌生存。在1972年12顆被認定疑似為蛀牙的牙齒，其中6顆到1977年仍是無菌的(表 15-10)。在未封閉的牙齒上不能找到沒有無菌的牙齒。在控制組裡14顆有活耀蛀牙的牙齒，到了1977年，每毫克的牙本質比起其他組有顯著更多的細菌，包含在溝隙封填劑組的那四顆牙齒也有相同的狀況(表 15-10)。這也表示這四顆牙齒仍被認定為有蛀牙，可以說是在轉換的過程中朝向蛀牙停止caries arrest的方向進行。
These studies, in which carious teeth were purposely sealed with an adhesive resin, indicate that if leakage occurs, the amount of nutrients that become available to these buried bacteria is so minimal that bacterial viability in most instances cannot be sustained. In fact, the nutrient supply may be even less than that which can occur when sealants are placed on caries-free surfaces, because of the increased retention of the sealant to the caries-demineralized enamel. Over time the bacterial counts drop to such low levels that an acid metabolism capable of continued tooth demineralization ceases and the decay arrests. In many instances the majority of the bacteria die, as is illustrated in Figure 15-3. Thus instead of concern over continued progression of the carious lesion beneath the sealant, the reality appears to be that the sealant can abort this progression and actually lead to caries arrest. The improved retention of the sealant on a carious surface plus the decreased viability of the bacteria in the carious lesion suggests that sealants may have some therapeutic applications.
這些研究裡，蛀牙的牙齒以樹脂封閉起來，若是有漏洞發生，則可以供給給底下細菌的營養量是很有限的，所以細菌在大部分的情況下是不能生存的。事實上，可供給的營養會比在無蛀牙表面上放上溝隙封填劑來得更少，因為溝隙封填劑在去礦物質的牙本質固持力上會增加。
經過一段時間細菌量掉至一個較低的基準時，酸蝕會造成牙齒脫鈣的狀況停止而且蛀牙也趨於停緩的狀態。在大多數情況下，如圖15-3所示，大部分的細菌已死亡。事實上溝隙封填劑可以將蛀牙過程中斷使蛀牙停止。因著封填劑在蛀牙表面上固持力的增加，加上變少的細菌量，可以說溝隙封填劑有治療的用途。
Change in S. mutans Percentages on Sealant-Treated Occlusal Surfaces
The placement of the sealant over the fissure changes the topography of the occlusal surface from one which provides retentive sites for bacterial colonization, to one in which the surface is relatively smooth and has great access to the saliva. Under these conditions the micro-environment on the occlusal surface might not select for S. mutans. We have cultured occlusal fissures in children participating in the Ypsilanti study (Table 13-11) before and after the placement of an ultraviolet polymerized sealant. These treated children were also given restorative dental treatment and periodic topical fluoride applications, whereas the untreated group received none of these modalities. Thus if a difference existed between the treated and untreated groups in regard to S. mutans proportions, it would not be possible to assign this difference to the sealants alone. However when the groups were compared, after eight and 12 months there was no apparent difference in the percent of S. mutans found in plaque samples taken from the sealant-enamel margin (Table 15-11). By 12 months the S. mutans/S. sanguis ratio had increased in the untreated group suggesting that an acidic environment had selected for S. mutans at the expense of S. sanguis.
在溝隙封填劑處理過咬合面S. mutans百分比的變化
溝隙封填劑的放置改變了咬合面的型態，將有溝縫易讓細菌群聚的地方改變成相對較平滑且口水有較大的接觸。在這樣的狀況下，咬合面可能不會有S. mutans存在。在Ypsilanti 研究裡(表13-11)，我們收集在放封填劑前、後咬合面溝縫的細菌。這些有放封填劑的小朋友同時給予補牙及定期局部塗氟，然而未放封填劑組則未接受任何治療。因此這兩組若有關於S. mutans比例上的不同，不會是僅僅和有無放溝隙封填劑有關。然而經過8和12個月後，從封填劑和牙釉質邊緣取出的S. mutans細菌量並無顯著的不同(表 15-11)。 經過12個月後，S. mutans/S. sanguis比例在未治療組裡是增加的，顯示出酸性環境對於S. mutans是有利的。
These finding indicate that the conditions which promoted S. mutans colonization on the treated children's teeth had not been appreciably changed by the various treatment modalities used. Some variable(s) other than fissure-retentive sites was operating in regard to S. mutans colonization in these patients. This could be sucrose availability. Despite the persistence of S. mutans on the sealant-treated teeth, the treated children experience a caries reduction of about 70 percent on the occlusal surfaces compared to the untreated group.。Obviously microbial metabolic activity on the sealant surface has very little demineralizing activity due to the barrier function of the sealant and the availability of the salivary protective functions.
這個結果表示會使S. mutans 聚集在治療過的牙齒表面上增加的情況，並不會經由改變治療的形式而增加。有些變異除了有關S. mutans聚集的溝縫處。也有可能是有過多的蔗糖。除了S. mutans持續在有封填劑處理過牙齒上，治療過的小朋友比起未治療有70%咬合面蛀牙的下降。明顯地可看出細菌在封填劑表面只有些微去礦物質化作用，因為封填劑的阻隔功能還有唾液有保護的功能。
Sealant Evaluation
The sealants represent a major breakthrough in the preventive treatment of caries-prone retentive surfaces such as pits and fissures. Leakage beneath the sealant is minimal and not adequate to sustain bacterial viability of most organisms left beneath the sealant. Because of this nutrient blockage phenomenon, the sealant apparently can be placed over incipient fissure lesions without causing progression of the lesion. In fact, the lesions tend to arrest, and the numbers of surviving bacteria in the lesion approach zero with time. (Obviously in such a situation the tooth should be carefully followed radiologically). Cariogenic organisms can colonize the sealant surface, but their acid waste products are unable to penetrate the sealant and therefore do not cause tooth demineralization.
封填劑的評估
封填劑在易蛀牙區域(如溝縫)上的預防治療是一大突破。在溝縫下的漏洞是很小的，並不會讓底下的細菌維持生存。因為隔絕營養的來源，封填劑可以放在起初的蛀牙上且不會讓蛀牙在發展。事實上，蛀牙傾向停止，在病灶上細菌的存活量趨於零(因此在這個情況下牙齒必須用x光片定期追蹤觀察)。易蛀牙的細菌可以聚集在封填劑的表面，但是其產酸的廢物卻不能透過溝隙封填劑，因此不會造成牙齒去礦物質化。
SUMMARY
Mechanical debriding procedures such as brushing and flossing were unable to reduce caries incidence when performed by patients under supervision. These debriding procedures were able to reduce plaque and gingivitis scores, indicating that the failure to reduce decay was not due to the patient's inability to debride those tooth surfaces of their supragingival plaque. Rather the failure reflects the weakness of the NSPH's main contention that plaque mass per se is the prime etiologic agent in caries development. In fact, an argument can be made that flossing and brushing can be counterproductive in caries prevention in that they can serve as a vehicle for the spreading of an S. mutans infection about the dentition. However, if the mechanical debridement is rigorously applied, as was done by professional personnel either by daily flossing or frequent tooth cleanings with rotary dental turbines, then caries can be reduced. In these instances, the thoroughness of the debriding apparently can change a cariogenic plaque to a noncariogenic plaque by repeatedly selecting for rapid plaque-forming organisms and discriminating against those species like S. mutans, which need a stagnant environment in order to gain ascendancy. Part of the success of the Karlstad and Danish professional cleaning studies can be explained in this manner. Studies which employ sealants are successful because they remove caries-prone sites from colonization and exploitation by aciduric organisms. Organisms left beneath the sealant are effectively cut off from their nutrient supplies and tend to die off.
結論
機械性移除方法如刷牙、用牙線是由病人在監督下使用不能降低蛀牙。這些移除方法可以減少plaque和gingivitis score，所以不能降低蛀牙不是因為病人無法將牙齦上的plaque清潔乾淨。因此這樣的失敗指出NSPH的缺失，plaque mass per se對於蛀牙發展是很重要的。
事實上有爭議認為牙線和刷牙會造成將S. mutans傳遞出去的媒介。然而，若機械性移除被嚴厲執行，就像是由專業人員每天用牙線和經常的使用rotary器械，蛀牙會下降。以這些例子來說，完整的清除，可以明顯的將易蛀牙的plaque改變為不易蛀牙的plaque，經由反覆選擇快速形成plaque的微生物，並區辨S. mutans需要遲鈍的環境以取得優勢。
Karlstad 和Danish的專業潔牙研究有成功可以用下面來解釋。封填劑的成功是因為他們移除易蛀牙的區域，有酸性細菌群聚。對於在封填劑下的微生物很有效的切斷其養分來源，然後就會死亡。
Mechanical procedures that are frequently applied by dental personnel can be caries preventive, but this labor intensive approach is expensive. In the following chapters we will examine preventive treatment strategies and tactics which are inherently less costly.
機械性清潔方法經常被牙科來做蛀牙預防的動作，但是這樣卻是很貴。在接下來的章節裡會介紹一些較省錢的方法
Preventive treatment by the dentist in the United States consists, at least as is reported for income purposes (Table 13- 8), primarily of annual or biannual tooth cleanings administered by the hygienist. As this procedure, when given to children, is often followed by topical application of fluorides, the caries preventive efficacy of the mechanical component cannot be assessed. However, one may deduce that an annual cleaning in the absence of fluoride will not be a particularly effective preventive caries procedure. In particular, there is the potential to select in the recolonization process for organisms buried within pits, fissures and other inaccessible anatomic sites. This has been beautifully demonstrated by means of scanning electron photomicrographs taken at various intervals following a dental cleaning. In Figure 15-1A a tooth surface containing a crack is shown immediately after a dental prophylaxis. No bacteria are observed on the flat tooth surfaces nor on the visible walls of the crack. However, four hours later a line of dense microbial growth is observed along the entire length of the crack (Fig. 15-1B). The appearance of the growth indicates that the bacteria left behind in the crack had quickly recolonized the vicinity of the crack and had established dominance in that site. If these bacteria contained S. mutans, then a cariogenic plaque was selected for. If these bacteria contained noncariogenic organisms, then a noncariogenic plaque would occupy this caries-prone site and could serve to exclude cariogenic organisms from the niche. The identity of the recolonizing bacteria thus would be decisive in determining the eventual caries outcome of the site. If the professionally administered mechanical debriding procedures are repeated at two or three-week intervals and are supplemented with a fluoride paste as was done in the Karlstad studies (Fig. 13-3, Table 13-11), there is the possibility that the fluoride could sterilize or greatly reduce the number of organisms left behind in pits, fissures and cracks. In this event, recolonization of these retentive sites would come from organisms in the saliva and would lead to a repopulation of these caries-prone sites with noncariogenic organisms, as was illustrated in Figure 14-1. If this is so, then fluoride was essential for the efficacy of these Swedish studies.
專業潔牙
對美國的牙醫師而言，預防治療是建議一年有一次到兩次的專業潔牙，這樣潔牙動作是讓衛教師來執行，有報導部分是基於收入的因素。這樣的專業潔牙到最後都會給與局部塗氟，用這種機械方法來預防蛀牙的效率是不可被評估的。然而，可能會有人說這樣專業潔牙若不給以氟，不會被視為一有效的預防蛀牙方法。特別來說，藏在溝縫裡或是其他不可接觸的地方，對於細菌而言是有潛力可以去選擇再次聚集的過程。這可以經由在潔牙時不同階段所拍攝的微電子照片美麗地呈現出來。如圖15-1，牙齒經過專業潔牙後可看出有一個裂縫，在平滑表面或是裂縫的強壁上都未發現任何細菌。然而經過四小時後，在整條縫隙處可見密集地細菌成長，可見圖15-1 B。被藏在縫隙裡的細菌很快地又再次聚集成菌落，並且成為此處的主要菌落者。若這些細菌包含S. mutans，則這些形成的菌落會是易蛀牙的細菌。若這些細菌包含的是非蛀牙性細菌，則非蛀牙細菌則會佔滿這容易蛀牙的地方，並排除那些易蛀牙的細菌。所以再次聚集細菌的種類會是決定這地方是否蛀牙重要因素。在Karlstand 所做的研究，每兩到三個禮拜所做的專業機械性潔牙並佐用氟膏，研究顯示氟可以消毒或是大量地減少在溝縫、或裂痕裡的細菌。在這個事件裡，重新聚集在這些地方的細菌是從唾液中來的，在這些容易引起蛀牙的地方重新聚集非蛀牙的細菌，像圖14-1所示。若真如這個所說，對於這些瑞典研究所顯示，氟是最重要的。
A Danish group consisting of Poulsen, Agerbaek, Melsen, Glavind and their colleagues have conducted a series of clinical experiments in which the various components of the Karlstad regimen have been isolated and individually studied. They observed that oral hygiene instructions and dietary and bacteriological information had no effect on caries reduction (Table 15-2). In a separate study they evaluated the effect that frequent toothcleaning using a nonfluoridated paste would have on caries increment. Seven-year-old children were stratified according to the presence or absence of smooth-surface lesions and then children within each of the two strata were randomly assigned to an experimental and a control group. The experimental group was given careful professional cleaning of the teeth every second week during the two years of the study. Both groups received biweekly 0.2 percent sodium fluoride rinses and were given complete restorative dental treatment before the baseline examinations and another course of treatment at six-month intervals.
有一群丹麥研究員包含Poulsen, Agerbaek, Melsen, Glavind和其他成員進行了以Karlstad研究裡不同的因素應被隔離或是個別研究進行的一系列實驗。他們發現口腔衛教、飲食還有細菌的資訊對於降低蛀牙是不會有幫助(表15-2)。在另一個實驗中他們評估經常用不含氟的牙膏刷牙對於蛀牙的增加率。一群七歲的小朋友以有無平滑面的蛀牙病炤來分層，所以當小朋友有在兩層以下的就被平均分配到實驗組和控制組。在這兩年的實驗中，實驗組每兩個禮拜就給予專業潔牙一次。這兩組每兩個禮拜都給予0.2%鈉化氟的漱口水。而且在實驗開始前所有蛀牙都有填補，且每六個禮拜會定期檢查。
After one year the experimental group averaged one less decayed permanent surface than the control group, and after two years the experimental group had 1.7 fewer decayed surfaces (Table 15-6). This difference was low compared to the reduction of 5.5 surfaces observed after two years in the seven to eight-year-old children treated by the Karlstad regimen (Fig. 13-3). These findings indicate that repeated professional cleaning with a nonfluoridated paste decreased caries incidence, but that the treatment effect is only about 30 to 40 percent of that which was obtained when a fluoridated paste and motivational programs were also used. Motivational programs by themselves were without a noticeable treatment effect (Table 15-2), whereas topical fluorides alone yielded about a 70 percent reduction (See Table 18-8). This would suggest that the dramatic success of the Swedish studies had both a fluoride and a mechanical component. The fluoride most likely, via its antimicrobial and remineralizing actions, enhanced the ability of the mechanical debriding procedures to change the plaque flora from a cariogenic to a nondisease-associated flora (See "Fluoride" in Chap. 18).
經過一年後，實驗組在恆牙上蛀洞的面比起控制組平均少一面。過兩年後，實驗組則少1.7面(見表15-6)。這樣的差距比起Karlstad研究裡，觀察七到八歲的小朋友共兩年，降低5.5面的蛀牙所得的數據是些微的(圖13-3)。這樣觀察的結果是指使用不含氟的牙膏反覆潔牙是會降低蛀牙發生率。但是有用含氟牙膏和提高行動力下，其治療較率只有百分之三十到四十。提高行動力並不會有影響不同的治療結果(表15-2)；然而局部圖氟給予百分之七十的蛀牙降低率(表18-8)。這樣結果表示在瑞典研究裡用氟和機械性方法造成引人注目的成功，這是因為氟藉由抵抗微生物再礦化的作用，進而增加機械性移除的程序，並將這群菌落由蛀牙細菌改變成不會造成細菌的組合。
SEALANTS
The occlusal fissures are the most caries-prone sites in the dentition (Table 11-1). The bacteria contained therein subside into a micro-environment which is virtually inaccessible to mechanical debriding procedures (Figure 15-2). In the 1920s Hyatt recommended eradication of fissures by replacing them with Class I amalgam restorations, and Bodecker advocated reshaping of the fissure morphology to produce wide, non-retentive, self-cleaning grooves. In the latter procedure, called a prophylactic odontotomy, there was the problem that the extreme depths of some fissures would lead to dentinal exposures during the reshaping process. Neither procedure was subsequently adapted because of its invasive nature and its cost effectiveness relative to the placement of a dental restoration only after caries had developed. However, these procedures conceptualized a valid treatment strategy in preventive dentistry, namely the recontouring of the fissure anatomy, that was to become a reality in the 1970s with the introduction of plastic sealants. Only now the recontouring was achieved by an onlay of an adhesive resin which occluded the natural fissures so as to provide, in plastic, the same wide, non-retentive grooves that Bodecker recommended.
溝隙封填劑
在牙齒表面的縫隙是最容易蛀牙的地方(表11-1)。藏在溝縫裡的細菌是不可經由機械性移除的過程而被清除(圖15-2)。在1920年代，Hyatt建議以Class I 汞齊填補的方式來移除溝縫。Bodecker則提倡將溝縫的形狀重新塑形成較寬、無故持性，可以自行清潔的溝縫。在Bodecker的發法裡，又稱作預防性修行齒質，若有個極深的溝縫經過重新塑形後有可能會造成牙本質的暴露，這會造成問題。不管這些步驟是因為其侵略性的特質，或是在蛀牙發生後放上牙科填補材料之成本效益的考量。然而，這些步驟將在預防醫學有效的治療方法概念化，重新塑形溝縫，在1970年代開始有溝隙封填劑的引進。只有在現，用有黏性的樹脂做為一嵌體，封閉溝縫來重新塑形。
The technical knowledge of polymer chemistry which led to the development of the cyanoacrylates, polyurethanes and bisphenol A-glycidyl methacrylates (bis-GMA) plastics for clinical usage in dentistry are beyond the scope of this monograph. Suffice it to say that complex problems dealing with the binding of the resin to the inorganic tooth structure, control of setting time and exclusion of an aqueous environment have been solved to the extent that two generations of bis-GMA sealants have been evaluated clinically and been found to significantly reduce decay on fissure surfaces. The ability of these resins to reduce decay was initially demonstrated by Buonocore in a study in which a single application of bis-GMA was applied to one member of a contralateral pair of either permanent or primary teeth. The teeth were carefully dried and after pretreatment with a phosphoric acid etching solution, the adhesive was painted onto the fissure and then its polymerization was activated by means of an ultraviolet light. After either one or two years in vivo, the sealant was removed and the caries status of the underlying surface was determined and compared to the unsealed control teeth.
In plastic由Bodecker所介紹同樣較寬、無故持性的溝縫。
在化學上聚合物的知識增加，進而發明了氰基丙烯酸酯、聚氨酯和雙酚甲烷甘油基甲基丙烯酸酯(bis-GMA)塑膠，這些在牙科臨床上的運用遠超過此篇所討論的範圍。已有足夠能力去處理將樹脂黏到無機牙齒的表面，控制行成時間，並排除含水的環境，隨著這些問題的克服以有兩代的bis-GMA溝隙封填劑已在臨床運用評估過，且成功地降低溝縫的蛀牙。這些樹酯可降低蛀牙的發生，最先被Buonocore在研究中發現，將bis-GMA塗一次在任一恆牙或乳牙上。牙齒很小心被吹乾，接著用磷酸酸蝕，再塗上adhesive，接著用紫外光聚合。經過在人體一年或兩年的時間，溝隙封填劑被移除，來評估其下面的蛀牙，並和未封閉的牙齒來比較。
In the permanent teeth the adhesive was retained on all surfaces after one year and on 87 percent after two years (Table 15-7). The adhesive was not as well retained on the primary teeth. This was attributed to the prismless enamel layer found on these teeth which apparently did not dissolve upon acid etching, thereby preventing the formation of interprismatic voids which could be occupied by the resin. After two years only one sealant-treated permanent tooth had become carious, whereas 68 of 113 or 60 percent of the control teeth had become carious (Table 15-7). Over the same time period two sealant-treated primary teeth had become carious compared to 15 control teeth (Table 15-7).
在經一年後黏著劑仍全部保存在所有的恆牙牙齒表面上，經兩年後剩百分之87(表18-7)。黏著劑也沒有完全保存在乳牙表面上。這是因為牙齒上的無錐狀體的牙釉質，在酸蝕時沒有被溶解，如此就無法和樹脂形成錐體間的裂縫(interprismatic voids)。經兩年後只有一顆購隙封填劑處理的恆牙有蛀洞，然而在控制組中，113個牙齒中有68顆，或是百分之六十有蛀牙(表15-7)。經過相同的時間，有兩顆放有溝隙封填劑的牙齒有蛀牙，而控制組則是15顆。
Reductions in dental decay of this magnitude are impressive and have ushered in an era where preventive treatment of occlusal fissure decay is a distinct reality. However, other investigators have not achieved the same degree of success with sealants and have raised important practical questions concerning the retention of the sealant and the cost benefit of a procedure that requires exacting clinical conditions in regard to the dryness of the operating field, and which may need to be repeated several times during the caries-prone years of the patient. The great success of the Ypsilanti study in reducing occlusal fissure decay probably was related to the repeated applications of the sealant as needed (Table 13-12), but this vigilance contributed appreciably to the cost of the study.
溝隙封填劑這樣大量地降低蛀牙是令人印像深刻的，並帶領我們進入溝隙封填劑可以有效預防咬合面的蛀牙時代。然而其他的研究結果並不能完全達到這樣一般的成功率，並且還有許多實際的問題，如有關溝隙封填劑的故持力，還有在臨床操作上為了要保持有個乾燥的工作區域所需的成本效益，或是對於高蛀牙率的牙齒會需要重複治療。在Ypsilanti研究裡，在降低咬合面溝縫的蛀牙有很高的成功率，是因為能重複地放置溝隙封填劑(表13-12)，但這樣會影響到整個實驗的花費。
Some have raised questions concerning leakage along the sealant-enamel margin that could lead to decay beneath the sealant, as well as questions concerning the survival of the bacteria that were left beneath the sealant during placement. It would also be of interest to know whether the absence of a retentive surface had any effect on the ability of S. mutans to successfully colonize the occlusal surface. These bacteriological issues will comprise the remaining sections of this chapter.
有關溝隙封填劑和牙本質的交界可能會產生裂縫，並可能會在封填劑下產生蛀牙，或是在放溝隙封填劑時藏在底下細菌的存活率，這些問題都有被注意到。對於缺乏故持性的表面，會影響到S. mutans是否會成功聚集在咬合面上，是很有趣的一點。有關於細菌這方面的爭議在這章節剩餘的部分會繼續討論。
Bacterial Leakage Beneath Sealants
In-vitro tests employing extracted teeth demonstrated minimal if any leakage of water-soluble dyes or radioactive compounds between the resin-enamel junction. These results indicated that the resin bound so intimately to the enamel surface that it effectively "sealed" off the underlying fissure surface from the oral environment. When this "seal" was challenged in vitro with a bacterial system however, bacteria had no difficulty in penetrating methyl-2-cyanoacrylate or bis-GMA sealants.
在溝隙封填劑下細菌的滲透
一個在口外的實驗，用水溶性的染料或具放射性化合物去測試拔下來的牙齒在樹脂牙釉質交界處是否有任何裂縫。這結果說明樹脂可以和牙釉質非常緊密的黏合，所以這樣可以緊密地將溝縫和口外環境隔絕起來。在體外實驗時，這個封閉性面對細菌系統是很具挑戰性的，然而細菌對於穿透甲基二氰基丙烯酸酯或bis-GMA溝隙封填劑沒有困難的。
Extracted molars were prepared so as to have an open connection between the occlusal fissure and the root apex. The occlusal end was then closed by the placing of a cyanoacrylate sealant. The teeth were embedded in plastic petri dishes in such a way that their crown surfaces were bathed in a medium inoculated with either S. mutans or F. nucleatum (acidogenic and nonacidogenic organisms, respectively), while their roots extended into a second petri dish containing sterile medium. Growth occurred in the sterile medium in 47 of 48 teeth, indicating that the sealant posed no barrier to bacterial penetration. This model because of the gravity drop between the fluid levels bathing the crowns and the roots introduced an unrealistic sink condition that would exploit any defects in the adequacy of the sealant-enamel bond.
有一實驗把拔下來的臼齒用來做在咬合溝縫上和牙根尖的一開放連結。在咬合面放上氰基丙烯酸酯的溝隙封填劑。並將牙齒浸泡在有蓋培養皿裡，且牙冠的部分是泡在含有S. mutans 或F. nucleatum的容易裡(分別是酸性和非酸性的細菌)。而牙根的部份則是浸泡在第二層的培養皿中，期中包含無菌的培養液。而在無菌培養皿裡48個有47個發現有生長，這結果指出溝隙封填劑並不能阻止細菌的穿透。因為在牙冠和牙根間培養液有受重力影響，這樣不像現實的下沉現象會發現溝細封填劑和牙釉質黏合的任何缺陷。
The system was modified by obturating the apices of the extracted teeth with epoxy resin so as to minimize the influence of hydrostatic pressures. Sterile endodontic paper points were aseptically placed in the pulp canals, covered with a cotton pellet and followed by the placement of a bis-GMA sealant. The teeth were placed, as before, in a medium inoculated with S. mutans and F. nucleatum. Forty two of 68 paper points were contaminated with the test organisms indicating that the tested adhesive resins were not sealants in the literal sense. However, the fact that in 26 teeth the paper points were sterile suggested that the sealants, while not a perfect barrier to bacterial penetration, were indeed a formidable barrier.
這系統藉由用樹脂來阻塞拔下來牙齒的根間孔，這樣是用來降低流體淨力的壓力。將消毒過的指針無菌地放入根管內，用棉花覆蓋起來，接著放入bis-GMA溝隙封填劑。接著將牙齒放在像之前一樣的培養液裡。68隻指針裡有42隻受到測試的細菌所感染，這表示受測試的樹脂並不是如實的溝係封填劑。然而實際上26隻消毒的指針指出溝隙封填劑對於細菌並不是一個完美的阻隔，但的確也可算上一傑出的阻隔。
Subsequent studies were performed in vivo using noncarious primary teeth that were within months of exfoliation. A narrow preparation, 3 mm long, 1 mm wide and 2 mm deep was made in the central groove of the occlusal surface and filled with sterile paper points in 23 teeth and with paper points saturated with the patient's saliva in 21 teeth. All experimental points were sandwiched between two sterile paper points to avoid direct contact with the sealant. The experimental teeth were extracted at four to 16-week intervals after application of the sealant. The teeth were disinfected, carefully entered from the pulp chamber and the experimental points aseptically removed and cultured. Nine of 19 points in which the point had been initially sterile and in which the sealant had been retained were still sterile at the conclusion of the experiment (Table 15-8). The average CFU count for the ten contaminated points was 11,600, but this count reflected primarily the contribution of one point with a count of 92,000 CFUs. From this data it would appear that bacterial leakage can occur in about half the teeth but that the amount of leakage is low judging from the magnitude of the bacterial recoveries. If the fluid which seeps in has the same bacterial density as saliva, i.e., 10,000,000 CFU/ml, then the cumulative volume which could account for 11,000 CFUs is only 0.1 ml.
接下來的實驗是在人體內進行，是利用在幾個月內脫落下未蛀的乳牙。在咬合面的中央溝上做出一狹長的修行，3釐米長，1釐米寬，2釐米深，在23顆牙齒上修行的窩洞內放消毒過的指針，在21顆牙齒上則用沾滿病人的口水指針。在實驗組裡的指針是放在兩個消毒過指針的中間，去避免和溝係封填劑接觸。而實驗組裡的牙齒是在放溝係封填劑後四到十六週後再拔除。而拔下來牙齒被消毒過，小心地從牙髓腔進入，而實驗的指針小心低被取出並培養細菌。十九個一開始就被消毒過的指針，其中有九個其溝隙封填劑仍維持在上面，在實驗結尾後仍是維持無菌的(表15-8)。十個受污染指針的平均菌落數是11,600 CFU，這樣的數據反映出每個指針上大約有92,000 CFU。從這資料裡可得知約一半的牙齒其細菌會滲透，但從細菌中重新再覆蓋的觀點來看，這樣滲透的量是很低的。若滲透進來的液體和唾液裡細菌的有相同的密度，換言之每毫升有10,000,000 CFU，則累積的量可以達到僅0.1毫升就有11,000 CFU。
It is possible that somewhat larger volumes than 0.1 ml penetrated the sealant-enamel interface, but that the amount of nutrients available for bacterial growth was so low that some bacterial cells could not survive, let alone grow. This was suggested by the second experiment in which 18 paper points were inserted after they had been purposely contaminated with saliva to the extent that they contained about 733,000 CFUs (Table 15-8). When these points were examined after being in vivo beneath the sealant for 30 to 73 days, nine points showed a decrease in bacterial counts and two of these were sterile. This would indicate that the available nutrients were barely able to sustain the size of the initial inoculum.
對於稍微大於0.1毫升是可能滲入溝隙封填劑和牙釉質的交界面，但是對於剩餘可供細菌生長的養分是很低的，有時低到有些細菌細胞不可生存，更別說生長了。這一點可被第二個實驗證實，當18個指針被口水故意污染再放入，內含有733000 CFU。當這些指針在放入口中後，在溝係封填劑下30到73天，九個指針在細菌量上有減少，有兩個仍是無菌。這顯示出剩餘的養分幾乎可以維持一開始接種的量。
These bacterial studies demonstrate that some leakage occurred in about half the sealant-treated teeth, but that the magnitude was so low as to make questionable its biological significance. This incidence of leakage is probably no more than occurs with any dental restorative material. However, the question has been raised as to whether if incipient lesions were present, would this leakage sustain further bacterial growth and enlargement of the lesion. The answer appears to be no, as will be discussed in the next section.
這些細菌的研究顯示出部分的滲漏是發生在約一半有放溝隙封填劑的牙齒。但所改變的量是非常低，在生物重要性上是一個疑問。這樣的滲漏可能是不會發生在任何填補的材料上。然而，不知是否出初期蛀牙是否存在是一問題，是否滲露是否會讓更多的細菌生長，並將病炤擴大。這答案是否定的，會在下個部份來討論。
Survival of Bacteria Beneath the Sealant
In the previous study (Table 15-8) a small Class I cavity preparation was filled with contaminated paper points prior to being covered by an occlusal sealant. The topography of the cavity preparation bore little resemblance to the fissure surface and while the bacterial levels tended to decrease, this could have been an artifact due to the inability of paper points to provide the same nutritive support as the enamel. These objections have been eliminated by studies in which carious teeth were covered with a sealant, and by a study which used a modification of the artificial fissure model (See "Fissure Colonization" in Chap. 6). In this latter investigation, Theilade et al. removed blocks of enamel containing the occlusal fissure from unerupted third molars and inserted them into specially-prepared recesses in occlusal amalgam fillings. The molar fissures were allowed to become colonized by the oral flora and then some were sealed with an adhesive resin. Immediately thereafter both the sealed and unsealed molar fissures were removed and cultured. The viable anaerobic count in the sealed teeth was reduced about 50-fold compared to the unsealed teeth. This killing effect was attributed to the 50 percent phosphoric acid solution used to condition the enamel surface. The ultraviolet light used for sealant polymerization probably had no antibacterial effect because penetration was unlikely beyond the thickness of the sealant. Thus the procedures used to apply the sealant will exert a marked antibacterial action upon the organisms embedded in the fissure.
在溝隙封填劑下細菌的存活
在前一個實驗裡(15-8)，Class I 窩洞裡在放溝隙封填劑前放入受污染的指針。而修行的窩洞和溝縫是很相似的，而當細菌量是傾向降低的，這有可能會是加工的因素，因為指針不能像牙釉質一樣供應相同的營養。而這樣的缺點以被本實驗中有放溝隙封填劑給消除，還有另一實驗中用人造溝縫的模型(可見第六章”溝縫處的菌落”)。在後者的實驗中，Theiland 等學者移除未萌發的第三大臼齒上部份牙釉質包含咬合面的溝縫，將他們放入在咬合面上汞齊填補處特製的一個地方。而臼齒的溝縫有口內細菌的聚集，有部分牙齒是用樹脂將溝縫封閉起來。在封閉或是沒封閉的臼齒被立刻移除且被培養。在封閉牙齒上無菌細菌的數量是未封閉牙齒降低的50倍。而用於將溝係封填劑聚合的紫外光可能是沒有抑菌的效用，因為紫外光的穿透力是不可能透過溝縫的厚度。因此這樣放溝隙封填劑的步驟會對於藏在溝縫裡的細菌有很大抑制的效用。
The studies involving the placement of sealants over carious lesions demonstrated a definite decline in bacterial viabilities over time that would be independent of the acid etch procedure. Handelman et al. in two separate studies showed that both an ultraviolet polymerizing and an autopolymerizing bis-GMA sealant caused about a 1000-fold reduction in bacterial counts per mg of carious dentin (Table 15-9). The study involving the autopolymerizing sealant Delton“ extended only one month and included unsealed control teeth that had or had not been acid etched. The acid etch reduced the bacterial counts four-fold, but the sealant decreased the counts 35-fold after one to two weeks, and 925-fold after one month. When the ultraviolet polymerized sealant was used, the counts decreased 20-fold after one to two weeks, l95-fold after six months and about 1900-fold after 24 months (Table 15-9). The longer the sealant remained in place the lower the bacterial counts became. The bacterial density of 600 bacteria per mg of dentin observed after 24 months was extremely low, being approximately one millionth the bacterial density found in plaque. The amount of metabolic activity that this small level of bacteria could muster would be minuscule compared to plaque and would be more comparable to that of sterile tissue. Thus it was no surprise that the clinical appearance of this formerly carious dentin was dry and leathery, resembling the texture of an arrested carious lesion.
在蛀牙上放溝係封填劑表現出細菌量上的下降，這和酸蝕的步驟是獨立的。Handelman等人在兩個不同的實驗中顯示出用紫外光聚合或是自行聚合的bis-GMA溝係封填劑，造成在蛀牙牙本質的每毫克細菌量約減少一千倍(表15-9)。這實驗包含自行聚合的溝係封填劑Delton，只維持了一個月，並包含那些有或是沒有被酸蝕的未封閉牙齒。而酸蝕降低四倍的細菌量。而溝隙封填劑經一到兩個禮拜會降低細菌量35倍，而過一個月後會降低925倍的細菌量。當使用紫外光聚合的溝係封填劑時，經一到兩個禮拜會降低細菌量20倍，而過六個月後會降低細菌量195倍，過兩年後則將低1900倍(表15-9)。當封閉劑停留在牙齒上月久，則得到的細菌數越低。在經兩年後牙本質的細菌密度是每毫克600隻，這是非常低，大約是在聚落裡所得細菌量的百萬分之一。這樣微小的細菌和聚落的細菌量比較起來是渺小的，而這樣的量是比較能和無菌的細菌量做比較。而且臨床上這些之前形成的蛀牙是乾燥且向皮革般的，和那已停止的蛀牙病炤的質地是相似的。
The arrest of dentinal decay after being covered with a sealant was shown by Going et al. Teeth that were clinically carious or suspected to be carious had been sealed in 1972 with a single application of an ultraviolet polymerized bis-GMA sealant. In 1977 the carious and bacteriological status of these fissures was evaluated. The fissure site was carefully encircled by drilling and then an islet of tooth structure containing the fissure plus associated dentin was fractured off, weighed and immediately cultured. The remaining dentinal surface was examined for caries status Of 30 occlusal sites judged in 1972 to be either carious (18 sites) or suspected to be carious (12 sites), only four were deemed to be carious in 1977 (Table 15-10). Of 21 control sites judged in 1972 to be either carious (7 sites) or caries free (14 sites), all were carious in 1977 (Table 15-10). Thus the sealant had arrested caries in 87 percent of the previously carious surfaces, at the same time that the control teeth in the same mouth were developing new decay.
由Going等人有研究用溝係封填劑去覆蓋以停止的牙本質蛀牙。這些牙齒在臨床上評估為蛀牙或是疑似蛀牙，在1972年時，單次用紫外線聚合的bis-GMA溝係封填劑將牙齒封閉起來。等到1977年再去評估這些牙齒溝縫裡蛀牙及細菌分布的情況。在溝縫處用鑽針將含有溝縫和牙本質的齒質小心地分切割來，秤重並立即培養細菌。檢查剩餘齒質的蛀牙狀況。在1972年有放溝係封填劑的30顆牙齒，其中被認定18顆被任定為有蛀牙，12顆為疑似蛀牙。到1977回診時只有四顆有蛀牙 (Table 15-10)。在1972年沒放溝隙封填劑的21顆牙齒，其中被認定7顆被任定為有蛀牙，14顆為無蛀牙。到1977回診時全部都有蛀牙 (Table 15-10)。因此溝隙封填劑可以抑制８７％的咬合面蛀牙，而同個時間在對照組上卻是有蛀牙在發生。
The bacteriological findings confirmed the clinical diagnosis. In 9 of 18 teeth judged to be carious in 1972, no bacteria could be cultivated in 1977. Six of 12 teeth suspected of being carious in 1972, were also found to be sterile in 1977 (Table 15-10). No sterile teeth were found among the unsealed teeth. The 14 actively carious teeth in the control group in 1977 had significantly more bacteria per mg of dentin than any of the other groups, including the four carious teeth in the sealant group (Table 15-10). This suggested that while these four teeth were still considered to be carious, they could well be in a transition stage on their way to caries arrest.
從細菌分布上也證實其臨床診斷。在1972年18顆被認定為蛀牙的牙齒，其中9顆到1977年未有細菌生存。在1972年12顆被認定疑似為蛀牙的牙齒，其中6顆到1977年仍是無菌的(表 15-10)。在未封閉的牙齒上不能找到沒有無菌的牙齒。在控制組裡14顆有活耀蛀牙的牙齒，到了1977年，每毫克的牙本質比起其他組有顯著更多的細菌，包含在溝隙封填劑組的那四顆牙齒也有相同的狀況(表 15-10)。這也表示這四顆牙齒仍被認定為有蛀牙，可以說是在轉換的過程中朝向蛀牙停止caries arrest的方向進行。
These studies, in which carious teeth were purposely sealed with an adhesive resin, indicate that if leakage occurs, the amount of nutrients that become available to these buried bacteria is so minimal that bacterial viability in most instances cannot be sustained. In fact, the nutrient supply may be even less than that which can occur when sealants are placed on caries-free surfaces, because of the increased retention of the sealant to the caries-demineralized enamel. Over time the bacterial counts drop to such low levels that an acid metabolism capable of continued tooth demineralization ceases and the decay arrests. In many instances the majority of the bacteria die, as is illustrated in Figure 15-3. Thus instead of concern over continued progression of the carious lesion beneath the sealant, the reality appears to be that the sealant can abort this progression and actually lead to caries arrest. The improved retention of the sealant on a carious surface plus the decreased viability of the bacteria in the carious lesion suggests that sealants may have some therapeutic applications.
這些研究裡，蛀牙的牙齒以樹脂封閉起來，若是有漏洞發生，則可以供給給底下細菌的營養量是很有限的，所以細菌在大部分的情況下是不能生存的。事實上，可供給的營養會比在無蛀牙表面上放上溝隙封填劑來得更少，因為溝隙封填劑在去礦物質的牙本質固持力上會增加。
經過一段時間細菌量掉至一個較低的基準時，酸蝕會造成牙齒脫鈣的狀況停止而且蛀牙也趨於停緩的狀態。在大多數情況下，如圖15-3所示，大部分的細菌已死亡。事實上溝隙封填劑可以將蛀牙過程中斷使蛀牙停止。因著封填劑在蛀牙表面上固持力的增加，加上變少的細菌量，可以說溝隙封填劑有治療的用途。
Change in S. mutans Percentages on Sealant-Treated Occlusal Surfaces
The placement of the sealant over the fissure changes the topography of the occlusal surface from one which provides retentive sites for bacterial colonization, to one in which the surface is relatively smooth and has great access to the saliva. Under these conditions the micro-environment on the occlusal surface might not select for S. mutans. We have cultured occlusal fissures in children participating in the Ypsilanti study (Table 13-11) before and after the placement of an ultraviolet polymerized sealant. These treated children were also given restorative dental treatment and periodic topical fluoride applications, whereas the untreated group received none of these modalities. Thus if a difference existed between the treated and untreated groups in regard to S. mutans proportions, it would not be possible to assign this difference to the sealants alone. However when the groups were compared, after eight and 12 months there was no apparent difference in the percent of S. mutans found in plaque samples taken from the sealant-enamel margin (Table 15-11). By 12 months the S. mutans/S. sanguis ratio had increased in the untreated group suggesting that an acidic environment had selected for S. mutans at the expense of S. sanguis.
在溝隙封填劑處理過咬合面S. mutans百分比的變化
溝隙封填劑的放置改變了咬合面的型態，將有溝縫易讓細菌群聚的地方改變成相對較平滑且口水有較大的接觸。在這樣的狀況下，咬合面可能不會有S. mutans存在。在Ypsilanti 研究裡(表13-11)，我們收集在放封填劑前、後咬合面溝縫的細菌。這些有放封填劑的小朋友同時給予補牙及定期局部塗氟，然而未放封填劑組則未接受任何治療。因此這兩組若有關於S. mutans比例上的不同，不會是僅僅和有無放溝隙封填劑有關。然而經過8和12個月後，從封填劑和牙釉質邊緣取出的S. mutans細菌量並無顯著的不同(表 15-11)。 經過12個月後，S. mutans/S. sanguis比例在未治療組裡是增加的，顯示出酸性環境對於S. mutans是有利的。
These finding indicate that the conditions which promoted S. mutans colonization on the treated children's teeth had not been appreciably changed by the various treatment modalities used. Some variable(s) other than fissure-retentive sites was operating in regard to S. mutans colonization in these patients. This could be sucrose availability. Despite the persistence of S. mutans on the sealant-treated teeth, the treated children experience a caries reduction of about 70 percent on the occlusal surfaces compared to the untreated group.。Obviously microbial metabolic activity on the sealant surface has very little demineralizing activity due to the barrier function of the sealant and the availability of the salivary protective functions.
這個結果表示會使S. mutans 聚集在治療過的牙齒表面上增加的情況，並不會經由改變治療的形式而增加。有些變異除了有關S. mutans聚集的溝縫處。也有可能是有過多的蔗糖。除了S. mutans持續在有封填劑處理過牙齒上，治療過的小朋友比起未治療有70%咬合面蛀牙的下降。明顯地可看出細菌在封填劑表面只有些微去礦物質化作用，因為封填劑的阻隔功能還有唾液有保護的功能。
Sealant Evaluation
The sealants represent a major breakthrough in the preventive treatment of caries-prone retentive surfaces such as pits and fissures. Leakage beneath the sealant is minimal and not adequate to sustain bacterial viability of most organisms left beneath the sealant. Because of this nutrient blockage phenomenon, the sealant apparently can be placed over incipient fissure lesions without causing progression of the lesion. In fact, the lesions tend to arrest, and the numbers of surviving bacteria in the lesion approach zero with time. (Obviously in such a situation the tooth should be carefully followed radiologically). Cariogenic organisms can colonize the sealant surface, but their acid waste products are unable to penetrate the sealant and therefore do not cause tooth demineralization.
封填劑的評估
封填劑在易蛀牙區域(如溝縫)上的預防治療是一大突破。在溝縫下的漏洞是很小的，並不會讓底下的細菌維持生存。因為隔絕營養的來源，封填劑可以放在起初的蛀牙上且不會讓蛀牙在發展。事實上，蛀牙傾向停止，在病灶上細菌的存活量趨於零(因此在這個情況下牙齒必須用x光片定期追蹤觀察)。易蛀牙的細菌可以聚集在封填劑的表面，但是其產酸的廢物卻不能透過溝隙封填劑，因此不會造成牙齒去礦物質化。
SUMMARY
Mechanical debriding procedures such as brushing and flossing were unable to reduce caries incidence when performed by patients under supervision. These debriding procedures were able to reduce plaque and gingivitis scores, indicating that the failure to reduce decay was not due to the patient's inability to debride those tooth surfaces of their supragingival plaque. Rather the failure reflects the weakness of the NSPH's main contention that plaque mass per se is the prime etiologic agent in caries development. In fact, an argument can be made that flossing and brushing can be counterproductive in caries prevention in that they can serve as a vehicle for the spreading of an S. mutans infection about the dentition. However, if the mechanical debridement is rigorously applied, as was done by professional personnel either by daily flossing or frequent tooth cleanings with rotary dental turbines, then caries can be reduced. In these instances, the thoroughness of the debriding apparently can change a cariogenic plaque to a noncariogenic plaque by repeatedly selecting for rapid plaque-forming organisms and discriminating against those species like S. mutans, which need a stagnant environment in order to gain ascendancy. Part of the success of the Karlstad and Danish professional cleaning studies can be explained in this manner. Studies which employ sealants are successful because they remove caries-prone sites from colonization and exploitation by aciduric organisms. Organisms left beneath the sealant are effectively cut off from their nutrient supplies and tend to die off.
結論
機械性移除方法如刷牙、用牙線是由病人在監督下使用不能降低蛀牙。這些移除方法可以減少plaque和gingivitis score，所以不能降低蛀牙不是因為病人無法將牙齦上的plaque清潔乾淨。因此這樣的失敗指出NSPH的缺失，plaque mass per se對於蛀牙發展是很重要的。
事實上有爭議認為牙線和刷牙會造成將S. mutans傳遞出去的媒介。然而，若機械性移除被嚴厲執行，就像是由專業人員每天用牙線和經常的使用rotary器械，蛀牙會下降。以這些例子來說，完整的清除，可以明顯的將易蛀牙的plaque改變為不易蛀牙的plaque，經由反覆選擇快速形成plaque的微生物，並區辨S. mutans需要遲鈍的環境以取得優勢。
Karlstad 和Danish的專業潔牙研究有成功可以用下面來解釋。封填劑的成功是因為他們移除易蛀牙的區域，有酸性細菌群聚。對於在封填劑下的微生物很有效的切斷其養分來源，然後就會死亡。
Mechanical procedures that are frequently applied by dental personnel can be caries preventive, but this labor intensive approach is expensive. In the following chapters we will examine preventive treatment strategies and tactics which are inherently less costly.
機械性清潔方法經常被牙科來做蛀牙預防的動作，但是這樣卻是很貴。在接下來的章節裡會介紹一些較省錢的方法
第12章 P267-287
Fissure Surface Caries
The fissures quickly become impacted with food and bacteria shortly after they erupt into the mouth. It is difficult to imagine bacteria trapped in the bottom of the fissure obtaining enough nutrients for growth, or even finding space for cell division, except at the expense of lysis of other bacteria. These buried bacteria are either dead or dormant. The viable cells are located near the fissure opening along a diffusion gradient, where nutrients would be available. These are the bacteria which would contribute to initiation of fissure caries. Konig has shown that in rats, this is the site of early enamel demineralization, but comparable data in humans is lacking.
溝隙面(Fissure surface)的齲齒
牙齒萌發至口腔中後不久，溝隙內很快就會被食物和細菌塞滿，很難想像困在溝隙底部的細菌該怎麼攝取足夠的養分來提供生長，甚至除了那些分解掉的細菌騰出的空間外，還要找到可供細胞分裂的空間，這些埋藏在溝隙內的細菌不是死亡了，就是休眠著。而能活著的細胞則在能獲取養分的溝隙的開口附近呈現著濃度差的分布，這些細胞也就是會起始溝隙齲齒(fissure caries)的細菌。Konig證實在老鼠的實驗中，這就是早期牙釉質去礦化(early enamel demineralization)的位置，但是在人體上相對的實驗是不足的。
The bacteria near the fissure orifice can be removed by a dental explorer or by other sharp pointed instruments such as hypodermic needles. The data shown in Table 12-1 for single-fissure surfaces were obtained by sampling with a 26-gauge hypodermic needle, which on the average removed about 500,000 CFU. The discreteness of the sampling site contributed to the already strong statistical association between S. mutans and caries, as the sample was not mixed with bacteria resident on the occlusal cusps. Even so, note that some caries-free fissures can harbor S. mutans in appreciable proportions. In such an instance either S. mutans is not causing caries because some resistance factor(s) is operating, or an infection has been detected prior to the appearance of cavitation.
位於靠近溝隙開口處的細菌是可以被牙科探針或其他尖銳的器械移除的，例如注射針。如表12-1所顯示，若利用26-gauge的注射針去對溝隙表面做採樣，平均可取得約500,000 CFU。這樣的取樣方式，更能印證S. mutans與蛀牙之間的強烈關聯(因為取出的菌具代表性，不會與occlusal cusp上的菌相混)。即使如此，某些無齲齒的溝隙也存在著可觀比例的S. mutans。像這樣S. mutans沒有引起齲齒的情形，不是某些抵抗的因素正在產生效果，就是在形成窩洞前，感染的狀況就已經被探測出來了。
There are cases where caries was diagnosed but no S. mutans was detected. This could be attributed to several causes (1) S. mutans was present but not removed by the sampling procedure, (2) the diagnosis of caries was incorrect, i.e., the catch was due to a developmental defect, (3) bacteria other than S. mutans were causing caries. In regard to this latter possibility, recall the data obtained from experiments with germfree animals (Chap. 8) where several species were found capable of causing fissure decay. Data, such as shown in Table 12-1, indicate a strong association between S. mutans and fissure caries, but does not distinguish whether S. mutans is the cause or the result of caries.
有些案例則是診斷已齲齒，但卻沒探測到S. mutans的存在。原因可能為：(1) S. mutans是存在的，可是並沒有被取樣到；(2) 齲齒的診斷是錯誤的，探測到的是發育造成的缺陷；(3) 是除了S. mutans以外的細菌引起齲齒。考慮到最後的這個原因，我們找出了以無菌動物所做的實驗結果(第八章)，實驗研究了許多能引起溝隙齲齒的細菌種類，表12-1顯示出S. mutans和fissure caries之間很強的關聯性，但並無法辨別是否S. mutans就是引起齲齒的原因。
表12-1
Approximal Surface Caries
Approximal caries is difficult to diagnose and sample at the stage of the early enamel lesion. The available data suggests that S. mutans is not as prominent in this plaque. However, sampling is usually done by passing floss between the teeth and culturing the plaque removed by the floss. This floss would miss whatever bacteria might be present in a site of cavitation. Littleton et al. have shown that carious approximal sites contain S. mutans in appreciable levels, whereas in noncarious sites S. mutans was discovered in only six of 26 samples.
鄰接面(proximal surface)的齲齒
在早期牙釉質的階段，鄰接面的齲齒是很難被診斷以及採樣的。目前可獲得的資料中顯示，鄰接面牙菌斑中S.mutans的量並不是很顯著。然而，鄰接面的取樣通常是將牙線通過牙齒間，再將牙線上的牙菌斑取下培養。但是無論如何，牙線病是無法取到窩洞內的細菌。Little et al.的研究顯示，在鄰接面的齲齒處含有可觀的S. mutans，而其餘未齲齒處，在26個樣本中，只有6個被檢測出來含有S. mutans。
Smooth Surface Caries - Rampant Caries
Buccal and lingual smooth surface plaques usually have the lowest levels of S. mutans. This is somewhat ironic because this plaque, which is easy to sample and usually present in appreciable amounts, had in early clinical studies been sampled most often by dental investigators. Bacteriological studies on smooth surface plaque removed from sites that are caries free can be misleading. Several studies have compared S. mutans levels in pooled plaque samples, which contained mostly smooth surface plaque, with the DMFT scores of individuals. The results do not show much of an association between S. mutans and DMFT scores. This reflects the inappropriateness of pooling plaque from noncarious sites and of attempting to relate the findings to active decay on the other tooth surfaces or to a morbidity index such as the DMFT score.
平滑面(smooth surface)的齲齒 – 猛爆性齲齒(rampant caries)
頰側及舌側平滑面的牙菌斑通常是S. mutans量最低的地方，諷刺的是，因為這是很容易取樣和會有較大量牙菌斑的位置，因此早期臨床研究最常採集這裡的樣本。關於平滑面齲齒的細菌學研究中，自無齲齒表面取得的牙菌斑通常會令人誤解。幾個研究比較了牙菌斑樣本中S. mutans的量和個人的DMFT值，但牙菌斑的樣本大部分都是取自於平滑面，結果顯示S. mutans和個人的DMFT值之間沒什麼多大的相關性。這反映出使用平滑面的牙菌斑樣本，以證明和齲齒之間或和個人DMFT值之間的相關性是不恰當的。
Table 12-2
The smooth surface, because it can be directly viewed, offers an opportunity to diagnose the clinical caries status of the surface in a more precise fashion than can be done on fissure or approximal surfaces. Thus it was possible for de Stoppelaar et al. to demonstrate a proportional increase in S. mutans in sites diagnosed as white spots or clinically carious compared to those diagnosed as sound (Table 12-2). Subsequently, van Houte and colleagues showed that the proportions of S. mutans increased going from a clinically sound site on the smooth surface to a clinically carious site on the same tooth. These findings strongly support the involvement of S. mutans at the stage of the white spot lesion.
和溝隙的齲齒或鄰接面的齲齒相較下，因為較好觀察，平滑面提供一個能更精準診斷齲齒的機會。因此de Stoppelaar et al.才能證明在有白斑(white spot)或已蛀牙的地方，S. mutans的量比沒有蛀牙的多(table 12-2)。接著，van Houte and colleagues表示在同一顆牙齒的平滑面上，S. mutans的量從沒有蛀牙的區域到已蛀牙的區域是逐漸增加的。這些學者的發現是證明S .mutans從白斑的階段就開始參與蛀牙的有力的證明。
Smooth surface caries is not usually observed in humans unless a rampant caries situation exists. A dietary history taken of rampant-caries individuals invariably reveals a frequent intake of sucrose and/or decreased salivation. The frequent sucrose ingestion resembles the factors present in the S. mutans animal infections. If this animal infection has any validity for the human, S. mutans should be found in human cases of rampant caries. Loesche et al. have examined pooled fissure plaque taken from children with 10 or more carious teeth. S. mutans was found in high numbers in 26 of 27 subjects and averaged 22 percent of the colony-forming units.
除非是猛爆性齲齒，否則一般人的口內很少觀察到平滑面的齲齒。替猛爆性齲齒病人做飲食病史的回顧發現，他們不約而同的都呈現蔗糖的高頻率攝取和/或唾液分泌的減少。經常性的攝取蔗糖和在動物上S. mutans的感染很類似，若這種動物的感染可以類推到人類，則我們應該可以在猛爆性齲齒的人口內驗出S. mutans的存在。Loesch et al.檢查了口內有超過10顆齲齒的小朋友溝隙內的牙菌斑，他發現在27人中有26人有很多的S. mutans，而且平均有22%的CFU。
Rampant caries is also found in instances where salivation is reduced for various reasons. The dry mouth syndrome is found following irradiation for treatment of jaw cancer, with habitual use of narcotics and with increasing age. Individuals with dry mouths tend to increase their intake of sucking-type candies, thereby providing more sucrose for the selection of organisms such as S. mutans. An increase in S. mutans following jaw irradiation occurs within weeks (Fig. 11-3).
猛爆性齲齒也會被發現存在於唾液分泌減少的人身上。顎骨癌在放射線治療後、習慣性使用麻醉藥物、或年齡的增長通常會出導致口乾症的出現，而有口乾症的人通常會傾向於增加吸吮類型糖果的攝取，因此也提高了適合存在於口內有蔗糖的細菌的選擇，例如S. mutans。在顎骨癌接受放射線治療的病人裡，口乾症會在幾個星期內就發生。
The caries found in drug users is unique. Lovenstat described in institutionalized drug addicts an atypical caries which consisted of shallow, broad-based lesions found mostly on facial surfaces. The lesions had a brown, leathery appearance and seemed to be found mainly in heavy drug users. The use of narcotics decreases salivary flow. The drug user will usually relieve the discomfort of a dry mouth by sucking hard candies, or by holding soda pop in the mouth for long periods of time before swallowing. This prolonged exposure to both sucrose and acidic solutions should select for aciduric organisms in the plaque. We have found high levels of S. mutans in facial caries in an individual who was a habitual marijuana smoker and who held soda pop in his mouth for 5 to 10 minutes before swallowing each mouthful.
在藥物使用的病人身上發生乾口症的狀況比較特別。Lovenstat針對在勒戒所內一種淺而廣泛、通常發生於頰側的齲齒進行研究，這些齲齒呈現棕色、似皮革的外表、且通常會在重症藥癮者身上發現。麻醉類藥物的使用會降低唾液的量，因此使用這類藥物的病人通常會藉由吸吮硬糖或將棒棒糖含在口內較長的時間再吞嚥，這樣延長蔗糖及酸性食物在口內的時間，會對牙菌斑內可耐酸的細菌進行選擇。我們發現在一個習慣性吸食大麻和一個會把棒棒糖至放在口內5至10分鐘後才吞下的病患身上有大量的S. mutans存在於頰側的齲齒內。
Root Surface Caries
Root surface caries is found after the gingiva has receded. It is thus found mainly in adults, and increases in frequency with age according to the degree of gingival recession. Root surface caries could be an unfortunate consequence of periodontal surgery. Despite its frequent occurrence, a root surface lesion is often not diagnosed, as the clinician is more concerned with the associated bone loss. As this lesion is found on the nonretentive root surface, plaque formation is essential to its occurrence.
牙根面(root surface)的齲齒
牙齦萎縮後，牙根面的齲齒才會被發現，因此這種類型的齲齒通常常見於成人，隨著年紀的增長和牙齦退縮的程度而越來越常見。牙根面的齲齒也可能是牙周手術後的不幸結果。儘管這種齲齒是很常見的，可是因為牙醫師通常只專注於喪失了多少骨頭，而忽略了牙根面上的齲齒。因為這樣的齲齒是發生在平滑的牙根表面，因此發生齲齒的原因主要是牙菌斑的形成。
In animals, an A. viscosus infection, which destroys the root surface, can occur with a starch diet. This suggests that any starchy food residues which are not mechanically removed by oral hygiene procedures, could select for an A. viscosus-type plaque. Thus root surface caries would be found in human populations that have a low level of oral hygiene and subsist on starch diets. This proves to be the case. Corbett and Moore have described the caries pattern in several thousand English skulls from pre-Roman to modern times. Root surface caries without coronal caries was found in the ancient skulls. It was not until England imported sucrose that a sudden rise in coronal caries occurred. Today many isolated native cultures do not have access to refined sucrose, but subsist mainly on starch diets. Schamshula and Keyes described severe root surface caries in natives of the New Guinea rain forests. Large accumulations of cervical plaque can be present, which when removed, revealed extensive destruction of the root surface in the absence of coronal enamel caries (Fig. 12-1).
在動物研究中，造成牙根表面破壞的A. viscosus的感染會出現在飲食中含有澱粉的動物上。這表示任何含有澱粉的食物殘渣若不被刷牙時機械式的方式清除掉，則會對A. viscosus類的牙菌斑進行選擇。因此，牙根面的齲齒通常會被發現存在於口腔衛生不好且以澱粉為主食的人身上。Corbett和Moore曾研究數千個從前羅馬時代到現代英國人的蛀牙型態，在古代人身上可以觀察到只有牙根面齲齒而沒有牙冠齲齒的型態。直到英國開始進口蔗糖之後，才開始發現牙冠的齲齒。現在許多土著的文化並沒有精製蔗糖的技術，且以澱粉為主食，Schamshula和Keyes就在新幾內亞雨林內土著身上，發現嚴重的牙根面齲齒。在他們齒頸部有大量的牙菌斑堆積，將牙菌斑清除掉後，可發現牙根面的廣泛破壞，但並沒有牙冠部的齲齒。(fig. 12-1)
A cross section through such a tooth shows that the only significant pathology is in the root and on up into the coronal dentin. The enamel appears to be resistant to attack. These natives eat substantial amounts of sweet potatoes, little meat, and no sucrose or dairy products.
將這種牙齒做橫切面後，可以發現主要病變的地方是在牙根表面，最多頂多到牙冠的牙本質，牙釉質似乎可以抵抗這類的齲齒，這些土著主要食用大量的番薯、極少的肉類，沒有蔗糖或乳類製品。
When plaque from human root surfaces is cultured, A. viscosus and S. mutans are often isolated. Sumney and Jordan studied the flora in the advancing front of root surface caries and found an aerobic Gram-positive rod which they tentatively identified as belonging to the genus Arthrobacter. There is yet no evidence that these Arthrobacter isolates can cause root surface caries. They may be secondary pathogens in this lesion in a manner analogous to the secondary involvement of lactobacilli in coronal caries.
將人類牙根面的牙菌斑進行培養，通常可以發現A. viscosus和S. mutans。Sumney和Jordan研究了牙根面齲齒較前端的部分，發現了好氧性格蘭氏陽性的桿菌，他們將它歸類於Arthrobacter屬。目前並沒有證據顯示Arthrobacter類的細菌會引起牙根面的齲齒，他們的出現可能是類似於lactobacilli在牙冠齲齒般，屬於較晚期出現的。
In experimental animals, A. viscosus invades the cementum and dentin and may eventually infect the pulpal tissue. Some bacterial cells seem to be almost totally surrounded by fairly intact crystallites and collagen. This recalls an observation made by Miller in 1883, who noted that he "found one type of fungus which undoubtedly is able to bore directly into sound dentin. It seems to generate an acid at its tip which helps to drill into or eat the hardest dental tissue".
在動物實驗中，A. viscosus會侵犯牙骨質和牙本質，最後可能造成牙髓組織的感染，某些細菌細胞似乎被完整的晶體和膠原蛋白包覆著，回想到Miller在1983年的研究，他說：｢發現一種能鑽入牙本質內的真菌，似乎能在尖端處產生酸以幫助鑽入或吃噬掉最堅硬的牙齒組織。｣
Fig. 12-1
In humans the pattern of bacterial invasion is not well defined and seems to consist of primary penetration into the tubules and lateral spread between tubules. If lesions involved the deeper regions of the dentin, small numbers of organisms could be seen following the tubules. This failure to dissolve massive amounts of dentinal substance further distinguishes A. viscosus-associated caries from that associated with S. mutans and lactobacilli.
細菌侵犯的模式在人類身上尚未被完全定義，可能和初期的侵入牙本質小管和之後延伸至側方的牙本質小管間有關。若病變處已涉及較深層的牙本質，小量的有機物可以在牙本質小管內被發現。可藉由這種無法分解大量牙本質的特性，分辨為A. viscosus引起的齲齒，而不是S. mutans或lactobacilli引起的齲齒。
LONGITUDINAL STUDIES
The investigations described previously showed a strong statistical association between S. mutans and the presence of cavitation on various tooth surfaces. These studies cannot distinguish whether the increase in S. mutans initiated the decay or was the result of the micro-environment caused by the carious lesion itself. Longitudinal studies presumably would demonstrate whether the elevated proportions and/or levels of S. mutans preceded or coincided with caries development rather than following it. A prospective clinical study to detect changes in the tooth surface flora before and at the time of caries development would be expensive, since it would have to be large enough to accommodate the uncertainties of patient cooperation and the likelihood of any given tooth surface becoming carious during the period of observation. The findings would have to be interpreted against the variability related to diet, fluoride exposure, use of antimicrobial medication, oral hygiene habits, salivary composition and flow, microbial interactions in the plaque, and host immunological experience, among other factors. These considerations indicate that the idealized study will not be performed and that practical longitudinal investigations will have certain limitations inherent in their design.
縱貫性研究(longitudinal studies)
之前提到過的種種研究都顯示S. mutans和牙齒各種面上齲齒的存在有極強的相關性，但這些研究並無法分辨到底是S. mutans的量增加導致齲齒，或是窩洞內自己的微環境(micro-environment)造成的。縱貫性的研究可以呈現出到底S. mutans的比例和/或量的增加是早於齲齒的產生，或是與之同時產生，或是繼之之後產生。一個研究齲齒前中後期的牙齒表面菌落變化的前瞻性研究(prospective study)可能非常昂貴，考慮到病人的配合程度、以及在過程中任何時間牙齒的任何一個面都可能出現齲齒，研究必須涵括夠多的人數，這個研究還必須解釋飲食、氟化物的攝取、抗生素藥物使用、口腔衛生的維持、唾液成分和流量、牙菌斑內微生物間的互動和宿主免疫反應的經驗等因素。這些顧慮使得理想的縱貫性研究是無法實現的，實際的縱貫性研究將會有許多限制。
Two types of longitudinal investigations have been performed. In the prospective study the S. mutans status of various caries-free surfaces is monitored over time in order to determine whether prior colonization and/or dominance of S. mutans on that surface invariably leads to cavitation of that surface. In the response to treatment study, caries-active patients are treated with one or more modalities in order to determine whether suppression or elimination of S. mutans is synonymous with rendering that surface, or patient caries free in the succeeding months to years. In this section we will describe prospective studies while the response to treatment studies will be discussed in Chapter 19.
目前已有兩種縱貫線研究。在前瞻性研究中，一開始就要從未齲齒區長期監測S. mutans的量，以決定是否S. mutans一開始的聚集(colonization)和/或成為優勢菌種會導致蛀牙的產生。而在治療型研究中(treatment study)，以一或多種模式治療有齲齒的病人(caries-active)，已決定是否減低或去除S. mutans等於讓病人在未來數個月至數年不再有齲齒。在此段落，我們將會討論前瞻性研究的部分，而治療型研究的部分將會在第19章討論。
Fissure Surfaces
Fissures in the permanent molars often become decayed within the first year after eruption. If the initial bacterial colonization of the fissure is an important determinant of eventual cariogenicity, then the sampling of these sites should begin shortly after their eruption. This has been difficult to achieve. Nonetheless, there is strong evidence that S. mutans is involved in caries development in the fissures. Ikeda et al. monitored both S. mutans and lactobacilli found in fissures of mandibular molars over a 12-18 month period. The results showed great individual variability, but all surfaces which became carious exhibited a prior colonization by S. mutans. Some surfaces with high levels of S. mutans did not become carious, suggesting that colonization with S. mutans does not automatically give rise to decay. The lactobacilli increased only after the diagnosis of caries was made, which would seem to discredit the lactobacilli as the initiators of caries. Shklair et al. observed that 17 of 21 caries-free naval recruits harbored S. mutans. Within the next year, 10 of the S. mutans carriers developed their first carious lesion, while none of the four men without S. mutans had detectable caries.
溝隙面(fissure surface)
恆牙的溝隙通常在萌發至口內的一年內就會產生齲齒，如果一開始的細菌具及對於後來齲齒的發生有關鍵性的影響，則這些地方細菌的採樣應該在萌發後不久就要進行，但是這很難做到。但是，S. mutans和溝隙面的齲齒間有很強的關聯性。Ikeda et al.花了12-18個月的時間觀測下顎臼齒溝隙中S. mutans和lactobacilli的量，儘管結果顯示有很大的個別差異，但也發現之後產生蛀牙的面，其蛀牙之前有S. mutans的聚集。某些有大量S. mutans的牙面並沒有蛀牙的產生，因此S. mutans的聚集並不是造成蛀牙的主因。在齲齒發生之後，lactobacilli的量才升高，因此lactobacilli也不是引起齲齒的細菌。Shklair et al.在21位無齲齒的海軍軍人口內發現17位有S. mutans的存在，過了一年後，有S. mutans的其中10位口內出現了第一顆齲齒，而一開始口內就沒有S. mutans的軍人，仍沒有任何的齲齒發生。
A prospective study was initiated in order to detect changes in the levels and proportions of S. mutans, S. sanguis, and lactobacilli before and at the time of caries development on occlusal fissures. The bacteriological analysis was performed on 195 teeth that received four examinations at approximately 6-month intervals. The data obtained from 42 carious fissures and 153 caries-free fissures strongly indicated an etiological role for S. mutans in most of the diagnosed fissure lesions. This was demonstrated by the longitudinal analysis, which showed the proportions of S. mutans to increase significantly at the time of caries diagnosis. (Table 12-3).
有一個前瞻性實驗內容為研究在齲齒發生的前後，咬合面上溝隙內的S. mutans、
S. sanguis和Lactobacillus量和比例的變化。總共有195顆牙齒，約每六個月進行一次檢查，共接受四次檢查，其中42顆牙齒的溝隙內有齲齒，153顆為無齲齒的，結果強烈顯示S. mutans是造成溝隙內的齲齒的因子。在縱貫性研究中也顯示S. mutans的比例在診斷為齲齒時也同時升高。(table 12-3)
Table 12-3
The subject's past caries experience as measured by the DFS score plus caries activity during the study period was used to stratify the subjects into five groups. Six subjects were caries free (CF) (DFS=0); 16 subjects were caries inactive (CI) (no new decayed surfaces on any tooth during the study, FS > 0); and 30 subjects had one or more new decayed surfaces somewhere in their dentition during the study and were therefore caries active (CA) (DFS > 0). Within the CI and CA groups, subgroups were defined by using a caries score of five as the partition and sorting the subjects into a low caries group (L) and a high caries group (H). These five groups, CF, LCI, HCI, LCA, and HCA, served as the basis for analyzing the bacteriological data.
依照被研究者過去齲齒的DFS值和目前齲齒的活性，將所有被研究者分成五類。六位被研究者為零齲齒的(caries-free，CF)，在研究期間沒有新的齲齒的16位被研究者歸為無齲齒活性(caries-inactive，CI)，30位有一或多面新齲齒者為有齲齒活性組(caries-active，CA)。在CI和CA組，再依照齲齒數小於5為少齲齒組，多於5為多齲齒組，總共分成CF、LCI、HCI、LCA和HCA五組。
The mean and median percentages of S. mutans in plaque removed from carious fissures in the HCA subjects increased significantly at the time of caries diagnosis compared with the proportions seen six and twelve months before this diagnosis (Table 12-3). No other fissures showed significant changes in the proportions of S. mutans during this time span. S. mutans was a minor component, less than one percent of the fissure flora in the five teeth that became carious in the LCA subjects. S. mutans comprised about 10 percent mean value of the flora in caries-free fissures in the HCI and HCA subjects, but was not a prominent member of the caries-free fissure flora in the CF, LCI, and LCA groups.
在HCA組中，從齲齒的溝隙中取得的牙菌斑內，其S. mutans在新齲齒後的平均值和中數都明顯較齲齒前六個月或十二個月多(table 12-3)。而其他組的溝隙則沒有顯著的不同。在LCA組後來發生齲齒的那五顆牙齒，S. mutans在口內細菌中只占少於1%。在HCI和HCA組中，沒有齲齒的溝隙裡，可發現S. mutans占約10%，而在CF、LCI和LCA組沒有齲齒的溝隙中，則沒有這麼多的S. mutans。
S. sanguis proportions did not exhibit any significant changes over time in any of the fissures, but there was a tendency for the proportions of this organism to be higher in caries-free fissures. The proportions of lactobacilli were low or zero in all subjects at all times except for the few carious fissures in LCA subjects. Six months before the diagnosis of caries, lactobacilli accounted for 25 percent of the flora and then declined to 4 percent at the time caries was diagnosed. Too few teeth were available for this difference to be significant.
在各組中，S. sanguis的比例並沒有多大的改變，不過在沒有齲齒的溝隙中，S. sanguis的量有較多的傾向。除了LCA組中幾個齲齒的溝隙以外，各組內lactobacilli的量都很低或是零。在診斷為齲齒前六個月時，lactobacilli的量約為25%，在診斷為齲齒時，量減低為4%，這部分的研究牙齒的數量太少，無法達到統計上的意義。
The diagnosis of caries was based on the catch of the explorer in a cavitation in the occlusal fissure (Fig. 12-2). This criterion would eliminate the white spot lesion from consideration, but might include as caries any surface defects which enlarged during the period of observation. Bite wing radiographs were taken at each visit; in no instance did they exhibit evidence of decay indicating that what was recorded as decay represented very early lesions. Although the results are striking in that they implicate S. mutans in the earliest detectable form of fissure decay, they show that clinical decay can occur in a few instances in the presence of very low proportions of S. mutans, as was observed in the fissures high in lactobacilli. The fact that these latter fissures were found in the LCA subjects is of interest, for this suggests that if these subjects had higher levels of S. mutans colonizing their teeth, their caries scores might have been higher.
齲齒的診斷是以探針探出咬合面上溝隙有窩洞為準，這樣的標準會把白斑排除在外，但卻可能把牙齒上的缺陷列為齲齒。每次檢查都會拍攝咬翼片，in no instance did they exhibit evidence of decay indicating that what was recorded as decay represented very early lesions。令人震驚的是研究結果認為在齲齒可被探測到的最一開始，就已經有S. mutans的存在，可是也有幾個臨床上的案例可以觀察到S. mutans的量很少、lactobacilli量多也會引起齲齒。後者這種齲齒為什麼發生在LCA組的原因令人產生興趣，這表示若這組的S. mutans量較高的話，齲齒的量也可能會隨之變多。
Fig. 12-2
初期的溝隙齲齒。請注意在第二臼齒溝隙上小的圓形病變處，六個月前此處並無法讓探針有勾住(catch)的感覺。
These results have been confirmed in a second study involving 500 children who were six to seven years old at the initial examination. Over 90 percent of the first-grade students, resident in a nonfluoridated community, were examined at six-month intervals over a three-year period. Fissure plaque was collected from occlusal surfaces of each mandibular first molar and correlated with the caries experience of that surface, as judged by either the presence of an obvious catch or the presence of a dental restoration. The proportions of S. mutans were significantly elevated in those teeth destined to become carious, compared to those teeth which remained caries free. The proportions of S. sanguis declined over time in those teeth destined to become carious. These data obtained from the most caries-prone surface, in the most caries-prone tooth, during the two- to three-year period following eruption, provide strong evidence that S. mutans is a human odontopathogen.
後來有另一個研究也證實了這些結果，這個研究包含了500位孩子，在第一次檢查時的年紀介於6到7歲。住在未飲水加氟區域的一年級生，多於90%的人每六個月進行一次檢查，期間持續了三年。從下顎第一大臼齒的咬合面溝隙中取得牙菌斑，並和該顆牙齒的齲齒經驗做相關聯研究，包括是否有明顯探針可以勾住，或是已經有填補物的存在。在被診斷為齲齒的牙齒上，S. mutans的量明顯多。後來成為齲齒的牙齒，S. sanguis的量是越來越少。這些數據是取自於最容易齲齒的牙面和牙齒和在最容易齲齒的時間，表示S. mutans的確是個引起人類牙齒病變的細菌(odontopathogen)。
Approximal Surfaces
The decay on approximal surfaces occurs apical to the contact point, and usually the early stages can only be detected by x-ray. X-ray diagnosis is amenable to standardization, thereby eliminating some of the clinical error possible with a dental explorer examination. This location of the caries-prone sites makes bacteriological sampling difficult. Bowden, Hardie and their colleagues have removed plaque from this site by means of a standardized abrasive strip. However, plaque is unavoidably removed from the subgingival surfaces, leading to a dilution of the sought-after cariogenic flora by members of the gingival flora. Plaque samples have been removed from the distal surfaces of the upper first premolars, four times a year for a three-year period and cultured using a serial dilution procedure. Approximately 100-120 isolates per sample are being characterized for a total of about 40,000 isolates per year. The magnitude of this study precludes rapid reporting of the findings. Thus far about 10 sites have become carious. Interim reports indicate that S. mutans can dominate a site which subsequently developed a carious lesion. However, domination by S. mutans is not obligatory for the production of a lesion. A combination of organisms which may include moderate levels of S. mutans and lactobacilli can produce a lesion. All representative colonies in a plaque sample will be identified so that it may be possible to determine whether certain bacterial profiles are highly cariogenic and others noncariogenic. In this manner it may be possible to identify bacterial combinations which appear to enhance or antagonize the cariogenicity of S. mutans.
鄰接面(Approximal Surfaces)
在鄰接面的齲齒通常發生在牙齒接觸點(contact point)之下，而且早期的鄰接面齲齒只能從X光片上發現，利用X光片的診斷應為不可缺少的標準動作，他可以偵測出探針檢測不出的齲齒。在這個容易齲齒的地方做細菌採樣是困難的，Bowden、Hardie和他們的同事曾利用abrasive strip收集鄰接面的牙菌斑，然而，無可避免的也同時採樣到了牙齦下的牙菌斑，使得這些致齲性的菌落被牙齦下的菌落稀釋了。曾有學者採集上顎第一小臼齒遠心端的牙菌斑樣本，一年採集四次，持續了三年，並以序列性稀釋(serial dilution)將牙菌斑進行培養。每個樣本約含有100至120個細菌菌落，每年收集的樣本數可提供約40,000個細菌菌落，這個實驗研究的數量太大，因此無法太早發表實驗結果，到目前為止，約有10個採樣處已經有齲齒發生。短期(interim)的研究顯示，在發生齲齒的位置，S. mutans在發生齲齒前會成為優勢菌種(dominate)。然而，S. mutans成為優勢菌種並不代表一定會產生齲齒。多種的細菌合併可能包括有中等數量的S. mutans和Lactobacilli才會造成齲齒。牙菌斑裡的所有具有代表性的細菌都必須被分離出來，才能得知哪些細菌為高度致齲性(cariogenic)，或為非致齲性(noncariogenic)。由此我們才可能分辨其他的細菌是否會加強或抵抗S. mutans的致齲力(cariogenicity)。
Smooth-Surface Rampant Caries
Krasse showed that if school children were ranked according to the proportions of S. mutans in their smooth surface plaque, the children with high levels were more likely to exhibit caries one year later, than children with low levels. The study was done with pooled plaque and included about 40 subjects. De Stoppelaar showed that the development of smooth surface caries on the buccal surfaces of molars was associated with an increase in the proportions of S. mutans in the plaque (Table 12-4). There was a direct relationship between the number of new carious sites and the percentage of S. mutans in the plaque.
平滑面猛爆型齲齒 (Smooth-Surface Rampant Caries)
Krasse表示，將就學兒童牙齒平滑面的牙菌斑以S. mutans的量高低分類，在一年後，較多牙菌斑中具有高含量S. mutans的兒童會發現齲齒。這個研究使用了pooled牙菌斑和約40個個案。De Stoppelaar表示，在臼齒頰側面齲齒的發生，和牙菌斑中S. mutans的量有相關 (表12-4)。新的齲齒發生和牙菌斑中S. mutans的比例有直接的關係。
The ideal population to study for a longitudinal analysis of the relationship between S. mutans and caries development would be individuals who are likely to experience rampant caries. If the Vipeholm study could be repeated, definitive data presumably could be obtained. However, as ethical considerations preclude this type of study, attention was focused on the irradiation-xerostomia patients who develop rampant caries as a consequence of their medical treatment.
長期研究S. mutans和發生齲齒之間的關係，最理想的對象為猛爆型齲齒。如果可以再次進行Vipeholm的實驗，就可以得到更正確的數據。然而，基於道德的考量，這樣的實驗無法再進行，因此轉而將重心放在由放射線引起口乾症，導致猛爆型齲齒的病人身上。
Llory et al. cultured the saliva and plaque of these individuals before, and six months after, radiation treatment for jaw cancer. S. mutans was found to increase dramatically, rising from 0.6 percent to 43.8 percent of the streptococci in plaque. Brown, Dreizen and their colleagues studied both the caries development and the microbial shifts in the plaque in xerostomia patients. The salivary shut down was accompanied by a marked reduction in the physical, chemical and biological anticaries activity of saliva and by a compensatory increase in the frequency of eating of soft, carbohydrate-rich foods. A pronounced shift to a highly acidogenic-aciduric flora occurred at the expense of noncariogenic organisms such as S. sanguis and Bacteroides, Fusobacterium and Neisseria species (Fig. 11-3).
Llory et al.在顎骨癌病人進行放射線治療的前後六個月，對他們的唾液和牙菌斑進行培養，發現S. mutans的量有非常明顯的增加，牙菌斑中的streptococci量從0.6%增加為43.8%。Brown、Dreizen和同事則研究了口乾症病人身上齲齒的發生和牙菌斑中菌種的變化。唾液分泌的停止使得唾液在物理性、化學性及生物性上的抗齲能力明顯下降，且病人會補償性的食用更多較軟且富含碳水化合物的食物。細菌方面，則是有明顯從非致齲性的細菌，例如：S. sanguis 和Bacteroides，Fusobacterium and Neisseria，轉為高產酸-耐酸的菌種。(圖11-3)
蔡醫師: 我不太確定這部分的意思是不是我翻譯的這樣，麻煩你幫我看看！
S. mutans and lactobacilli were present in low proportions prior to irradiation but were already on the increase following the 6-week radiation therapy (Table 12-5). Three months later the proportions of S. mutans peaked and five new carious surfaces were present. Thereafter lactobacilli became the dominant aciduric species as the lesions became larger and more numerous. The striking increases in S. mutans and lactobacilli were sucrose dependent, as when high sucrose foods were excluded during the 6-week period of irradiation; their plaque proportions did not increase, regardless of the severity of the xerostomia.
進行放射線治療前的S. mutans和lactobacilli含量是很低的，但在治療後六個星期就發現含量的增加(表12-5)。三個月後，S. mutans的含量達到高峰，並出現了五個齲齒面。之後，隨著齲齒越來越大、越來越多，lactobacilli成為耐酸菌的優勢菌種。S. mutans和lactobacilli數量的高峰是和蔗糖有關的，放射線治療的六個星期，將高蔗糖的食物去除，發現這些細菌在牙菌斑的組成並沒有改變，與口乾症的嚴重度無關。
MODEL FOR CARIES DEVELOPMENT
The clinical association between S. mutans and lactobacilli and human dental decay has been shown in many studies. Longitudinal investigations have confirmed the important role of S. mutans in most fissure, approximal and smooth surface decay and have suggested that dominance by S. mutans preceded dominance by lactobacilli. The complexity of the flora-caries relationship over time and the difficulties of sampling the actual site of caries development, precludes the making of absolute statements concerning the sequence of events involved in the initiation of the carious lesion. The model shown in Figure 12-3 posits the sequence of events which could occur on caries-free teeth destined to either become carious or remain caries free.
齲齒發生的模型(MODEL FOR CARIES DEVELOPMENT)
已經有許多研究顯示S. mutans和lactobacilli與人類齲齒是有臨床上的相關。縱貫性研究者已證實了S. mutans在溝隙面、鄰接面和平滑面齲齒扮演著重要的角色，並認為S. mutans成為優勢早於lactobacilli。隨著時間變化，菌落和齲齒間複雜的關係，和取得正確齲齒發生處牙菌斑的困難度，使得提出一個正確的齲齒發生順序變得困難。圖12-3表示了一個無齲齒的牙齒可能發生齲齒或維持無齲齒的發生順序。
Both tooth surfaces are initially shown as being in a carrier state relative to harboring a primary cariogen such as S. mutans in the plaque on a smooth surface. The proportions of the cariogen in the flora are similar in the two plaques, but the location of S. mutans within the plaques differs. In the tooth destined to develop decay, S. mutans is located on the enamel surface, whereas in the tooth destined to remain caries free, S. mutans is confined to the saliva-plaque interface. This spatial orientation has implications regarding the future caries status of the respective surfaces. Debriding procedures such as toothbrushing and flossing might remove most plaque organisms, but could leave untouched those bacteria either firmly attached to the enamel surface or sequestered in defects in the enamel surface. In the surfaces destined to become carious, the residual organisms would include the cariogen, whereas in the surfaces destined to remain caries free, the cariogen would be absent. Over time these caries-free surfaces might alternately acquire and lose the cariogen, thereby having an intermittent carrier state status. However, in those surfaces in which caries will eventually develop, the cariogen becomes a dominant member of the flora, undoubtedly secondary to frequent sucrose ingestion.
假設在帶有初期齲原(primary cariogen)的兩個牙面上，例如：在有S. mutans的平滑面上，其牙菌斑中齲原的比例是相似的，但是S. mutans在牙菌斑中的相對位置是不同的，在會發生齲齒的牙面上，S. mutans的位置是在牙釉質上的，而在不會發生齲齒的牙面上，S. mutans則是位於牙菌斑和唾液的交界面上，像這樣空間上位置的不同可能會造成齲齒結果的不同。牙菌斑清除的動作，例如：刷牙和使用牙線，可能可以移除大部份的牙菌斑，但是無法將黏附在牙釉質上的細菌去除，因此，在未來會形成齲齒的牙面上，會發現刷不掉的齲原；而不會形成齲齒的牙面上，則不會發現齲原。隨著時間過去，這些無齲齒的牙面也可能會得到和失去齲原，形成短暫的帶原狀態。然而，在那些最後會形成齲齒的牙面上，這些齲原會成為菌落中的優勢菌種，且毫無疑問的是因為頻繁攝取蔗糖緣故。
The incipient lesion occurs when the acidogenic activity of the cariogen causes tooth mineral to be mobilized from the subsurface enamel in order to buffer the pH at the plaque-enamel interface. Bacteriological sampling at this stage should reveal both a proportional and an absolute increase in the levels of the cariogen, as was the case with S. mutans (Tables 12-3, 12-4, 12-5). When the lesion progresses to the stage of cavitation, the organisms penetrate into the enamel crystals (Fig. 12-4). If the surface is sampled by dental floss or an abrasive strip, these organisms at the advancing front could be missed. Low values of the primary cariogen could be encountered, which clearly are an artifact of the sampling methodology. Also, secondary cariogens, such as the lactobacilli, appear as a result of the selection for aciduric organisms in the plaque. When the lesion reaches the advanced clinical stage, conditions may be such that the primary cariogen can no longer survive and only secondary cariogens and opportunistic organisms can be found.
初期齲齒(incipient caries)的發生為當齲原開始產生酸，為了緩衝牙菌斑牙釉質介面的酸鹼值，牙齒會使得牙釉質的表面下的礦物質變得可移動。若在此階段做細菌學檢查，會發現齲原的比例相對的且絕對的增加了，在此指S. mutans(表12-3、12-4和12-5)。當開始進展成為一個蛀洞時，這些細菌會穿透牙釉質(圖12-4)，此時若用牙線或abrasive strip取樣，可能會漏取了蛀洞內的菌種。採集結果只驗出低量的初期齲原(primary cariogen)，很明顯的是取樣方法造成的人工誤差。同時，像是lactobacilli的二級齲原，是對耐酸細菌進行選擇後的結果。若齲齒進行到一個更後期的階段，可能初期齲原無法再生存，只剩下二級齲原和伺機性的菌種了。
This model predicts that a bacterial succession occurs during the progression of a carious lesion and that the flora of the advanced lesion may bear little resemblance to the flora of the incipient lesion.
這個模型預測了齲齒進展時細菌的演替，以及當齲齒進展到後期與齲齒剛發生的菌落間相似度是很低的。
DENTINAL CARIES
Decay appears to progress slowly through the enamel, and then to move quickly within the dentin. This rate change can be explained by the chemical composition of enamel and dentin. Enamel is 99 percent mineral and one percent protein, whereas dentin is 70 percent mineral and 30 percent collagen. Acid derived from plaque metabolism can be neutralized by salivary buffers, so that demineralization of the enamel will progress slowly. Once cavitation occurs, and especially when it extends into the dentin, the influence of salivary buffers decreases. The dentinal lesion becomes a retentive site where low pHs dominate. The low pH will in turn change the microenvironment. In addition to solubilizing the dentinal mineral, the low pHs will denature the dentinal collagen and select strongly for organisms capable of surviving and growing in acid conditions and perhaps capable of metabolizing the denatured collagen (gelatin). These last two factors make the dentinal lesions quite distinct from the enamel lesion, and offer an explanation for the rapid destruction of the dentinal tissue.
齲齒(DENTINAL CARIES)
齲齒在牙釉質的進展是很慢的，但在牙本質時是很快的。兩者間速率的不同可以用成分組成的不同做解釋。牙釉質為99%的礦物質和1%的蛋白質，而牙本質為70%的礦物質和30%的膠原蛋白。牙菌斑代謝產生的酸可以藉由唾液緩衝，因此牙釉質的齲齒進展是較緩慢的。一旦蛀洞形成，尤其是是當蛀洞已到達牙本質時，唾液緩衝的能力就會降低，牙本質的蛀洞變成一個維持低酸鹼值的地方。為了將牙本質的礦物質溶解，低酸鹼值的環境會使牙本質的膠原蛋白變性，並選擇能在酸性環境生存且能代謝膠原蛋白的細菌。最後這兩個原因使得牙本質的蛀洞和牙釉質的蛀洞不同，且使得牙本質組織被更快速的破壞。
When the lesion progresses into the dentin, the conditions may be such that only the most aciduric organisms will thrive. This pattern of succession explains the dominance of lactobacilli species in sites of cavitation. This increase was quickly noted by early investigators (See "Lactobacillus Era" in Chap. 7) and served as the basis for caries diagnosis. However, it is apparent that in most instances the upsurge in lactobacilli is the result of cavitation. In this context they are important secondary pathogens contributing to the progression of the lesion.
當蛀洞進展至牙本質時，只有最耐酸的細菌可以存活下來，這解釋了蛀洞內lactobacilli的優勢。這個狀況很快就被早期的學者發現(請見第七章)，並成為齲齒診斷的基本。但是，很明顯的在大部份的情況，lactobacilli的增長是來自於蛀洞的產生，他們是造成蛀洞進展重要的次級病原菌。
The acid destruction of a tissue with 30 percent collagen differs from the destruction of a tissue with no collagen. Very few oral bacteria possess collagenases. However, collagen is readily denatured by acid, forming gelatin which is degraded by many oral organisms. Thus, the following sequence is possible in the dentinal lesion. Acid solubilizes the tooth mineral, exposing the collagen scaffold. The acid, as well as the high Ca++ salt content, denatures the collagen. Bacterial proteases degrade the collagen- gelatin to low-molecular-weight peptides and amino acids which can be used for microbial biosynthesis. The process is self repeating, causing expansion of the lesion with the collagen breakdown products transformed into microbial protein.
以酸去破壞含有30%膠原蛋白的組織和破壞不含膠原蛋白的組織是不同的，極少細菌含有膠原蛋白酶，然而，當膠原蛋白被酸變性之後，產生的凝膠(gelatin)可被許多口腔內微生物所分解。因此，接下來的敘述可能為牙本質蛀洞的發生順序。酸使得牙齒內的礦物質可移動，使膠原蛋白的支架暴露出來，酸和高含量的鈣鹽使膠原蛋白變性，細菌的蛋白酶將膠原蛋白-gelatin分解為低分子量的肽胜(peptide)和胺基酸，這些肽胜和胺基酸可被細菌所利用。這個過程不斷的重複，造成蛀洞的擴大，而膠原蛋白的分解產物則成為細菌可利用的蛋白質。
Dentinal lesions are not necessarily bacteriologically similar. The large lesion shown in Figure 12-5 is older than the lesion just developing at the dentino-enamel junction and because of its larger opening, would have access to impacted food and saliva. The nutrient availability would differ between the two lesions, and this should result in selection for a different flora.
在細菌學上，牙本質的蛀洞並不一定相似。和剛蛀進牙本質牙釉質交界的小蛀洞相較，在圖12-5的大蛀洞為較久的蛀洞，較大的開口可以塞入更多的食物和唾液，這兩種蛀洞(大蛀洞和小蛀洞)獲得營養的難易度不同，因此，蛀洞內菌落的組成也不盡相同。
Proteolytic Organisms
The prominence of proteolytic organisms in carious dentin was shown by Burnett and Scherp (Table 12-6). These investigators, using in most instances, aerobic procedures, cultured saliva, enamel lesions, carious dentin and scrapings from the junction between decalcified and intact dentin. Aciduric organisms were more prominent in the enamel lesion while proteolytic organisms dominated in the decalcified scrapings. These proteolytic organisms were heterogeneous but included anaerobic streptococci, micrococci and members of the genera Bacillus and Pseudomonas. Other investigators have isolated other proteolytic species. Hartles and McDonald isolated Clostridium welchii from about 60 percent of 252 carious teeth; and Engel showed that a filtrate of C. welchii, which contained collagenase, could liberate nitrogen from decalcified dentin. Roth isolated from dentinal lesions an aerobic, proteolytic organism (Rothia dentocariosa), which was capable of degrading denatured collagen. These studies indicate that not only are there a variety of proteolytic organisms in the carious dentin, but that the flora at this stage of the lesion is bacteriologically distinct from that found in cariogenic plaque.
分解蛋白的生物體 (Proteolytic organisms)
Burnett和Scherp提出在牙本質的齲齒內大多數為可分解蛋白質的生物體(表12-6)。這些學者在進行唾液、牙釉質齲齒、牙本質齲齒、以及從脫鈣和完整的牙本質交界處刮除下來的成分進行培養時，大多數都是使用有氧的程序，在牙釉質的齲齒裡大多是耐酸性的生物體，而在脫鈣處刮除下的成分裡大多是可分解蛋白質的生物體。這些可分解蛋白質的生物體是包含很多種類的，包括厭氧的鏈球菌、微球菌(micrococci)，以及Bacillus和Pseudomonas屬的細菌。其他學者更分出了其他可分解蛋白質的生物體。Hartles和McDonald分析了252顆齲齒，其中的60%分出了Clostridium welchii，而Engel將含有膠原蛋白酶的C. welchii濾出，發現這隻細菌可從脫鈣的牙本質中釋放氮。另外，Roth在牙本質的齲齒處分出了一種好氧、可分解蛋白質的生物體(Rothia dentocariosa)，這種細菌可以分解變性的膠原蛋白。這些研究並不只是陳述在牙本質內有許多可分解蛋白質的生物體種類的觀點，更點出了在齲齒的這個階段，這些可分解蛋白質的生物體比有致齲性的牙菌斑內的細菌更顯著。
Quantitative Cultural Studies
In many early studies of the carious lesion, the carious dentin was placed into broth media or cultured directly on selective media. In this manner the rapidly-growing species or the sought-after species would be the main organisms isolated, and little information would be available as to the proportional distribution of these cultivable species in the carious dentin.
定量的培養研究 (Quantitative Cultural Studies)
早期許多關於齲齒的研究，都是將齲蛀的牙本質置放在培養液(broth media)或直接在選擇性介質(selective media)中培養。這樣一來，最後分離出來的菌種大多為生長快速的菌種或是較強勢(sougjt-after)的菌種，除此以外，占小比例的菌種就很難被分離出來，也很難獲得關於這些菌種的資訊了。
Loesche and Syed cultured plaque from over an interproximal lesion and also the soft carious dentin from the lesion using a quantitative anaerobic procedure. S. mutans and lactobacilli were present in low proportions in the plaque, but accounted for 28 percent and 20 percent respectively of the organisms in the dentin (Table 12-6). Thus as the lesion penetrated into the dentin, both the primary and secondary cariogens were prominent members of the dentinal flora but not the plaque flora. This spatial distribution of these organisms in the lesion indicates that at the stage of the clinical and/or advanced lesion (Fig. 12-2), plaque samples may no longer be representative of the cariogenic flora within the lesion.
Loesche和Syed 取得鄰接面有齲齒的牙菌斑和齲蛀的牙本質，並以無氧、定量的方式進行培養，在鄰接面的牙菌斑中，S. mutans和lactobacilli只占了很小的比例，卻分別在牙本質的齲齒內占了28 %和 20 %的比例(表12-6)。因此，當齲齒穿透至牙本質的時候，初級和二級齲原皆成為齲齒內主要的細菌，而不是牙菌斑內主要的細菌。這個結果告訴我們，當齲齒已進入到這個階段時，牙菌斑的樣本已無法代表齲齒內細菌的生態了。
Carious dentin can be enucleated from the lesion leaving behind a decalcified surface that represents the front of the lesion. Barnett and Scherp cultured scrapings from this surface and found a sparse flora consisting of high proportions of streptococci and low proportions of lactobacilli and actinomyces (Table 12-6). Edwardsson cultured the same material but approached the site from the pulpal chamber. Extracted teeth were prepared so that dentin could be aseptically removed one layer or portion at a time moving from the intact dentin toward the carious lesion. All initial layers were sterile but thereafter bacteria were encountered in the various layers until the carious dentin was reached. The flora found in the first layer with visible growth was subcultured and extensively characterized. S. mutans was found in less than 10 percent of the decalcified lesions, whereas lactobacilli and Gram-positive rods were found in 33 percent and 50 percent of the lesions. No single organism or group of organisms was unique to the decalcified front (Table l2-6).
將齲蛀的齒質去除後，可在齲齒前端發現脫鈣的表面。Barnett和Scherp將這些脫鈣的表面進行培養，發現一個稀疏的菌落群，包含有高比例的streptococci以及低比例的lactobacilli和actinomyces(表12-6)。Edwardsson也對脫鈣的表面進行培養，只是取得的方向是從牙髓腔往外，他將拔下的牙齒從牙髓腔往齲齒的方向一層一層去除，最一開始取得的幾層牙本質皆為無菌的，之後慢慢開始發現有微生物的存在，最後才到達齲齒處。將開始發現到有微生物的那層牙本質進行培養，發現S. mutans的量低於10%，而lactobacilli和革蘭氏陽性球菌則分別佔了33%和50%。並沒有哪一隻細菌或哪一種細菌是特別存在於脫鈣處的。 (表l2-6).
This lack of bacterial specificity was even more apparent when the various isolates were classified. No single species was found in more than 20 percent of the lesions. The flora was simple, consisting of from one to seven bacterial types. In about 45 percent of the lesions the flora was dominated by one of the following species, Arachnia spp., nine percent; Bifidobacterium spp., nine percent; E. alactolyticum, 11 percent; L. casei, 16 percent. Apparently each of these species at a specific moment found the environment suitable for growth, and acted as a pioneer bacterium which entered the dentinal tubule and produced micro-colonies along the length of the tubule. These findings support a nonspecific bacterial involvement at the level of decalcified dentin.
很明顯的，在此處並沒有細菌的專一性，沒有任何一隻細菌的量占超過20%，在這裡細菌群是很簡單的，只包括1至7種細菌，在45%的齲齒處可發現下列的優勢細菌：Arachnia類占9%，Bifidobacterium類占9%，E. alactolyticum占11%，而L. casei占16%。很明顯的，這些菌種在某一特定時刻發現到這個適合生長的環境，進入到牙本質小管內成為先驅菌種，並沿著牙本質小管形成菌落，這些發現支持了"在脫鈣的牙本質處，細菌是非專一性的(nonspecific bacterial involvement)"的說法。
PULPAL INFECTIONS
An untreated carious lesion can progress through the dentin and into the pulp causing pulpal inflammation and necrosis. The culturing of the canal could provide some information concerning the types of bacteria at the front of the carious lesion. However, by the time these lesions are cultured, there is no adequate way to document the length of time that the pulp had been infected. Also, many pulpal lesions have been cultured in a qualitative manner in that a paper point, after insertion into the pulp canal, is placed into broth media and incubated aerobically. Facultative organisms by virtue of their rapid growth rate predominated in such cultures. In the past these isolates were not well characterized, but this situation has changed.
牙髓腔的感染 PULPAL INFECTIONS
當齲齒未受到治療，持續進行至牙本質，甚至進入到牙髓腔時，會造成牙髓的發炎及壞死。根管內的細菌培養可提供一些關於齲齒前端細菌的資訊。然而，當我們開始進行培養的時候，已無法得知牙髓受到感染的時間有多長，而且，許多牙髓腔內細菌的定性培養已經被做過了，這部分可經由在根管內置入紙針(paper point)，再放置於培養液中，於含氧的環境下進行培養。兼養性細菌因為有生長快速的優點，成為這類培養主要的細菌。從前這類的細菌分離並無法好好的被分類，但這個情況現在已經改變了。
Sundquist and Carlsson found streptococci, enterococci, staphylococci and lactobacilli to be prominent isolates among 566 positive cultures obtained from 1282 root canals. The lactobacilli were classified to the species level and found to be L. casei (41% of the isolates), L. salivarius (28%), L. acidophilus (17%), L. fermentum (10%) and L. plantarum (4%). This profile with the exception of L. salivarius is comparable to the lactobacilli found in the decalcified dentin. This suggests that in the 27 percent of the canals found to be positive for lactobacilli, these organisms entered the canal via extension of the carious lesion. This is not the case when necrotic pulps from traumatized teeth were cultured, as lactobacilli were not found, but anaerobic organisms similar to the periodontal flora were encountered.
Sundquist和Carlsson研究了1282個根管，其中有566個培養基有細菌可被培養出來，被培養出來的細菌裡，又以streptococci、enterococci、staphylococci和lactobacilli占多數，lactobacilli被仔細的分離後發現有：L. casei (41%)、L. salivarius (28%)、L. acidophilus (17%)、L. fermentum (10%)和L. plantarum (4%)。在這裡並沒有分離出L. salivarius，這和在脫鈣牙本質的結果相同，表示在27%含有lactobacilli的根管中，lactobacilli其實是由齲齒延伸至根管的。不過，當牙髓組織的壞死是來自於外傷時，情況便不同了，在這個狀況下不會發現lactobacilli，但是會發現類似於牙周菌落的厭氧細菌。
The presence of L. salivarius in the pulp-canal cultures suggested that salivary contamination had occurred. This was further supported in a separate study in which Mejare examined the streptococcal flora found in 587 positive cultures obtained from l958 root canals. S. sanguis was isolated from 12 percent, S. mutans from four percent and S. salivarius from seven percent of the positive cultures. The frequency of S. mutans recovery was compatible with its prevalence in the flora of decalcified dentin. However, the recoveries of S. sanguis and especially S. salivarius were higher than could be expected. S. salivarius was found significantly more often in teeth with open pulp cavities than in teeth with closed pulp cavities; more often in teeth without, than with periradicular bone rarefactions; and more often among positive cultures when the previous culture had been negative versus positive. These observations indicated that S. salivarius was a salivary contaminant and not indigenous to the infected root canal. Thus, about seven percent of all positive root canal cultures might be expected to be contaminated with saliva. The culturing of caries-infected root canals has not shed much information upon caries etiology.
若在根管內發現L. salivarius，表示根管已受到口水汙染，Mejare的實驗證實了這個說法。Mejare研究了1958個根管，其中在streptococci陽性反應的587個菌落中發現，S. sanguis占了12%，S. mutans占4%，S. salivarius占7%。S. mutans的培養結果和脫鈣處牙本質的相差不遠，然而，S. sanguis和S. salivarius卻遠高於期望值。在牙髓腔已對外相通的牙齒，S. salivarius的量顯著的較沒對外相通的高，在沒有根尖骨頭破壞處S. salivarius的量也較多，在培養結果從陰性轉陽性的S. salivarius的量也較多，以上這些結果表示S. salivarius的來源並不是根管內生的，而是口水汙染來的。因此，在呈現細菌陽性反應的根管中，約有7%已被口水汙染了，這樣的培養並無法提供關於齲齒病因學方面的資訊。
SUMMARY
Dental caries is a multifactoral disease with genetic, environmental, dietary and bacterial factors. In the past the bacterial component appeared to be so complex that it was conceptualized as a constant that produced acid upon exposure to carbohydrates. This simplification became the basis of the nonspecific plaque hypothesis as it related to dental caries. The only way that acid production could be reduced would be by decreasing the plaque and/or carbohydrate intake. Both of these approaches have been the cornerstone of traditional preventive treatment. Keyes' demonstration of bacterial specificity in animal caries models was followed by the demonstration of S. mutans in human plaques. A considerable number of studies have found a significant association of S. mutans with human dental decay. Longitudinal investigations indicate that S. mutans peaks at about the time that caries is diagnosed. However, the correlation is never absolute as there are usually a few teeth that are either highly colonized with S. mutans which do not become carious, or which become carious in the absence of S. mutans. These exceptions probably reflect, in the first instance, that the virulence of S. mutans can be modified and in the second instance, that other bacteria can contribute to the caries process. They do not detract from the basic finding that S. mutans is statistically involved in the majority of human carious lesions. This observation forms the basis of the specific plaque hypothesis and is the departure point for the preventive treatments described in Chapters 15-20.
總結 (SUMMARY)
齲齒是多因性的疾病，包含了基因、環境、飲食和細菌幾個因素。在以前，細菌這項因素太過複雜，以致於被簡略成一個暴露在碳水化合物下會產酸的因子，這個簡化的動作成為了"非專一性牙菌斑假說(nonspecific plaque hypothesis )"用於解釋齲齒的基礎，因此減少產酸的方法只能靠減少牙菌斑和/或碳水化合物的攝取，這兩個方法為傳統預防齲齒的主要方式，Keyes在動物的齲齒模型證明了細菌的專一性，接著證明S. mutans在人類牙菌斑中的存在。許多實驗都證明了S. mutans和人類齲齒間的強力相關性。縱貫性的研究學者指出，當齲齒被診斷出來的時候，S. mutans的量也達到高峰。然而，這之間的相關性卻無法成為完全絕對的，因為在某些無齲齒的牙齒發現高比例的S. mutans，或在齲齒的牙齒上沒有發現到S. mutans。這些例外可能反映出幾個可能性，首先，S. mutans 的毒性可以被修改，另外一個可能就是也許還有其他細菌能造成齲齒。 不過無可否認的是S. mutans is的確和大部分人類的齲齒是相關的。這項觀察成為了"專一性牙菌斑假說(specific plaque hypothesis)"的基礎，並且在第15-20章關於預防這部分產生了不同的治療理念。
The fissures quickly become impacted with food and bacteria shortly after they erupt into the mouth. It is difficult to imagine bacteria trapped in the bottom of the fissure obtaining enough nutrients for growth, or even finding space for cell division, except at the expense of lysis of other bacteria. These buried bacteria are either dead or dormant. The viable cells are located near the fissure opening along a diffusion gradient, where nutrients would be available. These are the bacteria which would contribute to initiation of fissure caries. Konig has shown that in rats, this is the site of early enamel demineralization, but comparable data in humans is lacking.
溝隙面(Fissure surface)的齲齒
牙齒萌發至口腔中後不久，溝隙內很快就會被食物和細菌塞滿，很難想像困在溝隙底部的細菌該怎麼攝取足夠的養分來提供生長，甚至除了那些分解掉的細菌騰出的空間外，還要找到可供細胞分裂的空間，這些埋藏在溝隙內的細菌不是死亡了，就是休眠著。而能活著的細胞則在能獲取養分的溝隙的開口附近呈現著濃度差的分布，這些細胞也就是會起始溝隙齲齒(fissure caries)的細菌。Konig證實在老鼠的實驗中，這就是早期牙釉質去礦化(early enamel demineralization)的位置，但是在人體上相對的實驗是不足的。
The bacteria near the fissure orifice can be removed by a dental explorer or by other sharp pointed instruments such as hypodermic needles. The data shown in Table 12-1 for single-fissure surfaces were obtained by sampling with a 26-gauge hypodermic needle, which on the average removed about 500,000 CFU. The discreteness of the sampling site contributed to the already strong statistical association between S. mutans and caries, as the sample was not mixed with bacteria resident on the occlusal cusps. Even so, note that some caries-free fissures can harbor S. mutans in appreciable proportions. In such an instance either S. mutans is not causing caries because some resistance factor(s) is operating, or an infection has been detected prior to the appearance of cavitation.
位於靠近溝隙開口處的細菌是可以被牙科探針或其他尖銳的器械移除的，例如注射針。如表12-1所顯示，若利用26-gauge的注射針去對溝隙表面做採樣，平均可取得約500,000 CFU。這樣的取樣方式，更能印證S. mutans與蛀牙之間的強烈關聯(因為取出的菌具代表性，不會與occlusal cusp上的菌相混)。即使如此，某些無齲齒的溝隙也存在著可觀比例的S. mutans。像這樣S. mutans沒有引起齲齒的情形，不是某些抵抗的因素正在產生效果，就是在形成窩洞前，感染的狀況就已經被探測出來了。
There are cases where caries was diagnosed but no S. mutans was detected. This could be attributed to several causes (1) S. mutans was present but not removed by the sampling procedure, (2) the diagnosis of caries was incorrect, i.e., the catch was due to a developmental defect, (3) bacteria other than S. mutans were causing caries. In regard to this latter possibility, recall the data obtained from experiments with germfree animals (Chap. 8) where several species were found capable of causing fissure decay. Data, such as shown in Table 12-1, indicate a strong association between S. mutans and fissure caries, but does not distinguish whether S. mutans is the cause or the result of caries.
有些案例則是診斷已齲齒，但卻沒探測到S. mutans的存在。原因可能為：(1) S. mutans是存在的，可是並沒有被取樣到；(2) 齲齒的診斷是錯誤的，探測到的是發育造成的缺陷；(3) 是除了S. mutans以外的細菌引起齲齒。考慮到最後的這個原因，我們找出了以無菌動物所做的實驗結果(第八章)，實驗研究了許多能引起溝隙齲齒的細菌種類，表12-1顯示出S. mutans和fissure caries之間很強的關聯性，但並無法辨別是否S. mutans就是引起齲齒的原因。
表12-1
Approximal Surface Caries
Approximal caries is difficult to diagnose and sample at the stage of the early enamel lesion. The available data suggests that S. mutans is not as prominent in this plaque. However, sampling is usually done by passing floss between the teeth and culturing the plaque removed by the floss. This floss would miss whatever bacteria might be present in a site of cavitation. Littleton et al. have shown that carious approximal sites contain S. mutans in appreciable levels, whereas in noncarious sites S. mutans was discovered in only six of 26 samples.
鄰接面(proximal surface)的齲齒
在早期牙釉質的階段，鄰接面的齲齒是很難被診斷以及採樣的。目前可獲得的資料中顯示，鄰接面牙菌斑中S.mutans的量並不是很顯著。然而，鄰接面的取樣通常是將牙線通過牙齒間，再將牙線上的牙菌斑取下培養。但是無論如何，牙線病是無法取到窩洞內的細菌。Little et al.的研究顯示，在鄰接面的齲齒處含有可觀的S. mutans，而其餘未齲齒處，在26個樣本中，只有6個被檢測出來含有S. mutans。
Smooth Surface Caries - Rampant Caries
Buccal and lingual smooth surface plaques usually have the lowest levels of S. mutans. This is somewhat ironic because this plaque, which is easy to sample and usually present in appreciable amounts, had in early clinical studies been sampled most often by dental investigators. Bacteriological studies on smooth surface plaque removed from sites that are caries free can be misleading. Several studies have compared S. mutans levels in pooled plaque samples, which contained mostly smooth surface plaque, with the DMFT scores of individuals. The results do not show much of an association between S. mutans and DMFT scores. This reflects the inappropriateness of pooling plaque from noncarious sites and of attempting to relate the findings to active decay on the other tooth surfaces or to a morbidity index such as the DMFT score.
平滑面(smooth surface)的齲齒 – 猛爆性齲齒(rampant caries)
頰側及舌側平滑面的牙菌斑通常是S. mutans量最低的地方，諷刺的是，因為這是很容易取樣和會有較大量牙菌斑的位置，因此早期臨床研究最常採集這裡的樣本。關於平滑面齲齒的細菌學研究中，自無齲齒表面取得的牙菌斑通常會令人誤解。幾個研究比較了牙菌斑樣本中S. mutans的量和個人的DMFT值，但牙菌斑的樣本大部分都是取自於平滑面，結果顯示S. mutans和個人的DMFT值之間沒什麼多大的相關性。這反映出使用平滑面的牙菌斑樣本，以證明和齲齒之間或和個人DMFT值之間的相關性是不恰當的。
Table 12-2
The smooth surface, because it can be directly viewed, offers an opportunity to diagnose the clinical caries status of the surface in a more precise fashion than can be done on fissure or approximal surfaces. Thus it was possible for de Stoppelaar et al. to demonstrate a proportional increase in S. mutans in sites diagnosed as white spots or clinically carious compared to those diagnosed as sound (Table 12-2). Subsequently, van Houte and colleagues showed that the proportions of S. mutans increased going from a clinically sound site on the smooth surface to a clinically carious site on the same tooth. These findings strongly support the involvement of S. mutans at the stage of the white spot lesion.
和溝隙的齲齒或鄰接面的齲齒相較下，因為較好觀察，平滑面提供一個能更精準診斷齲齒的機會。因此de Stoppelaar et al.才能證明在有白斑(white spot)或已蛀牙的地方，S. mutans的量比沒有蛀牙的多(table 12-2)。接著，van Houte and colleagues表示在同一顆牙齒的平滑面上，S. mutans的量從沒有蛀牙的區域到已蛀牙的區域是逐漸增加的。這些學者的發現是證明S .mutans從白斑的階段就開始參與蛀牙的有力的證明。
Smooth surface caries is not usually observed in humans unless a rampant caries situation exists. A dietary history taken of rampant-caries individuals invariably reveals a frequent intake of sucrose and/or decreased salivation. The frequent sucrose ingestion resembles the factors present in the S. mutans animal infections. If this animal infection has any validity for the human, S. mutans should be found in human cases of rampant caries. Loesche et al. have examined pooled fissure plaque taken from children with 10 or more carious teeth. S. mutans was found in high numbers in 26 of 27 subjects and averaged 22 percent of the colony-forming units.
除非是猛爆性齲齒，否則一般人的口內很少觀察到平滑面的齲齒。替猛爆性齲齒病人做飲食病史的回顧發現，他們不約而同的都呈現蔗糖的高頻率攝取和/或唾液分泌的減少。經常性的攝取蔗糖和在動物上S. mutans的感染很類似，若這種動物的感染可以類推到人類，則我們應該可以在猛爆性齲齒的人口內驗出S. mutans的存在。Loesch et al.檢查了口內有超過10顆齲齒的小朋友溝隙內的牙菌斑，他發現在27人中有26人有很多的S. mutans，而且平均有22%的CFU。
Rampant caries is also found in instances where salivation is reduced for various reasons. The dry mouth syndrome is found following irradiation for treatment of jaw cancer, with habitual use of narcotics and with increasing age. Individuals with dry mouths tend to increase their intake of sucking-type candies, thereby providing more sucrose for the selection of organisms such as S. mutans. An increase in S. mutans following jaw irradiation occurs within weeks (Fig. 11-3).
猛爆性齲齒也會被發現存在於唾液分泌減少的人身上。顎骨癌在放射線治療後、習慣性使用麻醉藥物、或年齡的增長通常會出導致口乾症的出現，而有口乾症的人通常會傾向於增加吸吮類型糖果的攝取，因此也提高了適合存在於口內有蔗糖的細菌的選擇，例如S. mutans。在顎骨癌接受放射線治療的病人裡，口乾症會在幾個星期內就發生。
The caries found in drug users is unique. Lovenstat described in institutionalized drug addicts an atypical caries which consisted of shallow, broad-based lesions found mostly on facial surfaces. The lesions had a brown, leathery appearance and seemed to be found mainly in heavy drug users. The use of narcotics decreases salivary flow. The drug user will usually relieve the discomfort of a dry mouth by sucking hard candies, or by holding soda pop in the mouth for long periods of time before swallowing. This prolonged exposure to both sucrose and acidic solutions should select for aciduric organisms in the plaque. We have found high levels of S. mutans in facial caries in an individual who was a habitual marijuana smoker and who held soda pop in his mouth for 5 to 10 minutes before swallowing each mouthful.
在藥物使用的病人身上發生乾口症的狀況比較特別。Lovenstat針對在勒戒所內一種淺而廣泛、通常發生於頰側的齲齒進行研究，這些齲齒呈現棕色、似皮革的外表、且通常會在重症藥癮者身上發現。麻醉類藥物的使用會降低唾液的量，因此使用這類藥物的病人通常會藉由吸吮硬糖或將棒棒糖含在口內較長的時間再吞嚥，這樣延長蔗糖及酸性食物在口內的時間，會對牙菌斑內可耐酸的細菌進行選擇。我們發現在一個習慣性吸食大麻和一個會把棒棒糖至放在口內5至10分鐘後才吞下的病患身上有大量的S. mutans存在於頰側的齲齒內。
Root Surface Caries
Root surface caries is found after the gingiva has receded. It is thus found mainly in adults, and increases in frequency with age according to the degree of gingival recession. Root surface caries could be an unfortunate consequence of periodontal surgery. Despite its frequent occurrence, a root surface lesion is often not diagnosed, as the clinician is more concerned with the associated bone loss. As this lesion is found on the nonretentive root surface, plaque formation is essential to its occurrence.
牙根面(root surface)的齲齒
牙齦萎縮後，牙根面的齲齒才會被發現，因此這種類型的齲齒通常常見於成人，隨著年紀的增長和牙齦退縮的程度而越來越常見。牙根面的齲齒也可能是牙周手術後的不幸結果。儘管這種齲齒是很常見的，可是因為牙醫師通常只專注於喪失了多少骨頭，而忽略了牙根面上的齲齒。因為這樣的齲齒是發生在平滑的牙根表面，因此發生齲齒的原因主要是牙菌斑的形成。
In animals, an A. viscosus infection, which destroys the root surface, can occur with a starch diet. This suggests that any starchy food residues which are not mechanically removed by oral hygiene procedures, could select for an A. viscosus-type plaque. Thus root surface caries would be found in human populations that have a low level of oral hygiene and subsist on starch diets. This proves to be the case. Corbett and Moore have described the caries pattern in several thousand English skulls from pre-Roman to modern times. Root surface caries without coronal caries was found in the ancient skulls. It was not until England imported sucrose that a sudden rise in coronal caries occurred. Today many isolated native cultures do not have access to refined sucrose, but subsist mainly on starch diets. Schamshula and Keyes described severe root surface caries in natives of the New Guinea rain forests. Large accumulations of cervical plaque can be present, which when removed, revealed extensive destruction of the root surface in the absence of coronal enamel caries (Fig. 12-1).
在動物研究中，造成牙根表面破壞的A. viscosus的感染會出現在飲食中含有澱粉的動物上。這表示任何含有澱粉的食物殘渣若不被刷牙時機械式的方式清除掉，則會對A. viscosus類的牙菌斑進行選擇。因此，牙根面的齲齒通常會被發現存在於口腔衛生不好且以澱粉為主食的人身上。Corbett和Moore曾研究數千個從前羅馬時代到現代英國人的蛀牙型態，在古代人身上可以觀察到只有牙根面齲齒而沒有牙冠齲齒的型態。直到英國開始進口蔗糖之後，才開始發現牙冠的齲齒。現在許多土著的文化並沒有精製蔗糖的技術，且以澱粉為主食，Schamshula和Keyes就在新幾內亞雨林內土著身上，發現嚴重的牙根面齲齒。在他們齒頸部有大量的牙菌斑堆積，將牙菌斑清除掉後，可發現牙根面的廣泛破壞，但並沒有牙冠部的齲齒。(fig. 12-1)
A cross section through such a tooth shows that the only significant pathology is in the root and on up into the coronal dentin. The enamel appears to be resistant to attack. These natives eat substantial amounts of sweet potatoes, little meat, and no sucrose or dairy products.
將這種牙齒做橫切面後，可以發現主要病變的地方是在牙根表面，最多頂多到牙冠的牙本質，牙釉質似乎可以抵抗這類的齲齒，這些土著主要食用大量的番薯、極少的肉類，沒有蔗糖或乳類製品。
When plaque from human root surfaces is cultured, A. viscosus and S. mutans are often isolated. Sumney and Jordan studied the flora in the advancing front of root surface caries and found an aerobic Gram-positive rod which they tentatively identified as belonging to the genus Arthrobacter. There is yet no evidence that these Arthrobacter isolates can cause root surface caries. They may be secondary pathogens in this lesion in a manner analogous to the secondary involvement of lactobacilli in coronal caries.
將人類牙根面的牙菌斑進行培養，通常可以發現A. viscosus和S. mutans。Sumney和Jordan研究了牙根面齲齒較前端的部分，發現了好氧性格蘭氏陽性的桿菌，他們將它歸類於Arthrobacter屬。目前並沒有證據顯示Arthrobacter類的細菌會引起牙根面的齲齒，他們的出現可能是類似於lactobacilli在牙冠齲齒般，屬於較晚期出現的。
In experimental animals, A. viscosus invades the cementum and dentin and may eventually infect the pulpal tissue. Some bacterial cells seem to be almost totally surrounded by fairly intact crystallites and collagen. This recalls an observation made by Miller in 1883, who noted that he "found one type of fungus which undoubtedly is able to bore directly into sound dentin. It seems to generate an acid at its tip which helps to drill into or eat the hardest dental tissue".
在動物實驗中，A. viscosus會侵犯牙骨質和牙本質，最後可能造成牙髓組織的感染，某些細菌細胞似乎被完整的晶體和膠原蛋白包覆著，回想到Miller在1983年的研究，他說：｢發現一種能鑽入牙本質內的真菌，似乎能在尖端處產生酸以幫助鑽入或吃噬掉最堅硬的牙齒組織。｣
Fig. 12-1
In humans the pattern of bacterial invasion is not well defined and seems to consist of primary penetration into the tubules and lateral spread between tubules. If lesions involved the deeper regions of the dentin, small numbers of organisms could be seen following the tubules. This failure to dissolve massive amounts of dentinal substance further distinguishes A. viscosus-associated caries from that associated with S. mutans and lactobacilli.
細菌侵犯的模式在人類身上尚未被完全定義，可能和初期的侵入牙本質小管和之後延伸至側方的牙本質小管間有關。若病變處已涉及較深層的牙本質，小量的有機物可以在牙本質小管內被發現。可藉由這種無法分解大量牙本質的特性，分辨為A. viscosus引起的齲齒，而不是S. mutans或lactobacilli引起的齲齒。
LONGITUDINAL STUDIES
The investigations described previously showed a strong statistical association between S. mutans and the presence of cavitation on various tooth surfaces. These studies cannot distinguish whether the increase in S. mutans initiated the decay or was the result of the micro-environment caused by the carious lesion itself. Longitudinal studies presumably would demonstrate whether the elevated proportions and/or levels of S. mutans preceded or coincided with caries development rather than following it. A prospective clinical study to detect changes in the tooth surface flora before and at the time of caries development would be expensive, since it would have to be large enough to accommodate the uncertainties of patient cooperation and the likelihood of any given tooth surface becoming carious during the period of observation. The findings would have to be interpreted against the variability related to diet, fluoride exposure, use of antimicrobial medication, oral hygiene habits, salivary composition and flow, microbial interactions in the plaque, and host immunological experience, among other factors. These considerations indicate that the idealized study will not be performed and that practical longitudinal investigations will have certain limitations inherent in their design.
縱貫性研究(longitudinal studies)
之前提到過的種種研究都顯示S. mutans和牙齒各種面上齲齒的存在有極強的相關性，但這些研究並無法分辨到底是S. mutans的量增加導致齲齒，或是窩洞內自己的微環境(micro-environment)造成的。縱貫性的研究可以呈現出到底S. mutans的比例和/或量的增加是早於齲齒的產生，或是與之同時產生，或是繼之之後產生。一個研究齲齒前中後期的牙齒表面菌落變化的前瞻性研究(prospective study)可能非常昂貴，考慮到病人的配合程度、以及在過程中任何時間牙齒的任何一個面都可能出現齲齒，研究必須涵括夠多的人數，這個研究還必須解釋飲食、氟化物的攝取、抗生素藥物使用、口腔衛生的維持、唾液成分和流量、牙菌斑內微生物間的互動和宿主免疫反應的經驗等因素。這些顧慮使得理想的縱貫性研究是無法實現的，實際的縱貫性研究將會有許多限制。
Two types of longitudinal investigations have been performed. In the prospective study the S. mutans status of various caries-free surfaces is monitored over time in order to determine whether prior colonization and/or dominance of S. mutans on that surface invariably leads to cavitation of that surface. In the response to treatment study, caries-active patients are treated with one or more modalities in order to determine whether suppression or elimination of S. mutans is synonymous with rendering that surface, or patient caries free in the succeeding months to years. In this section we will describe prospective studies while the response to treatment studies will be discussed in Chapter 19.
目前已有兩種縱貫線研究。在前瞻性研究中，一開始就要從未齲齒區長期監測S. mutans的量，以決定是否S. mutans一開始的聚集(colonization)和/或成為優勢菌種會導致蛀牙的產生。而在治療型研究中(treatment study)，以一或多種模式治療有齲齒的病人(caries-active)，已決定是否減低或去除S. mutans等於讓病人在未來數個月至數年不再有齲齒。在此段落，我們將會討論前瞻性研究的部分，而治療型研究的部分將會在第19章討論。
Fissure Surfaces
Fissures in the permanent molars often become decayed within the first year after eruption. If the initial bacterial colonization of the fissure is an important determinant of eventual cariogenicity, then the sampling of these sites should begin shortly after their eruption. This has been difficult to achieve. Nonetheless, there is strong evidence that S. mutans is involved in caries development in the fissures. Ikeda et al. monitored both S. mutans and lactobacilli found in fissures of mandibular molars over a 12-18 month period. The results showed great individual variability, but all surfaces which became carious exhibited a prior colonization by S. mutans. Some surfaces with high levels of S. mutans did not become carious, suggesting that colonization with S. mutans does not automatically give rise to decay. The lactobacilli increased only after the diagnosis of caries was made, which would seem to discredit the lactobacilli as the initiators of caries. Shklair et al. observed that 17 of 21 caries-free naval recruits harbored S. mutans. Within the next year, 10 of the S. mutans carriers developed their first carious lesion, while none of the four men without S. mutans had detectable caries.
溝隙面(fissure surface)
恆牙的溝隙通常在萌發至口內的一年內就會產生齲齒，如果一開始的細菌具及對於後來齲齒的發生有關鍵性的影響，則這些地方細菌的採樣應該在萌發後不久就要進行，但是這很難做到。但是，S. mutans和溝隙面的齲齒間有很強的關聯性。Ikeda et al.花了12-18個月的時間觀測下顎臼齒溝隙中S. mutans和lactobacilli的量，儘管結果顯示有很大的個別差異，但也發現之後產生蛀牙的面，其蛀牙之前有S. mutans的聚集。某些有大量S. mutans的牙面並沒有蛀牙的產生，因此S. mutans的聚集並不是造成蛀牙的主因。在齲齒發生之後，lactobacilli的量才升高，因此lactobacilli也不是引起齲齒的細菌。Shklair et al.在21位無齲齒的海軍軍人口內發現17位有S. mutans的存在，過了一年後，有S. mutans的其中10位口內出現了第一顆齲齒，而一開始口內就沒有S. mutans的軍人，仍沒有任何的齲齒發生。
A prospective study was initiated in order to detect changes in the levels and proportions of S. mutans, S. sanguis, and lactobacilli before and at the time of caries development on occlusal fissures. The bacteriological analysis was performed on 195 teeth that received four examinations at approximately 6-month intervals. The data obtained from 42 carious fissures and 153 caries-free fissures strongly indicated an etiological role for S. mutans in most of the diagnosed fissure lesions. This was demonstrated by the longitudinal analysis, which showed the proportions of S. mutans to increase significantly at the time of caries diagnosis. (Table 12-3).
有一個前瞻性實驗內容為研究在齲齒發生的前後，咬合面上溝隙內的S. mutans、
S. sanguis和Lactobacillus量和比例的變化。總共有195顆牙齒，約每六個月進行一次檢查，共接受四次檢查，其中42顆牙齒的溝隙內有齲齒，153顆為無齲齒的，結果強烈顯示S. mutans是造成溝隙內的齲齒的因子。在縱貫性研究中也顯示S. mutans的比例在診斷為齲齒時也同時升高。(table 12-3)
Table 12-3
The subject's past caries experience as measured by the DFS score plus caries activity during the study period was used to stratify the subjects into five groups. Six subjects were caries free (CF) (DFS=0); 16 subjects were caries inactive (CI) (no new decayed surfaces on any tooth during the study, FS > 0); and 30 subjects had one or more new decayed surfaces somewhere in their dentition during the study and were therefore caries active (CA) (DFS > 0). Within the CI and CA groups, subgroups were defined by using a caries score of five as the partition and sorting the subjects into a low caries group (L) and a high caries group (H). These five groups, CF, LCI, HCI, LCA, and HCA, served as the basis for analyzing the bacteriological data.
依照被研究者過去齲齒的DFS值和目前齲齒的活性，將所有被研究者分成五類。六位被研究者為零齲齒的(caries-free，CF)，在研究期間沒有新的齲齒的16位被研究者歸為無齲齒活性(caries-inactive，CI)，30位有一或多面新齲齒者為有齲齒活性組(caries-active，CA)。在CI和CA組，再依照齲齒數小於5為少齲齒組，多於5為多齲齒組，總共分成CF、LCI、HCI、LCA和HCA五組。
The mean and median percentages of S. mutans in plaque removed from carious fissures in the HCA subjects increased significantly at the time of caries diagnosis compared with the proportions seen six and twelve months before this diagnosis (Table 12-3). No other fissures showed significant changes in the proportions of S. mutans during this time span. S. mutans was a minor component, less than one percent of the fissure flora in the five teeth that became carious in the LCA subjects. S. mutans comprised about 10 percent mean value of the flora in caries-free fissures in the HCI and HCA subjects, but was not a prominent member of the caries-free fissure flora in the CF, LCI, and LCA groups.
在HCA組中，從齲齒的溝隙中取得的牙菌斑內，其S. mutans在新齲齒後的平均值和中數都明顯較齲齒前六個月或十二個月多(table 12-3)。而其他組的溝隙則沒有顯著的不同。在LCA組後來發生齲齒的那五顆牙齒，S. mutans在口內細菌中只占少於1%。在HCI和HCA組中，沒有齲齒的溝隙裡，可發現S. mutans占約10%，而在CF、LCI和LCA組沒有齲齒的溝隙中，則沒有這麼多的S. mutans。
S. sanguis proportions did not exhibit any significant changes over time in any of the fissures, but there was a tendency for the proportions of this organism to be higher in caries-free fissures. The proportions of lactobacilli were low or zero in all subjects at all times except for the few carious fissures in LCA subjects. Six months before the diagnosis of caries, lactobacilli accounted for 25 percent of the flora and then declined to 4 percent at the time caries was diagnosed. Too few teeth were available for this difference to be significant.
在各組中，S. sanguis的比例並沒有多大的改變，不過在沒有齲齒的溝隙中，S. sanguis的量有較多的傾向。除了LCA組中幾個齲齒的溝隙以外，各組內lactobacilli的量都很低或是零。在診斷為齲齒前六個月時，lactobacilli的量約為25%，在診斷為齲齒時，量減低為4%，這部分的研究牙齒的數量太少，無法達到統計上的意義。
The diagnosis of caries was based on the catch of the explorer in a cavitation in the occlusal fissure (Fig. 12-2). This criterion would eliminate the white spot lesion from consideration, but might include as caries any surface defects which enlarged during the period of observation. Bite wing radiographs were taken at each visit; in no instance did they exhibit evidence of decay indicating that what was recorded as decay represented very early lesions. Although the results are striking in that they implicate S. mutans in the earliest detectable form of fissure decay, they show that clinical decay can occur in a few instances in the presence of very low proportions of S. mutans, as was observed in the fissures high in lactobacilli. The fact that these latter fissures were found in the LCA subjects is of interest, for this suggests that if these subjects had higher levels of S. mutans colonizing their teeth, their caries scores might have been higher.
齲齒的診斷是以探針探出咬合面上溝隙有窩洞為準，這樣的標準會把白斑排除在外，但卻可能把牙齒上的缺陷列為齲齒。每次檢查都會拍攝咬翼片，in no instance did they exhibit evidence of decay indicating that what was recorded as decay represented very early lesions。令人震驚的是研究結果認為在齲齒可被探測到的最一開始，就已經有S. mutans的存在，可是也有幾個臨床上的案例可以觀察到S. mutans的量很少、lactobacilli量多也會引起齲齒。後者這種齲齒為什麼發生在LCA組的原因令人產生興趣，這表示若這組的S. mutans量較高的話，齲齒的量也可能會隨之變多。
Fig. 12-2
初期的溝隙齲齒。請注意在第二臼齒溝隙上小的圓形病變處，六個月前此處並無法讓探針有勾住(catch)的感覺。
These results have been confirmed in a second study involving 500 children who were six to seven years old at the initial examination. Over 90 percent of the first-grade students, resident in a nonfluoridated community, were examined at six-month intervals over a three-year period. Fissure plaque was collected from occlusal surfaces of each mandibular first molar and correlated with the caries experience of that surface, as judged by either the presence of an obvious catch or the presence of a dental restoration. The proportions of S. mutans were significantly elevated in those teeth destined to become carious, compared to those teeth which remained caries free. The proportions of S. sanguis declined over time in those teeth destined to become carious. These data obtained from the most caries-prone surface, in the most caries-prone tooth, during the two- to three-year period following eruption, provide strong evidence that S. mutans is a human odontopathogen.
後來有另一個研究也證實了這些結果，這個研究包含了500位孩子，在第一次檢查時的年紀介於6到7歲。住在未飲水加氟區域的一年級生，多於90%的人每六個月進行一次檢查，期間持續了三年。從下顎第一大臼齒的咬合面溝隙中取得牙菌斑，並和該顆牙齒的齲齒經驗做相關聯研究，包括是否有明顯探針可以勾住，或是已經有填補物的存在。在被診斷為齲齒的牙齒上，S. mutans的量明顯多。後來成為齲齒的牙齒，S. sanguis的量是越來越少。這些數據是取自於最容易齲齒的牙面和牙齒和在最容易齲齒的時間，表示S. mutans的確是個引起人類牙齒病變的細菌(odontopathogen)。
Approximal Surfaces
The decay on approximal surfaces occurs apical to the contact point, and usually the early stages can only be detected by x-ray. X-ray diagnosis is amenable to standardization, thereby eliminating some of the clinical error possible with a dental explorer examination. This location of the caries-prone sites makes bacteriological sampling difficult. Bowden, Hardie and their colleagues have removed plaque from this site by means of a standardized abrasive strip. However, plaque is unavoidably removed from the subgingival surfaces, leading to a dilution of the sought-after cariogenic flora by members of the gingival flora. Plaque samples have been removed from the distal surfaces of the upper first premolars, four times a year for a three-year period and cultured using a serial dilution procedure. Approximately 100-120 isolates per sample are being characterized for a total of about 40,000 isolates per year. The magnitude of this study precludes rapid reporting of the findings. Thus far about 10 sites have become carious. Interim reports indicate that S. mutans can dominate a site which subsequently developed a carious lesion. However, domination by S. mutans is not obligatory for the production of a lesion. A combination of organisms which may include moderate levels of S. mutans and lactobacilli can produce a lesion. All representative colonies in a plaque sample will be identified so that it may be possible to determine whether certain bacterial profiles are highly cariogenic and others noncariogenic. In this manner it may be possible to identify bacterial combinations which appear to enhance or antagonize the cariogenicity of S. mutans.
鄰接面(Approximal Surfaces)
在鄰接面的齲齒通常發生在牙齒接觸點(contact point)之下，而且早期的鄰接面齲齒只能從X光片上發現，利用X光片的診斷應為不可缺少的標準動作，他可以偵測出探針檢測不出的齲齒。在這個容易齲齒的地方做細菌採樣是困難的，Bowden、Hardie和他們的同事曾利用abrasive strip收集鄰接面的牙菌斑，然而，無可避免的也同時採樣到了牙齦下的牙菌斑，使得這些致齲性的菌落被牙齦下的菌落稀釋了。曾有學者採集上顎第一小臼齒遠心端的牙菌斑樣本，一年採集四次，持續了三年，並以序列性稀釋(serial dilution)將牙菌斑進行培養。每個樣本約含有100至120個細菌菌落，每年收集的樣本數可提供約40,000個細菌菌落，這個實驗研究的數量太大，因此無法太早發表實驗結果，到目前為止，約有10個採樣處已經有齲齒發生。短期(interim)的研究顯示，在發生齲齒的位置，S. mutans在發生齲齒前會成為優勢菌種(dominate)。然而，S. mutans成為優勢菌種並不代表一定會產生齲齒。多種的細菌合併可能包括有中等數量的S. mutans和Lactobacilli才會造成齲齒。牙菌斑裡的所有具有代表性的細菌都必須被分離出來，才能得知哪些細菌為高度致齲性(cariogenic)，或為非致齲性(noncariogenic)。由此我們才可能分辨其他的細菌是否會加強或抵抗S. mutans的致齲力(cariogenicity)。
Smooth-Surface Rampant Caries
Krasse showed that if school children were ranked according to the proportions of S. mutans in their smooth surface plaque, the children with high levels were more likely to exhibit caries one year later, than children with low levels. The study was done with pooled plaque and included about 40 subjects. De Stoppelaar showed that the development of smooth surface caries on the buccal surfaces of molars was associated with an increase in the proportions of S. mutans in the plaque (Table 12-4). There was a direct relationship between the number of new carious sites and the percentage of S. mutans in the plaque.
平滑面猛爆型齲齒 (Smooth-Surface Rampant Caries)
Krasse表示，將就學兒童牙齒平滑面的牙菌斑以S. mutans的量高低分類，在一年後，較多牙菌斑中具有高含量S. mutans的兒童會發現齲齒。這個研究使用了pooled牙菌斑和約40個個案。De Stoppelaar表示，在臼齒頰側面齲齒的發生，和牙菌斑中S. mutans的量有相關 (表12-4)。新的齲齒發生和牙菌斑中S. mutans的比例有直接的關係。
The ideal population to study for a longitudinal analysis of the relationship between S. mutans and caries development would be individuals who are likely to experience rampant caries. If the Vipeholm study could be repeated, definitive data presumably could be obtained. However, as ethical considerations preclude this type of study, attention was focused on the irradiation-xerostomia patients who develop rampant caries as a consequence of their medical treatment.
長期研究S. mutans和發生齲齒之間的關係，最理想的對象為猛爆型齲齒。如果可以再次進行Vipeholm的實驗，就可以得到更正確的數據。然而，基於道德的考量，這樣的實驗無法再進行，因此轉而將重心放在由放射線引起口乾症，導致猛爆型齲齒的病人身上。
Llory et al. cultured the saliva and plaque of these individuals before, and six months after, radiation treatment for jaw cancer. S. mutans was found to increase dramatically, rising from 0.6 percent to 43.8 percent of the streptococci in plaque. Brown, Dreizen and their colleagues studied both the caries development and the microbial shifts in the plaque in xerostomia patients. The salivary shut down was accompanied by a marked reduction in the physical, chemical and biological anticaries activity of saliva and by a compensatory increase in the frequency of eating of soft, carbohydrate-rich foods. A pronounced shift to a highly acidogenic-aciduric flora occurred at the expense of noncariogenic organisms such as S. sanguis and Bacteroides, Fusobacterium and Neisseria species (Fig. 11-3).
Llory et al.在顎骨癌病人進行放射線治療的前後六個月，對他們的唾液和牙菌斑進行培養，發現S. mutans的量有非常明顯的增加，牙菌斑中的streptococci量從0.6%增加為43.8%。Brown、Dreizen和同事則研究了口乾症病人身上齲齒的發生和牙菌斑中菌種的變化。唾液分泌的停止使得唾液在物理性、化學性及生物性上的抗齲能力明顯下降，且病人會補償性的食用更多較軟且富含碳水化合物的食物。細菌方面，則是有明顯從非致齲性的細菌，例如：S. sanguis 和Bacteroides，Fusobacterium and Neisseria，轉為高產酸-耐酸的菌種。(圖11-3)
蔡醫師: 我不太確定這部分的意思是不是我翻譯的這樣，麻煩你幫我看看！
S. mutans and lactobacilli were present in low proportions prior to irradiation but were already on the increase following the 6-week radiation therapy (Table 12-5). Three months later the proportions of S. mutans peaked and five new carious surfaces were present. Thereafter lactobacilli became the dominant aciduric species as the lesions became larger and more numerous. The striking increases in S. mutans and lactobacilli were sucrose dependent, as when high sucrose foods were excluded during the 6-week period of irradiation; their plaque proportions did not increase, regardless of the severity of the xerostomia.
進行放射線治療前的S. mutans和lactobacilli含量是很低的，但在治療後六個星期就發現含量的增加(表12-5)。三個月後，S. mutans的含量達到高峰，並出現了五個齲齒面。之後，隨著齲齒越來越大、越來越多，lactobacilli成為耐酸菌的優勢菌種。S. mutans和lactobacilli數量的高峰是和蔗糖有關的，放射線治療的六個星期，將高蔗糖的食物去除，發現這些細菌在牙菌斑的組成並沒有改變，與口乾症的嚴重度無關。
MODEL FOR CARIES DEVELOPMENT
The clinical association between S. mutans and lactobacilli and human dental decay has been shown in many studies. Longitudinal investigations have confirmed the important role of S. mutans in most fissure, approximal and smooth surface decay and have suggested that dominance by S. mutans preceded dominance by lactobacilli. The complexity of the flora-caries relationship over time and the difficulties of sampling the actual site of caries development, precludes the making of absolute statements concerning the sequence of events involved in the initiation of the carious lesion. The model shown in Figure 12-3 posits the sequence of events which could occur on caries-free teeth destined to either become carious or remain caries free.
齲齒發生的模型(MODEL FOR CARIES DEVELOPMENT)
已經有許多研究顯示S. mutans和lactobacilli與人類齲齒是有臨床上的相關。縱貫性研究者已證實了S. mutans在溝隙面、鄰接面和平滑面齲齒扮演著重要的角色，並認為S. mutans成為優勢早於lactobacilli。隨著時間變化，菌落和齲齒間複雜的關係，和取得正確齲齒發生處牙菌斑的困難度，使得提出一個正確的齲齒發生順序變得困難。圖12-3表示了一個無齲齒的牙齒可能發生齲齒或維持無齲齒的發生順序。
Both tooth surfaces are initially shown as being in a carrier state relative to harboring a primary cariogen such as S. mutans in the plaque on a smooth surface. The proportions of the cariogen in the flora are similar in the two plaques, but the location of S. mutans within the plaques differs. In the tooth destined to develop decay, S. mutans is located on the enamel surface, whereas in the tooth destined to remain caries free, S. mutans is confined to the saliva-plaque interface. This spatial orientation has implications regarding the future caries status of the respective surfaces. Debriding procedures such as toothbrushing and flossing might remove most plaque organisms, but could leave untouched those bacteria either firmly attached to the enamel surface or sequestered in defects in the enamel surface. In the surfaces destined to become carious, the residual organisms would include the cariogen, whereas in the surfaces destined to remain caries free, the cariogen would be absent. Over time these caries-free surfaces might alternately acquire and lose the cariogen, thereby having an intermittent carrier state status. However, in those surfaces in which caries will eventually develop, the cariogen becomes a dominant member of the flora, undoubtedly secondary to frequent sucrose ingestion.
假設在帶有初期齲原(primary cariogen)的兩個牙面上，例如：在有S. mutans的平滑面上，其牙菌斑中齲原的比例是相似的，但是S. mutans在牙菌斑中的相對位置是不同的，在會發生齲齒的牙面上，S. mutans的位置是在牙釉質上的，而在不會發生齲齒的牙面上，S. mutans則是位於牙菌斑和唾液的交界面上，像這樣空間上位置的不同可能會造成齲齒結果的不同。牙菌斑清除的動作，例如：刷牙和使用牙線，可能可以移除大部份的牙菌斑，但是無法將黏附在牙釉質上的細菌去除，因此，在未來會形成齲齒的牙面上，會發現刷不掉的齲原；而不會形成齲齒的牙面上，則不會發現齲原。隨著時間過去，這些無齲齒的牙面也可能會得到和失去齲原，形成短暫的帶原狀態。然而，在那些最後會形成齲齒的牙面上，這些齲原會成為菌落中的優勢菌種，且毫無疑問的是因為頻繁攝取蔗糖緣故。
The incipient lesion occurs when the acidogenic activity of the cariogen causes tooth mineral to be mobilized from the subsurface enamel in order to buffer the pH at the plaque-enamel interface. Bacteriological sampling at this stage should reveal both a proportional and an absolute increase in the levels of the cariogen, as was the case with S. mutans (Tables 12-3, 12-4, 12-5). When the lesion progresses to the stage of cavitation, the organisms penetrate into the enamel crystals (Fig. 12-4). If the surface is sampled by dental floss or an abrasive strip, these organisms at the advancing front could be missed. Low values of the primary cariogen could be encountered, which clearly are an artifact of the sampling methodology. Also, secondary cariogens, such as the lactobacilli, appear as a result of the selection for aciduric organisms in the plaque. When the lesion reaches the advanced clinical stage, conditions may be such that the primary cariogen can no longer survive and only secondary cariogens and opportunistic organisms can be found.
初期齲齒(incipient caries)的發生為當齲原開始產生酸，為了緩衝牙菌斑牙釉質介面的酸鹼值，牙齒會使得牙釉質的表面下的礦物質變得可移動。若在此階段做細菌學檢查，會發現齲原的比例相對的且絕對的增加了，在此指S. mutans(表12-3、12-4和12-5)。當開始進展成為一個蛀洞時，這些細菌會穿透牙釉質(圖12-4)，此時若用牙線或abrasive strip取樣，可能會漏取了蛀洞內的菌種。採集結果只驗出低量的初期齲原(primary cariogen)，很明顯的是取樣方法造成的人工誤差。同時，像是lactobacilli的二級齲原，是對耐酸細菌進行選擇後的結果。若齲齒進行到一個更後期的階段，可能初期齲原無法再生存，只剩下二級齲原和伺機性的菌種了。
This model predicts that a bacterial succession occurs during the progression of a carious lesion and that the flora of the advanced lesion may bear little resemblance to the flora of the incipient lesion.
這個模型預測了齲齒進展時細菌的演替，以及當齲齒進展到後期與齲齒剛發生的菌落間相似度是很低的。
DENTINAL CARIES
Decay appears to progress slowly through the enamel, and then to move quickly within the dentin. This rate change can be explained by the chemical composition of enamel and dentin. Enamel is 99 percent mineral and one percent protein, whereas dentin is 70 percent mineral and 30 percent collagen. Acid derived from plaque metabolism can be neutralized by salivary buffers, so that demineralization of the enamel will progress slowly. Once cavitation occurs, and especially when it extends into the dentin, the influence of salivary buffers decreases. The dentinal lesion becomes a retentive site where low pHs dominate. The low pH will in turn change the microenvironment. In addition to solubilizing the dentinal mineral, the low pHs will denature the dentinal collagen and select strongly for organisms capable of surviving and growing in acid conditions and perhaps capable of metabolizing the denatured collagen (gelatin). These last two factors make the dentinal lesions quite distinct from the enamel lesion, and offer an explanation for the rapid destruction of the dentinal tissue.
齲齒(DENTINAL CARIES)
齲齒在牙釉質的進展是很慢的，但在牙本質時是很快的。兩者間速率的不同可以用成分組成的不同做解釋。牙釉質為99%的礦物質和1%的蛋白質，而牙本質為70%的礦物質和30%的膠原蛋白。牙菌斑代謝產生的酸可以藉由唾液緩衝，因此牙釉質的齲齒進展是較緩慢的。一旦蛀洞形成，尤其是是當蛀洞已到達牙本質時，唾液緩衝的能力就會降低，牙本質的蛀洞變成一個維持低酸鹼值的地方。為了將牙本質的礦物質溶解，低酸鹼值的環境會使牙本質的膠原蛋白變性，並選擇能在酸性環境生存且能代謝膠原蛋白的細菌。最後這兩個原因使得牙本質的蛀洞和牙釉質的蛀洞不同，且使得牙本質組織被更快速的破壞。
When the lesion progresses into the dentin, the conditions may be such that only the most aciduric organisms will thrive. This pattern of succession explains the dominance of lactobacilli species in sites of cavitation. This increase was quickly noted by early investigators (See "Lactobacillus Era" in Chap. 7) and served as the basis for caries diagnosis. However, it is apparent that in most instances the upsurge in lactobacilli is the result of cavitation. In this context they are important secondary pathogens contributing to the progression of the lesion.
當蛀洞進展至牙本質時，只有最耐酸的細菌可以存活下來，這解釋了蛀洞內lactobacilli的優勢。這個狀況很快就被早期的學者發現(請見第七章)，並成為齲齒診斷的基本。但是，很明顯的在大部份的情況，lactobacilli的增長是來自於蛀洞的產生，他們是造成蛀洞進展重要的次級病原菌。
The acid destruction of a tissue with 30 percent collagen differs from the destruction of a tissue with no collagen. Very few oral bacteria possess collagenases. However, collagen is readily denatured by acid, forming gelatin which is degraded by many oral organisms. Thus, the following sequence is possible in the dentinal lesion. Acid solubilizes the tooth mineral, exposing the collagen scaffold. The acid, as well as the high Ca++ salt content, denatures the collagen. Bacterial proteases degrade the collagen- gelatin to low-molecular-weight peptides and amino acids which can be used for microbial biosynthesis. The process is self repeating, causing expansion of the lesion with the collagen breakdown products transformed into microbial protein.
以酸去破壞含有30%膠原蛋白的組織和破壞不含膠原蛋白的組織是不同的，極少細菌含有膠原蛋白酶，然而，當膠原蛋白被酸變性之後，產生的凝膠(gelatin)可被許多口腔內微生物所分解。因此，接下來的敘述可能為牙本質蛀洞的發生順序。酸使得牙齒內的礦物質可移動，使膠原蛋白的支架暴露出來，酸和高含量的鈣鹽使膠原蛋白變性，細菌的蛋白酶將膠原蛋白-gelatin分解為低分子量的肽胜(peptide)和胺基酸，這些肽胜和胺基酸可被細菌所利用。這個過程不斷的重複，造成蛀洞的擴大，而膠原蛋白的分解產物則成為細菌可利用的蛋白質。
Dentinal lesions are not necessarily bacteriologically similar. The large lesion shown in Figure 12-5 is older than the lesion just developing at the dentino-enamel junction and because of its larger opening, would have access to impacted food and saliva. The nutrient availability would differ between the two lesions, and this should result in selection for a different flora.
在細菌學上，牙本質的蛀洞並不一定相似。和剛蛀進牙本質牙釉質交界的小蛀洞相較，在圖12-5的大蛀洞為較久的蛀洞，較大的開口可以塞入更多的食物和唾液，這兩種蛀洞(大蛀洞和小蛀洞)獲得營養的難易度不同，因此，蛀洞內菌落的組成也不盡相同。
Proteolytic Organisms
The prominence of proteolytic organisms in carious dentin was shown by Burnett and Scherp (Table 12-6). These investigators, using in most instances, aerobic procedures, cultured saliva, enamel lesions, carious dentin and scrapings from the junction between decalcified and intact dentin. Aciduric organisms were more prominent in the enamel lesion while proteolytic organisms dominated in the decalcified scrapings. These proteolytic organisms were heterogeneous but included anaerobic streptococci, micrococci and members of the genera Bacillus and Pseudomonas. Other investigators have isolated other proteolytic species. Hartles and McDonald isolated Clostridium welchii from about 60 percent of 252 carious teeth; and Engel showed that a filtrate of C. welchii, which contained collagenase, could liberate nitrogen from decalcified dentin. Roth isolated from dentinal lesions an aerobic, proteolytic organism (Rothia dentocariosa), which was capable of degrading denatured collagen. These studies indicate that not only are there a variety of proteolytic organisms in the carious dentin, but that the flora at this stage of the lesion is bacteriologically distinct from that found in cariogenic plaque.
分解蛋白的生物體 (Proteolytic organisms)
Burnett和Scherp提出在牙本質的齲齒內大多數為可分解蛋白質的生物體(表12-6)。這些學者在進行唾液、牙釉質齲齒、牙本質齲齒、以及從脫鈣和完整的牙本質交界處刮除下來的成分進行培養時，大多數都是使用有氧的程序，在牙釉質的齲齒裡大多是耐酸性的生物體，而在脫鈣處刮除下的成分裡大多是可分解蛋白質的生物體。這些可分解蛋白質的生物體是包含很多種類的，包括厭氧的鏈球菌、微球菌(micrococci)，以及Bacillus和Pseudomonas屬的細菌。其他學者更分出了其他可分解蛋白質的生物體。Hartles和McDonald分析了252顆齲齒，其中的60%分出了Clostridium welchii，而Engel將含有膠原蛋白酶的C. welchii濾出，發現這隻細菌可從脫鈣的牙本質中釋放氮。另外，Roth在牙本質的齲齒處分出了一種好氧、可分解蛋白質的生物體(Rothia dentocariosa)，這種細菌可以分解變性的膠原蛋白。這些研究並不只是陳述在牙本質內有許多可分解蛋白質的生物體種類的觀點，更點出了在齲齒的這個階段，這些可分解蛋白質的生物體比有致齲性的牙菌斑內的細菌更顯著。
Quantitative Cultural Studies
In many early studies of the carious lesion, the carious dentin was placed into broth media or cultured directly on selective media. In this manner the rapidly-growing species or the sought-after species would be the main organisms isolated, and little information would be available as to the proportional distribution of these cultivable species in the carious dentin.
定量的培養研究 (Quantitative Cultural Studies)
早期許多關於齲齒的研究，都是將齲蛀的牙本質置放在培養液(broth media)或直接在選擇性介質(selective media)中培養。這樣一來，最後分離出來的菌種大多為生長快速的菌種或是較強勢(sougjt-after)的菌種，除此以外，占小比例的菌種就很難被分離出來，也很難獲得關於這些菌種的資訊了。
Loesche and Syed cultured plaque from over an interproximal lesion and also the soft carious dentin from the lesion using a quantitative anaerobic procedure. S. mutans and lactobacilli were present in low proportions in the plaque, but accounted for 28 percent and 20 percent respectively of the organisms in the dentin (Table 12-6). Thus as the lesion penetrated into the dentin, both the primary and secondary cariogens were prominent members of the dentinal flora but not the plaque flora. This spatial distribution of these organisms in the lesion indicates that at the stage of the clinical and/or advanced lesion (Fig. 12-2), plaque samples may no longer be representative of the cariogenic flora within the lesion.
Loesche和Syed 取得鄰接面有齲齒的牙菌斑和齲蛀的牙本質，並以無氧、定量的方式進行培養，在鄰接面的牙菌斑中，S. mutans和lactobacilli只占了很小的比例，卻分別在牙本質的齲齒內占了28 %和 20 %的比例(表12-6)。因此，當齲齒穿透至牙本質的時候，初級和二級齲原皆成為齲齒內主要的細菌，而不是牙菌斑內主要的細菌。這個結果告訴我們，當齲齒已進入到這個階段時，牙菌斑的樣本已無法代表齲齒內細菌的生態了。
Carious dentin can be enucleated from the lesion leaving behind a decalcified surface that represents the front of the lesion. Barnett and Scherp cultured scrapings from this surface and found a sparse flora consisting of high proportions of streptococci and low proportions of lactobacilli and actinomyces (Table 12-6). Edwardsson cultured the same material but approached the site from the pulpal chamber. Extracted teeth were prepared so that dentin could be aseptically removed one layer or portion at a time moving from the intact dentin toward the carious lesion. All initial layers were sterile but thereafter bacteria were encountered in the various layers until the carious dentin was reached. The flora found in the first layer with visible growth was subcultured and extensively characterized. S. mutans was found in less than 10 percent of the decalcified lesions, whereas lactobacilli and Gram-positive rods were found in 33 percent and 50 percent of the lesions. No single organism or group of organisms was unique to the decalcified front (Table l2-6).
將齲蛀的齒質去除後，可在齲齒前端發現脫鈣的表面。Barnett和Scherp將這些脫鈣的表面進行培養，發現一個稀疏的菌落群，包含有高比例的streptococci以及低比例的lactobacilli和actinomyces(表12-6)。Edwardsson也對脫鈣的表面進行培養，只是取得的方向是從牙髓腔往外，他將拔下的牙齒從牙髓腔往齲齒的方向一層一層去除，最一開始取得的幾層牙本質皆為無菌的，之後慢慢開始發現有微生物的存在，最後才到達齲齒處。將開始發現到有微生物的那層牙本質進行培養，發現S. mutans的量低於10%，而lactobacilli和革蘭氏陽性球菌則分別佔了33%和50%。並沒有哪一隻細菌或哪一種細菌是特別存在於脫鈣處的。 (表l2-6).
This lack of bacterial specificity was even more apparent when the various isolates were classified. No single species was found in more than 20 percent of the lesions. The flora was simple, consisting of from one to seven bacterial types. In about 45 percent of the lesions the flora was dominated by one of the following species, Arachnia spp., nine percent; Bifidobacterium spp., nine percent; E. alactolyticum, 11 percent; L. casei, 16 percent. Apparently each of these species at a specific moment found the environment suitable for growth, and acted as a pioneer bacterium which entered the dentinal tubule and produced micro-colonies along the length of the tubule. These findings support a nonspecific bacterial involvement at the level of decalcified dentin.
很明顯的，在此處並沒有細菌的專一性，沒有任何一隻細菌的量占超過20%，在這裡細菌群是很簡單的，只包括1至7種細菌，在45%的齲齒處可發現下列的優勢細菌：Arachnia類占9%，Bifidobacterium類占9%，E. alactolyticum占11%，而L. casei占16%。很明顯的，這些菌種在某一特定時刻發現到這個適合生長的環境，進入到牙本質小管內成為先驅菌種，並沿著牙本質小管形成菌落，這些發現支持了"在脫鈣的牙本質處，細菌是非專一性的(nonspecific bacterial involvement)"的說法。
PULPAL INFECTIONS
An untreated carious lesion can progress through the dentin and into the pulp causing pulpal inflammation and necrosis. The culturing of the canal could provide some information concerning the types of bacteria at the front of the carious lesion. However, by the time these lesions are cultured, there is no adequate way to document the length of time that the pulp had been infected. Also, many pulpal lesions have been cultured in a qualitative manner in that a paper point, after insertion into the pulp canal, is placed into broth media and incubated aerobically. Facultative organisms by virtue of their rapid growth rate predominated in such cultures. In the past these isolates were not well characterized, but this situation has changed.
牙髓腔的感染 PULPAL INFECTIONS
當齲齒未受到治療，持續進行至牙本質，甚至進入到牙髓腔時，會造成牙髓的發炎及壞死。根管內的細菌培養可提供一些關於齲齒前端細菌的資訊。然而，當我們開始進行培養的時候，已無法得知牙髓受到感染的時間有多長，而且，許多牙髓腔內細菌的定性培養已經被做過了，這部分可經由在根管內置入紙針(paper point)，再放置於培養液中，於含氧的環境下進行培養。兼養性細菌因為有生長快速的優點，成為這類培養主要的細菌。從前這類的細菌分離並無法好好的被分類，但這個情況現在已經改變了。
Sundquist and Carlsson found streptococci, enterococci, staphylococci and lactobacilli to be prominent isolates among 566 positive cultures obtained from 1282 root canals. The lactobacilli were classified to the species level and found to be L. casei (41% of the isolates), L. salivarius (28%), L. acidophilus (17%), L. fermentum (10%) and L. plantarum (4%). This profile with the exception of L. salivarius is comparable to the lactobacilli found in the decalcified dentin. This suggests that in the 27 percent of the canals found to be positive for lactobacilli, these organisms entered the canal via extension of the carious lesion. This is not the case when necrotic pulps from traumatized teeth were cultured, as lactobacilli were not found, but anaerobic organisms similar to the periodontal flora were encountered.
Sundquist和Carlsson研究了1282個根管，其中有566個培養基有細菌可被培養出來，被培養出來的細菌裡，又以streptococci、enterococci、staphylococci和lactobacilli占多數，lactobacilli被仔細的分離後發現有：L. casei (41%)、L. salivarius (28%)、L. acidophilus (17%)、L. fermentum (10%)和L. plantarum (4%)。在這裡並沒有分離出L. salivarius，這和在脫鈣牙本質的結果相同，表示在27%含有lactobacilli的根管中，lactobacilli其實是由齲齒延伸至根管的。不過，當牙髓組織的壞死是來自於外傷時，情況便不同了，在這個狀況下不會發現lactobacilli，但是會發現類似於牙周菌落的厭氧細菌。
The presence of L. salivarius in the pulp-canal cultures suggested that salivary contamination had occurred. This was further supported in a separate study in which Mejare examined the streptococcal flora found in 587 positive cultures obtained from l958 root canals. S. sanguis was isolated from 12 percent, S. mutans from four percent and S. salivarius from seven percent of the positive cultures. The frequency of S. mutans recovery was compatible with its prevalence in the flora of decalcified dentin. However, the recoveries of S. sanguis and especially S. salivarius were higher than could be expected. S. salivarius was found significantly more often in teeth with open pulp cavities than in teeth with closed pulp cavities; more often in teeth without, than with periradicular bone rarefactions; and more often among positive cultures when the previous culture had been negative versus positive. These observations indicated that S. salivarius was a salivary contaminant and not indigenous to the infected root canal. Thus, about seven percent of all positive root canal cultures might be expected to be contaminated with saliva. The culturing of caries-infected root canals has not shed much information upon caries etiology.
若在根管內發現L. salivarius，表示根管已受到口水汙染，Mejare的實驗證實了這個說法。Mejare研究了1958個根管，其中在streptococci陽性反應的587個菌落中發現，S. sanguis占了12%，S. mutans占4%，S. salivarius占7%。S. mutans的培養結果和脫鈣處牙本質的相差不遠，然而，S. sanguis和S. salivarius卻遠高於期望值。在牙髓腔已對外相通的牙齒，S. salivarius的量顯著的較沒對外相通的高，在沒有根尖骨頭破壞處S. salivarius的量也較多，在培養結果從陰性轉陽性的S. salivarius的量也較多，以上這些結果表示S. salivarius的來源並不是根管內生的，而是口水汙染來的。因此，在呈現細菌陽性反應的根管中，約有7%已被口水汙染了，這樣的培養並無法提供關於齲齒病因學方面的資訊。
SUMMARY
Dental caries is a multifactoral disease with genetic, environmental, dietary and bacterial factors. In the past the bacterial component appeared to be so complex that it was conceptualized as a constant that produced acid upon exposure to carbohydrates. This simplification became the basis of the nonspecific plaque hypothesis as it related to dental caries. The only way that acid production could be reduced would be by decreasing the plaque and/or carbohydrate intake. Both of these approaches have been the cornerstone of traditional preventive treatment. Keyes' demonstration of bacterial specificity in animal caries models was followed by the demonstration of S. mutans in human plaques. A considerable number of studies have found a significant association of S. mutans with human dental decay. Longitudinal investigations indicate that S. mutans peaks at about the time that caries is diagnosed. However, the correlation is never absolute as there are usually a few teeth that are either highly colonized with S. mutans which do not become carious, or which become carious in the absence of S. mutans. These exceptions probably reflect, in the first instance, that the virulence of S. mutans can be modified and in the second instance, that other bacteria can contribute to the caries process. They do not detract from the basic finding that S. mutans is statistically involved in the majority of human carious lesions. This observation forms the basis of the specific plaque hypothesis and is the departure point for the preventive treatments described in Chapters 15-20.
總結 (SUMMARY)
齲齒是多因性的疾病，包含了基因、環境、飲食和細菌幾個因素。在以前，細菌這項因素太過複雜，以致於被簡略成一個暴露在碳水化合物下會產酸的因子，這個簡化的動作成為了"非專一性牙菌斑假說(nonspecific plaque hypothesis )"用於解釋齲齒的基礎，因此減少產酸的方法只能靠減少牙菌斑和/或碳水化合物的攝取，這兩個方法為傳統預防齲齒的主要方式，Keyes在動物的齲齒模型證明了細菌的專一性，接著證明S. mutans在人類牙菌斑中的存在。許多實驗都證明了S. mutans和人類齲齒間的強力相關性。縱貫性的研究學者指出，當齲齒被診斷出來的時候，S. mutans的量也達到高峰。然而，這之間的相關性卻無法成為完全絕對的，因為在某些無齲齒的牙齒發現高比例的S. mutans，或在齲齒的牙齒上沒有發現到S. mutans。這些例外可能反映出幾個可能性，首先，S. mutans 的毒性可以被修改，另外一個可能就是也許還有其他細菌能造成齲齒。 不過無可否認的是S. mutans is的確和大部分人類的齲齒是相關的。這項觀察成為了"專一性牙菌斑假說(specific plaque hypothesis)"的基礎，並且在第15-20章關於預防這部分產生了不同的治療理念。
第10章 P211
Saliva is remarkably protective against decay, as illustrated by the rampant decay that ensues when salivary flow is low or absent (see "Salivary Factors" in Chap. 11), and by the fact that dental decay was and is a relatively minor health problem in the absence of frequent sucrose consumption (see "Nutritional Factors" in Chap. 11). These protective characteristics of saliva can be attributed primarily to its flushing and buffering capacities that come into play during food ingestion. Thus when food is masticated, the increased salivary flow serves not only to prepare the bolus for swallowing, but provides both a large liquid volume for plaque acids to diffuse into and a bicarbonate buffer to neutralize these acids. In recent years another protective mechanism has been identified which is concerned with the maintenance of a concentration gradient for calcium and phosphate ions which favors their diffusion into the enamel.
Saliva對預防decay這件事具有保護作用, 例如當salivary flow降低時就會發生rampant decay. 對於不常使用含糖食物的人, dental decay是minor health problem. Saliva的保護性質主要可歸功於當攝取食物時他們具有flushing and buffering capacities. 因此當食物被咀嚼時, increased salivary flow不只負責上食團較易被吞嚥, 也提供一個large liquid volume使plaque acids可擴散進去且當作bicarbonate buffer中和這些酸. 近幾年來另一個保護機轉也被確認, 維持calcium and phosphate ions的濃度梯度是其可擴散到enamel內.
Inhibitors of calcium-phosphate precipitation
Calcium-phosphate沉澱的抑制劑
The tooth surface selectively adsorbs acidic glycoproteins and proteins from the bathing saliva giving rise to the acquired enamel pellicle (see "The Acquired Enamel Pellicle" in Chap. 6). This is a normal condition but its biological significance, other than promoting the colonization of certain streptococcal species, is not fully understood. As the pellicle is interposed between the enamel surface and either the saliva or plaque, it has the potential to affect the diffusion of bacterial acids into the tooth and the loss of calcium and phosphate ions from the dissolved hydroxyapatite crystals within the enamel. Some of these adsorbed molecules have been identified as either acidic proline-rich proteins or as an unusual tyrosine-rich peptide that has been named statherin by Hays et al.
牙齒表面會選擇性地吸收acidic glycoproteins以及從bathing saliva附著到acquired enamel pellicle的proteins. 這是個正常情況, 但其除了促進某些streptococcal species colonization外, 在生化上的意義目前未被完全了解. 當pellicale出現在enamel surface及saliva or plaque中間時, 會影響bacterial acids擴散到牙齒及calcium and phosphate ions從enamel的dissolved hydroxyapatitie crystals中流失. 這些被吸收的粒子被認定為acidic proline-rich proteins, 或一種被命名為statherin的unusual tyrosine-rich peptide.
These proteins and peptides have distinct polar and nonpolar amino acid sequences giving rise to a fair amount of molecular asymmetry. In the case of statherin, the polar amino terminal end adsorbs to the tooth surface, resulting in the nonpolar end aligning itself at the pellicle-saliva interface, thereby presenting a new and primarily hydrophobic surface to the bathing saliva. This molecular rearrangement should have important implications in the process of bacterial colonization. However, this does not appear to be the main role of either statherin or the proline-rich peptides, as the presence of these components delays, in vitro both the onset and rate of precipitation of calcium phosphate salts from supersaturated solutions. If this happens in vivo, then it would explain why the teeth are not buried in calcium phosphate deposits.
這些proteins和peptides有明顯極化和非極化的amino acid sequences, 會賦予這些分子不對稱性. 例如statherin的極化端會附著於牙齒表面, 非極化端就會排列在pellicle-saliva的交界, 會使這個侵在唾液中的牙齒有一個疏水的表面. 這個分子的重新排列會影響到細菌colonization的過程. 然而這並不是statherin和proline-rich peptides的主要功能, 因為在非活體實驗中當這些分子延遲出現時, calcium phosphate會從過飽和溶液中儲存下來. 當發生在活體中時, 可以用來解釋為何牙齒沒被calcium phosphate deposits掩埋.
Saliva is supersaturated with calcium and phosphate ions and accordingly, their salts should precipitate out from solution, forming ectopic calcifications on the tooth surface. This occurs during calculus formation, but the incidence and magnitude of this precipitation is minimal compared to the calcifying potential that exists in each ml of saliva. It now appears that statherin and the proline-rich proteins, after adsorbing to the tooth surface, block the nucleation sites for crystal growth of the calcium phosphate salts from the supersaturated saliva. These inhibitors probably are partially degraded by the plaque microbes, but residues survive which presumably prevent precipitation, giving rise to high concentrations of calcium and phosphate ions in the plaque. The elevated concentrations of these ions constitute a constant and powerful remineralizing mechanism in those plaque and pellicle surfaces that are bathed by the saliva. The higher the degree of supersaturation maintained by these inhibitors, the greater the protection against demineralization.
Saliva中calcium ions和phosphate ions是過飽和的, 因此會沉澱成鹽類在牙齒表面形成ectopic calcifications. 這些事情是在calculus形成是會發生, 但這種沉澱的機率和量相對於每一ml saliva的calcifying potential是算少的. 現在知道是statherin和proline-rich proteins吸附在牙使表面後, 會阻斷由過飽和唾液來的calcium phosphate salts所產生的nucleation sites for crystal growth. 這些inhibitors可能會因plaque microbes的出現而減少, 但還是會有殘留以免過度沉澱, 使得plaque中的calcium ions和phosphate ions濃度偏高. 這些離子濃度的提高會在saliva中的plaque和pellicle surfaces形成一個連續且有力的在鈣化系統. 這些inhibitors所維持的過飽和程度越高, 對於脫鈣處所造成的保護效果越大.
These same inhibitory proteins adsorb preferentially onto fluorapatite surfaces compared to hydroxyapatite surfaces. Apparently, the incorporation of fluoride into the apatite lattice results in a solid having a lower surface energy and a decreased interaction with water. As a consequence, the salivary proteins are able to effectively compete with water for binding sites on the enamel surface. This leads to a greater adsorption and retention of these proteins on fluorapatite. As free fluoride ion is also likely to be present in such a milieu, conditions are favorable for remineralization (see "Fluoride" in Chap. 18).
這些inhibitory proteins較容易吸附在fluorapatite surfaces上. 很明顯地若將fluoride併到apatite lattice中會形成一個solid surface, 會有較低的surface energy且和水的交互作用會減少. 結果會造成salivary proteins和水競爭enamel surface的binding sites, 使得這些proteins較容易吸附停留在fluorapatite上. 因此當在這樣的環境下出現free fluoride ion時則較容易發生在鈣化.
NEUTRALIZATION OF PLAQUE ACIDS
中和牙菌斑酸性
The chemoparasitic theory predicted that acid solubilized the tooth mineral. The various in vitro models described how this could occur, and indicated that in a bathing medium such as saliva which is saturated with calcium and phosphate ions, the plaque pH would have to go below 5.0 in order for demineralization to occur. Early investigators focused briefly on saliva as the most likely variable to influence caries initiation. To their surprise, they found that the salivary pHs were remarkably constant near neutrality, and did not differ between highly caries-active and caries-free individuals. When saliva was stimulated during eating, both the flow rate and the levels of bicarbonate buffer rose dramatically, i.e., there was about a 20-fold increase in bicarbonate in the parotid saliva.
Chemoparasitic theory預言酸會溶掉牙齒的礦物質成分. 許多不同的非活體實驗中陳述其如何發生, 並指出當沉浸在充滿calcium ions和phosphate ions的saliva中, plaque pH必須降到5.0以下才有可能發生脫鈣. 早期研究者將焦點放在saliva, 因為認為saliva最可能影響caries initiation. 但令人驚訝的是他們發現salivary pHs不管在caries-active或caries-free的個體中幾乎都是接近中性的. 當進食刺激唾液分泌時, bicarbonate buffer的含量及流速都會提高, 例如parotid saliva的bicarbonate會提高20倍.
The question then became, why didn't the saliva neutralize the acids produced in the plaques of carious teeth? Miller had shown that blue litmus paper turned red or acidic when pressed against carious dentin. Did this indicate that the acid production in the carious lesion was greater than that which could be neutralized by the salivary bicarbonate buffer? These questions were not answered until the experiments of Stephan in the 1940s. Initially Stephan used pH color indicators to demonstrate that the pH in a carious lesion was as low as 4.2 and that the average pH of carious surfaces was 0.7 pH units lower than that of plaques from intact tooth surfaces. However, it was not until antimony pH electrodes were employed for direct pH measurements in the mouth, that the kinetics of acid formation and neutralization on the tooth surfaces were described.
問題是這些唾液為何無法中和plaque of carious teeth所產生的酸? Miller當現當藍色石蕊試紙碰到carious dentin會變成紅色. 但這就表示carious lesion所產生酸的量大於salivary bicarbonate buffer所能中和的量嗎? 這問題直到1940年Stephan的實驗才被解答. 一開始Stephan用pH color indicator發現carious lesion的pH值是4.2, 較完整牙齒表面的plaque pH值低0.7個pH units. 然而直到antimony pH electrodes用在口內直接做pH值測量, 牙齒表面酸的形成及被中和的動力學才有辦法被描述.
STEPHAN CURVE
Stephan selected patients who were caries free, caries inactive or who exhibited various degrees of caries activity. They were instructed not to brush their teeth for three to four days prior to the measurement of the pH on the labial surfaces of the maxillary and mandibular anterior teeth. The pH readings were obtained prior to rinsing for two minutes with a 10 percent glucose solution, and at intervals thereafter until the pH returned to its original value. The pH profiles for maxillary teeth are shown in Figure 10-3. In all instances, there was a rapid pH drop, indicating that the glucose was instantaneously converted to acid products by the plaque flora. The suddenness and magnitude of this acid production obviously overwhelmed the available salivary buffering capacity. The low pHs persisted, in some cases for more than 60 minutes after the glucose solution had been expectorated. This indicated that the salivary buffers were inadequate in neutralizing the acids in the plaque and/or that acid was continually being produced in the plaque. This latter possibility was suggested by the continued pH drop in the subjects in Group V, i.e., the extremely caries-active subjects.
Sephan選了一些病人, 他們分別是caries free, caries inactive及有各種不同程度的caries activity. 指示他們在測量上下顎前牙唇側面的pH值時前3~4天不要刷牙. 在測pH值時請他們先以10% glucose solution漱口2分鐘, 之後每間隔一段時間再去測, 直到其回復到original value. 上顎牙齒pH質變化圖呈現在Figure 10-3. 所有人的pH值會迅速下降, 表示glucose會立即被plaque flora轉換成acid products. 產酸的量及速度明顯地超越口水的緩衝能力. 在某些病人, 其葡萄糖水吐出後, 低pH值還持續超過60分鐘. 這表示口水緩衝能力對中和牙菌斑所產生的酸性物質和(或)其持續所產生的酸性物質是不足的. 後者可在Group V的持續pH drop看出, 這一組的受試者是extremely caries-active.
The clinical diagnosis used to initially stratify the subjects had biological significance as the pH profiles of the caries-free and caries-inactive groups were distinctly different from those of the caries-active groups (Fig. 10-3). This was most apparent in a comparison of the caries-free group with the extremely caries-active group where the pHs differed by almost 1 to 1.5 logs at each time interval. This difference can best be explained by assuming that the microbial composition of the caries-free plaques differed from that of the caries-active plaques. This is not surprising since most of the caries-active plaques were located over carious lesions, and it is now known that plaques from caries-active sites have significantly higher levels and proportions of S. mutans than plaques from caries-free sites (see "Bacterial Factors" in Chap. 12). These pH curves established the fact that plaque pH quickly dropped following a glucose rinse and stayed reduced for 30 to 60 minutes thereafter. If the patients had active caries, the lowest pHs obtained invariably went below 5.0, the critical pH for enamel demineralization (Table 10-5).
一開始用來分類受試者的臨床診斷有很重要的生物意義, 因為caries-free和caries-inactive組和caries-active組的pH profiles有明顯地不同(Figure 10-3). Caries-free組和extremely caries-active組的差別是最大的, 在每一個time interval其pH值會差到1~1.5 logs. 這個差異可以用caries-free組牙菌斑和caries-active組牙菌斑的微生物組成不同來解釋. 此現象並不令人驚訝, 因為caries-free plaques位在carious lesions上, 目前知道caries-active處的plaques較caries-free處的plaques相較下有明顯較高濃度的S.mutans. 這些pH curves顯示plaque pH值在漱完葡萄糖水後會迅速下降, 且會持續30~60分鐘. 如果病人有active caries, 最低的pH值不能低 於5.0, 這是enamel脫鈣的critical pH.
IN VITRO PLAQUE pH MEASUREMENTS
活體外牙菌斑pH值的測量
These plaque pH response curves have come to be known as Stephan Curves. Similar curves were obtained by an in vitro procedure in which aliquots of plaque were removed from the teeth and after suspension in a drop of distilled water the pH was read. In a typical experiment the plaque pH was determined before and after the subject rinsed his mouth with the test solution or consumed the test food. These in vitro studies could be performed without the use of special electrodes and could be standardized as to age of the plaque and the amount of plaque used. However, because of the need for enough plaque for the repeated samplings, the subjects usually went for several days without oral hygiene, and the plaque was then pooled from the most accessible sites, such as the buccal and labial smooth surfaces along the gingival margin. The predominant cultivable flora of such plaques includes, S. mitis, S. sanguis, and various Actinomyces species and would be considered a noncariogenic plaque (see "Bacterial Factors" in Chap. 12). Nevertheless, such noncariogenic plaques, whether from a single site (Fig. 10-3) or from many sites, displayed the characteristic pH drop following exposure to sugar solutions.
這些牙菌斑pH值的反應曲線後來就變成大家所知道的Stephan Curves. 在非活體步驟中也得到相同的曲線, 將牙菌斑從牙齒移除, 使其懸浮於一滴蒸餾水中, 讀取其pH值. 在典型實驗中, 在受試者以受試溶液漱口或攝取受試食物之前及之後測量其牙菌斑pH值.這些非活體研究可以不用用到特殊的電極且可以將牙菌斑的年紀及量做標準化. 然而, 因為需要足夠的牙菌斑作repeated samplings, 受試者需要好幾天不做口腔清潔, 且牙菌斑取得會從最容易取得之處, 例如沿著牙齦邊緣的頰側或唇側平滑面. 最多從牙菌斑培養到的細菌有S. mitis, S. samguis, 和各種不同的Actinomyces species, 這些細菌被認為是noncariogenic plaque. 不過這些noncariogenic plaques不管是從單一部位或很多部位取得, 它們在暴露於糖水後的pH drop反應特色都相同.
The pH distinctions between a noncariogenic and a cariogenic site, i.e., between Group I and Group V in Figure 10-3 were lost in these experiments with pooled plaques. Gone from consideration was the fact that Stephan separated his subjects into groups according to clinical caries status, and that these clinical diagnoses correlated with the resting pH levels of the plaques and with the magnitude of the pH depression in the plaques following the glucose rinse (Fig. 10-3). The dynamics of plaque acid production, per se, became the only parameter under investigation.
在noncariogenic處及cariogenic處的pH值差異, 例如在Figure 10-3中Group I和Group V的差異, 在pooled plaques的實驗就消失了. pH值差異的消失, 是因為它不像Stephan將其受試者依臨床蛀牙狀況分類, 這些臨床診斷和一開始牙菌斑的resting pH levels及在漱完葡萄糖水後pH depression的程度有關. 牙菌斑產酸物的動力平衡變成研究的唯一變數.
In this way Stephan's in vivo pH findings, which supported the specific plaque hypothesis, gave rise to experiments which championed the nonspecific plaque hypothesis. Subjects were studied without precisely defining their current caries status, and in some cases a salivary sediment system was substituted for a pooled plaque suspension. This latter substitution came about when it was demonstrated that noncariogenic plaque suspensions and the salivary sediments exhibited the same pH profiles after exposure in vitro to various carbohydrate and nitrogen substrates. The sediment was prepared by centrifuging whole saliva that had been collected from individuals who were instructed to neither eat nor drink and to avoid oral hygiene for finite periods prior to collection. This sediment would be composed of bacteria and epithelial cells shed primarily from the oral soft tissues and accordingly, would differ in some respects from the plaque flora. The fact that both systems produced acid in a similar manner probably reflected the dominance of the acidogenic streptococcal species, such as S. salivarius, S. mitis, and S. sanguis in the saliva and in the noncariogenic plaques. Studies employing these in vitro systems cannot describe the specific events which occur in cariogenic plaques, but provide information concerning the interactions of various substrates with a mixed oral flora.
Stephan在活體內的pH finding支持specific plaque hypothesis, 使nonspecific plaque hypothesis的擁護者開始做實驗. 受試者未明確定義其目前caries status, 在某些受試者的唾液沉澱系統被置換成pooled plaque suspension. 當noncriogenic plaque suspensions和唾液沉積在活體外接觸各種不同碳水化合物及nitrogen substrates後仍維持相同pH值, 就會出現pooled plaque suspension. 沉澱物是將每位受試者口水離心, 他們的口水在收及前一段時間不能吃或喝東西且要避免任何口腔清潔. 這樣的沉積物是由口腔軟組織的細菌及表皮細胞脫落所組成, 和plaque flora不同. 兩個系統在相同方式下都產酸很可能表示主要產酸的streptococcal species例如S. salivarius, S. mitis, 和S. sanguis會存在saliva及noncariogenic plaques中. 利用這些活體實驗的研究無法詳述在cariogenic plaques發生的事, 但提供在mixed oral flora中各種不同基質間的交互作用.
CONTINUOUS IN VIVO PLAQUE pH MEASUREMENTS
在活體中pH值的測量
Stephan had positioned a small antimony pH electrode in the plaque and measured the pH drop following a glucose rinse. An alternate approach that awaited the development of microelectronic telemetry, was the placement of a miniature glass electrode into a tooth in such a manner that the glass tip was flush with the tooth surface so that plaque would form over it.
Stephan放一個小的antimony pH electrode在牙菌斑中測量在葡萄糖水漱口後的pH drop. 另一個需要微電子遠距測量術幫忙的方式是放一個miniature glass electrode在牙齒上, glass tip會沖洗過牙齒表面, 牙菌斑就在它上面形成.
Such electrode assemblies were constructed in denture teeth by Graf and Muhlemann and are illustrated in Figure 10-4. In the upper appliance the interproximal area where the electrode was located, was bordered by the denture tooth and the abutment tooth. This arrangement was subjected to a pumping action due to the mobility of the denture saddle, which led to unexpectedly low pH values when the test substance was administered in the form of a chewable food. This was not observed when the electrode was situated in an interproximal area between two denture teeth as shown in the lower appliance in Figure 10-4. Thus a seemingly insignificant difference in the placement of the electrodes influenced the pH response, indicating how localized and specific plaque ecosystems are. The indwelling electrodes were located below the contact points of the teeth, so that they continuously monitored the pH in sites that mimicked the caries-prone interproximal surfaces in regard to salivary access and oral hygiene procedures.
這種電極裝置是由Graf和Muhlemann在denture teeth上建立出來的, 如圖10-4. 在上顎裝置, 放電極的interproximal area被denture tooth和支台齒包圍. 這樣的排列容易受到pumping action是因為denture saddle的mobility, 會導致受試者在咀嚼時會有特別低的pH值. 但是當在下顎裝置電極放在2個denture teeth的interproximal area時這種情況就不會發生, 如圖10-4. 所以似乎放電極的位置就會影響pH值的反應, 表示plaque ecosystems是很localized且specific. 在中間的電極應放在牙齒的接觸點之下, 才能追中這些在一般口水及口腔清潔活動下較容易蛀牙的鄰接面的pH值.
The discontinuous in vitro and continuous in vivo pH measuring techniques have not been directly compared in the same subjects. However, pH readings have been obtained with both methods, on different subjects, ingesting the same food items taken in the same sequence, with a fixed interval between items. In the experiment shown in Figure 10-5, six subjects per experimental group ingested one-half of a pear in 10 ml of juice, followed after one minute by the drinking of 120 ml of coffee containing 10 ml of milk and 12 g of sucrose. The dashed line reflects the pH readings obtained by the in vitro method, and the solid lines, the readings obtained by in vivo telemetry. In the in vitro experiment the acidic pear juice reduced the pH minimally, whereas the coffee decreased the pH to about 5.7. Thereafter the pH remained constant for a few minutes and then slowly increased. In the in vivo experiment, the pear juice led to an immediate drop of two pH units followed by a brief recovery which was interrupted by the ingestion of the coffee. The pH during the consumption of the coffee remained at about 4.9 and thereafter rose to about 5.2, only to drop again to about 4.5. At the 28-minute mark the in vitro method showed the pH to be about 6.0, whereas the in vivo method indicated that the pH was 4.5.
在活體外不連續的pH值和在活體內連續的pH值測量技術並沒有在相同個體內被比較. 然而這兩種方式的pH reading都用在不同個體, 以相同順序攝取相同食物且相同的interval被得知. Figure 10-5的實驗顯示, 在每一個實驗組的6個個體都攝取來自半顆洋梨10ml果汁, 接著1分鐘後喝120ml的咖啡, 內含10ml的牛奶和12g的葡萄糖. 虛線表示以非活體方式測量得到的pH 值, 實現表示以活體方式測量得到的pH 值. 在非活體實驗中, 酸性梨子汁會小小地降低pH值, 而咖啡會將pH值降到5.7. 之後pH值會維持數分鐘後再緩慢地增加. 在活體實驗中, 梨子汁會讓pH值立即下降2個單位, 之後在短暫的回覆後會再因攝取咖啡而降低. 在攝取咖啡時pH值會維持在4.9, 然後會升到5.2, 之後會再降到4.5. 在28分時非活體的方式pH值約6.0活體方式pH值為4.5.
Clearly, these methods measured the same directional movement, but differed greatly in their sensitivities. The in vivo method measures the response of plaque which formed in a caries-prone site where salivary access is limited and where acidogenic and aciduric bacteria would be selected for. The fact that the plaque pH is read on a glass surface and not on tooth surface means that there is no calcium and phosphate ions made available from the solubilized enamel to buffer the acid drop. For these reasons one would expect the pH in this location read by the continuous pH method, to be lower than the pH generated by smooth surface plaque and read either in vivo by microelectrodes applied to the enamel surface or by the in vitro method.
很明顯地這些方式測量的方向相同, 但其sensitivities差異很大. 活體方式測量的是較容易形成蛀牙處的牙菌斑, 這些地方口水流量較少且產酸性及耐酸性的細菌會選在這些地方生存. 牙菌斑pH值是在glass surface上測量而不是tooth surface, 表示沒有從溶掉enamel上calcium ions和phosphate ions來中和酸. 因為這些原因, 由continuous pH method讀出來的pH值會比在smooth surface plaque上讀出來的pH值第, 不管是活體中用microelectrode測量enamel表面或用非活體方式.
The in vivo methodology tests single site plaque samples and would yield data consistent with the specific plaque hypothesis. The in vitro method combines plaque from all accessible tooth surfaces and ignores the microbial uniqueness of cariogenic and noncariogenic plaques. The pH is read extraorally under conditions in which the metabolism of some plaque organisms could be inhibited due to the levels of atmospheric oxygen in the new environment .
活體方式側單一處牙菌斑樣本, 產生的資料和specific plaque hypothesis相符. 非活體方是測量多處牙齒表面收集來的牙菌斑, 忽略cariogenic plaques和noncariogenic plaques的microbial uniqueness.
The in vitro pH is thus measured under non-physiological conditions and reflects primarily the metabolic activity of noncariogenic plaque. Under these conditions the metabolic response is muted, but the in vitro methodology can still show differences between individuals, if the clinical caries status between them is great. Englander et al. measured the pH of pooled plaques before and after a sucrose rinse in rampant caries patients and in caries-free subjects. The initial pHs of the plaques from the caries-active patients were lower than those observed in the plaques of the caries-free subjects, which is in agreement with Stephan's findings (Fig. 10-3). Twenty minutes after the sucrose rinse, the pHs in the patients were depressed from the initial values, whereas in the caries-free subjects no changes from the baseline values were noted. Apparently the microbial differences between the plaques of the two different groups were so great, that they were able to express themselves despite the limitations of the in vitro pH methodology used.
非活體的pH值是在非生理情況下測量, 主要反應noncariogenic plaque的新陳代謝活性. 在這樣的情況下, 新陳代謝反應會被掩蓋, 但非活體方式還是可以顯示出個體差異, 如果這些個體臨床蛀牙情況差異很大的話. Englander et al.在猛爆性蛀牙和沒有蛀牙的個體分別測量其在使用葡萄糖漱口水前後pooled plaques的pH值. 一開始在caries-active病人上測到的牙菌斑pH值較caries-free病人低, 這點和Stephan的發現相符. 在以葡萄糖水漱口20分鐘後, caries-active的病人口腔內pH值較原來低, 而caries-free病人的pH值與原先相較下沒有改變. 很明顯地, 這兩組病人牙菌斑的microbial differences很大, 才能在非活體pH值測量方式的限制下, 顯現它們的差異.
THE EFFECT OF SALIVA ON PLAQUE ACID PRODUCTION
唾液對牙菌斑產酸的影響
Salivary flow, because of its volume, i.e., over one liter per day, and because of its buffering capacity, should exert an appreciable effect on plaque pH. This was established by Englander et al., who compared the changes in plaque pH in the presence and absence of saliva. Saliva was diverted away from the plaque by placing cups over the parotid duct, thereby directing the flow out of the mouth and by evacuating the submandibular saliva from the floor of the mouth by means of suction. The isolated teeth were then sprayed for 15 seconds with a 1.5 M sucrose solution (50 percent) and the pH measured in vitro at the times indicated in Table 10-6. In the absence of saliva the pHs dropped faster and attained values that were about 0.4 to 0.8 units lower than those observed in the presence of saliva.
人體的唾液, 因為一天的分泌量超過1升且有緩衝能力, 對牙菌斑pH值會有很大的影響. 這個理論是由Englander et al.建立, 他們比較在有唾液存在及無唾液存在時pH值的變化. 把小杯子放在parotid duct上將牙菌斑上的唾液導流出口外, 將吸唾管放在口底吸出submandibular saliva. 分離的牙齒以50%的葡萄糖容易沖15秒, 此時以非活體方式測量pH值, 結果紀錄在table10-6. 沒有唾液時pH值會下降較快, 比有唾液時低約0.4~0.8單位.
The in vivo experiments of Stephan (Table 10-5) indicated that the pHs of the lower anterior teeth before and after the glucose rinse were always higher than the values obtained on the upper anterior teeth. Subsequently, Kleinberg and Jenkins, with the in vitro method, showed that the resting pH of interproximal plaque taken from the lower anterior teeth was consistently higher than the pH on interproximal plaque taken from the upper anterior teeth. This was correlated with the higher pHs of the bathing submandibular and sublingual saliva about the lower teeth. In addition a correlation between salivary flow rate and pH was observed, with the faster secretors having the higher resting pH levels in their plaques.
Stephan的活體實驗(Table 10-5)指出下顎前牙的pH值不論在漱葡萄糖水之前或之後都比上顎前牙高. 接著Kleinberg和Jenkins以非活體方式淺是下顎前牙鄰接面牙菌斑的resting pH比上顎前牙鄰接面牙菌斑pH高. 這項發現符合下顎牙齒一直浸泡在在pH值較高的submandibular 和sublingual saliva. 另外也發現唾液流速和pH值間也有相關性, 流速較快的地方其牙菌斑的resting pH值較高.
There are several factors in saliva capable of restoring plaque pH towards neutrality (Table 10-7). The most obvious are the salivary fluid volume and bicarbonate content. Both of these factors are interdependent in parotid saliva in that the concentration of bicarbonate increases significantly with increased flow of saliva. As this usually occurs coincident with eating, this salivary buffer system is most suited to neutralize the pH depressions that occur during the eating of meals. This probably accounts for the fact that considerable amounts of sucrose, i.e., 3/4 pound per day, can be consumed at meal times without an obvious increase in caries activity (see "Vipeholm Study" in Chap. 11). This protective mechanism, which obviously evolved in conjunction with primitive man's pattern of eating when food was available, can be circumvented by modern man's habit of frequently ingesting high-sucrose-containing products which do not elicit a compensatory flow of saliva.
在唾液中有許多因素可以將牙菌斑pH值回復到中性(Table10-7). 效果最顯著的是唾液流量和bicarbonate content. 這兩個因素都和parotid saliva有關, 當唾液流量增加時, bicarbonate濃度就會增加. 這在吃飯時最常發生, 唾液緩衝系統最適合在此時中和pH值. 這可以用來解釋一定量的葡萄糖, 約3/4 pound, 可以在餐與餐之間食用而不會增加蛀牙活性. 人類近代的飲食習慣常攝取高葡萄糖含量製品, 會減少唾液流量, 會妨礙這個自人類攝取食物以來就有的保護機制.
Other salivary factors which neutralize plaque acidity are urea and sialin. Urea appears in the saliva in small amounts, i.e. 10mg/100ml and its levels are secondary to its levels in the serum. As such it is diet dependent and would peak in saliva a few hours after a protein food has been digested. The salivary levels of urea would be elevated in people ingesting low carbohydrate-high protein diets, and could contribute to the low caries experience associated with these diets (see "Low Carbohydrate Diets" in Chap. 16). Urea is converted by certain plaque bacteria to ammonia and carbon dioxide. At normal salivary pHs the pK of ammonia favors ammonia ion formation, thereby removing hydrogen ions from the plaque environment.
其他唾液中可以中和牙菌斑酸性的因子有urea和sialin. Urea在唾液中含量很少, 約10mg/100ml, 這個含量較血清中含量少. 它的含量和飲食有關, 在攝取含蛋白質食物數小時後在血清中會達到高峰. 攝取低碳水化合物高蛋白質飲食的人唾液中urea含量會升高, 這樣的飲食可以讓蛀牙的機會降低. 某些牙菌斑細菌會將urea轉換成ammonia和carbon dioxide. 在正常唾液pH值下, ammonia的pK值喜歡以ammonia ion的形式存在, 因此會移除牙菌斑內的hydrogen ions.
Saliva對預防decay這件事具有保護作用, 例如當salivary flow降低時就會發生rampant decay. 對於不常使用含糖食物的人, dental decay是minor health problem. Saliva的保護性質主要可歸功於當攝取食物時他們具有flushing and buffering capacities. 因此當食物被咀嚼時, increased salivary flow不只負責上食團較易被吞嚥, 也提供一個large liquid volume使plaque acids可擴散進去且當作bicarbonate buffer中和這些酸. 近幾年來另一個保護機轉也被確認, 維持calcium and phosphate ions的濃度梯度是其可擴散到enamel內.
Inhibitors of calcium-phosphate precipitation
Calcium-phosphate沉澱的抑制劑
The tooth surface selectively adsorbs acidic glycoproteins and proteins from the bathing saliva giving rise to the acquired enamel pellicle (see "The Acquired Enamel Pellicle" in Chap. 6). This is a normal condition but its biological significance, other than promoting the colonization of certain streptococcal species, is not fully understood. As the pellicle is interposed between the enamel surface and either the saliva or plaque, it has the potential to affect the diffusion of bacterial acids into the tooth and the loss of calcium and phosphate ions from the dissolved hydroxyapatite crystals within the enamel. Some of these adsorbed molecules have been identified as either acidic proline-rich proteins or as an unusual tyrosine-rich peptide that has been named statherin by Hays et al.
牙齒表面會選擇性地吸收acidic glycoproteins以及從bathing saliva附著到acquired enamel pellicle的proteins. 這是個正常情況, 但其除了促進某些streptococcal species colonization外, 在生化上的意義目前未被完全了解. 當pellicale出現在enamel surface及saliva or plaque中間時, 會影響bacterial acids擴散到牙齒及calcium and phosphate ions從enamel的dissolved hydroxyapatitie crystals中流失. 這些被吸收的粒子被認定為acidic proline-rich proteins, 或一種被命名為statherin的unusual tyrosine-rich peptide.
These proteins and peptides have distinct polar and nonpolar amino acid sequences giving rise to a fair amount of molecular asymmetry. In the case of statherin, the polar amino terminal end adsorbs to the tooth surface, resulting in the nonpolar end aligning itself at the pellicle-saliva interface, thereby presenting a new and primarily hydrophobic surface to the bathing saliva. This molecular rearrangement should have important implications in the process of bacterial colonization. However, this does not appear to be the main role of either statherin or the proline-rich peptides, as the presence of these components delays, in vitro both the onset and rate of precipitation of calcium phosphate salts from supersaturated solutions. If this happens in vivo, then it would explain why the teeth are not buried in calcium phosphate deposits.
這些proteins和peptides有明顯極化和非極化的amino acid sequences, 會賦予這些分子不對稱性. 例如statherin的極化端會附著於牙齒表面, 非極化端就會排列在pellicle-saliva的交界, 會使這個侵在唾液中的牙齒有一個疏水的表面. 這個分子的重新排列會影響到細菌colonization的過程. 然而這並不是statherin和proline-rich peptides的主要功能, 因為在非活體實驗中當這些分子延遲出現時, calcium phosphate會從過飽和溶液中儲存下來. 當發生在活體中時, 可以用來解釋為何牙齒沒被calcium phosphate deposits掩埋.
Saliva is supersaturated with calcium and phosphate ions and accordingly, their salts should precipitate out from solution, forming ectopic calcifications on the tooth surface. This occurs during calculus formation, but the incidence and magnitude of this precipitation is minimal compared to the calcifying potential that exists in each ml of saliva. It now appears that statherin and the proline-rich proteins, after adsorbing to the tooth surface, block the nucleation sites for crystal growth of the calcium phosphate salts from the supersaturated saliva. These inhibitors probably are partially degraded by the plaque microbes, but residues survive which presumably prevent precipitation, giving rise to high concentrations of calcium and phosphate ions in the plaque. The elevated concentrations of these ions constitute a constant and powerful remineralizing mechanism in those plaque and pellicle surfaces that are bathed by the saliva. The higher the degree of supersaturation maintained by these inhibitors, the greater the protection against demineralization.
Saliva中calcium ions和phosphate ions是過飽和的, 因此會沉澱成鹽類在牙齒表面形成ectopic calcifications. 這些事情是在calculus形成是會發生, 但這種沉澱的機率和量相對於每一ml saliva的calcifying potential是算少的. 現在知道是statherin和proline-rich proteins吸附在牙使表面後, 會阻斷由過飽和唾液來的calcium phosphate salts所產生的nucleation sites for crystal growth. 這些inhibitors可能會因plaque microbes的出現而減少, 但還是會有殘留以免過度沉澱, 使得plaque中的calcium ions和phosphate ions濃度偏高. 這些離子濃度的提高會在saliva中的plaque和pellicle surfaces形成一個連續且有力的在鈣化系統. 這些inhibitors所維持的過飽和程度越高, 對於脫鈣處所造成的保護效果越大.
These same inhibitory proteins adsorb preferentially onto fluorapatite surfaces compared to hydroxyapatite surfaces. Apparently, the incorporation of fluoride into the apatite lattice results in a solid having a lower surface energy and a decreased interaction with water. As a consequence, the salivary proteins are able to effectively compete with water for binding sites on the enamel surface. This leads to a greater adsorption and retention of these proteins on fluorapatite. As free fluoride ion is also likely to be present in such a milieu, conditions are favorable for remineralization (see "Fluoride" in Chap. 18).
這些inhibitory proteins較容易吸附在fluorapatite surfaces上. 很明顯地若將fluoride併到apatite lattice中會形成一個solid surface, 會有較低的surface energy且和水的交互作用會減少. 結果會造成salivary proteins和水競爭enamel surface的binding sites, 使得這些proteins較容易吸附停留在fluorapatite上. 因此當在這樣的環境下出現free fluoride ion時則較容易發生在鈣化.
NEUTRALIZATION OF PLAQUE ACIDS
中和牙菌斑酸性
The chemoparasitic theory predicted that acid solubilized the tooth mineral. The various in vitro models described how this could occur, and indicated that in a bathing medium such as saliva which is saturated with calcium and phosphate ions, the plaque pH would have to go below 5.0 in order for demineralization to occur. Early investigators focused briefly on saliva as the most likely variable to influence caries initiation. To their surprise, they found that the salivary pHs were remarkably constant near neutrality, and did not differ between highly caries-active and caries-free individuals. When saliva was stimulated during eating, both the flow rate and the levels of bicarbonate buffer rose dramatically, i.e., there was about a 20-fold increase in bicarbonate in the parotid saliva.
Chemoparasitic theory預言酸會溶掉牙齒的礦物質成分. 許多不同的非活體實驗中陳述其如何發生, 並指出當沉浸在充滿calcium ions和phosphate ions的saliva中, plaque pH必須降到5.0以下才有可能發生脫鈣. 早期研究者將焦點放在saliva, 因為認為saliva最可能影響caries initiation. 但令人驚訝的是他們發現salivary pHs不管在caries-active或caries-free的個體中幾乎都是接近中性的. 當進食刺激唾液分泌時, bicarbonate buffer的含量及流速都會提高, 例如parotid saliva的bicarbonate會提高20倍.
The question then became, why didn't the saliva neutralize the acids produced in the plaques of carious teeth? Miller had shown that blue litmus paper turned red or acidic when pressed against carious dentin. Did this indicate that the acid production in the carious lesion was greater than that which could be neutralized by the salivary bicarbonate buffer? These questions were not answered until the experiments of Stephan in the 1940s. Initially Stephan used pH color indicators to demonstrate that the pH in a carious lesion was as low as 4.2 and that the average pH of carious surfaces was 0.7 pH units lower than that of plaques from intact tooth surfaces. However, it was not until antimony pH electrodes were employed for direct pH measurements in the mouth, that the kinetics of acid formation and neutralization on the tooth surfaces were described.
問題是這些唾液為何無法中和plaque of carious teeth所產生的酸? Miller當現當藍色石蕊試紙碰到carious dentin會變成紅色. 但這就表示carious lesion所產生酸的量大於salivary bicarbonate buffer所能中和的量嗎? 這問題直到1940年Stephan的實驗才被解答. 一開始Stephan用pH color indicator發現carious lesion的pH值是4.2, 較完整牙齒表面的plaque pH值低0.7個pH units. 然而直到antimony pH electrodes用在口內直接做pH值測量, 牙齒表面酸的形成及被中和的動力學才有辦法被描述.
STEPHAN CURVE
Stephan selected patients who were caries free, caries inactive or who exhibited various degrees of caries activity. They were instructed not to brush their teeth for three to four days prior to the measurement of the pH on the labial surfaces of the maxillary and mandibular anterior teeth. The pH readings were obtained prior to rinsing for two minutes with a 10 percent glucose solution, and at intervals thereafter until the pH returned to its original value. The pH profiles for maxillary teeth are shown in Figure 10-3. In all instances, there was a rapid pH drop, indicating that the glucose was instantaneously converted to acid products by the plaque flora. The suddenness and magnitude of this acid production obviously overwhelmed the available salivary buffering capacity. The low pHs persisted, in some cases for more than 60 minutes after the glucose solution had been expectorated. This indicated that the salivary buffers were inadequate in neutralizing the acids in the plaque and/or that acid was continually being produced in the plaque. This latter possibility was suggested by the continued pH drop in the subjects in Group V, i.e., the extremely caries-active subjects.
Sephan選了一些病人, 他們分別是caries free, caries inactive及有各種不同程度的caries activity. 指示他們在測量上下顎前牙唇側面的pH值時前3~4天不要刷牙. 在測pH值時請他們先以10% glucose solution漱口2分鐘, 之後每間隔一段時間再去測, 直到其回復到original value. 上顎牙齒pH質變化圖呈現在Figure 10-3. 所有人的pH值會迅速下降, 表示glucose會立即被plaque flora轉換成acid products. 產酸的量及速度明顯地超越口水的緩衝能力. 在某些病人, 其葡萄糖水吐出後, 低pH值還持續超過60分鐘. 這表示口水緩衝能力對中和牙菌斑所產生的酸性物質和(或)其持續所產生的酸性物質是不足的. 後者可在Group V的持續pH drop看出, 這一組的受試者是extremely caries-active.
The clinical diagnosis used to initially stratify the subjects had biological significance as the pH profiles of the caries-free and caries-inactive groups were distinctly different from those of the caries-active groups (Fig. 10-3). This was most apparent in a comparison of the caries-free group with the extremely caries-active group where the pHs differed by almost 1 to 1.5 logs at each time interval. This difference can best be explained by assuming that the microbial composition of the caries-free plaques differed from that of the caries-active plaques. This is not surprising since most of the caries-active plaques were located over carious lesions, and it is now known that plaques from caries-active sites have significantly higher levels and proportions of S. mutans than plaques from caries-free sites (see "Bacterial Factors" in Chap. 12). These pH curves established the fact that plaque pH quickly dropped following a glucose rinse and stayed reduced for 30 to 60 minutes thereafter. If the patients had active caries, the lowest pHs obtained invariably went below 5.0, the critical pH for enamel demineralization (Table 10-5).
一開始用來分類受試者的臨床診斷有很重要的生物意義, 因為caries-free和caries-inactive組和caries-active組的pH profiles有明顯地不同(Figure 10-3). Caries-free組和extremely caries-active組的差別是最大的, 在每一個time interval其pH值會差到1~1.5 logs. 這個差異可以用caries-free組牙菌斑和caries-active組牙菌斑的微生物組成不同來解釋. 此現象並不令人驚訝, 因為caries-free plaques位在carious lesions上, 目前知道caries-active處的plaques較caries-free處的plaques相較下有明顯較高濃度的S.mutans. 這些pH curves顯示plaque pH值在漱完葡萄糖水後會迅速下降, 且會持續30~60分鐘. 如果病人有active caries, 最低的pH值不能低 於5.0, 這是enamel脫鈣的critical pH.
IN VITRO PLAQUE pH MEASUREMENTS
活體外牙菌斑pH值的測量
These plaque pH response curves have come to be known as Stephan Curves. Similar curves were obtained by an in vitro procedure in which aliquots of plaque were removed from the teeth and after suspension in a drop of distilled water the pH was read. In a typical experiment the plaque pH was determined before and after the subject rinsed his mouth with the test solution or consumed the test food. These in vitro studies could be performed without the use of special electrodes and could be standardized as to age of the plaque and the amount of plaque used. However, because of the need for enough plaque for the repeated samplings, the subjects usually went for several days without oral hygiene, and the plaque was then pooled from the most accessible sites, such as the buccal and labial smooth surfaces along the gingival margin. The predominant cultivable flora of such plaques includes, S. mitis, S. sanguis, and various Actinomyces species and would be considered a noncariogenic plaque (see "Bacterial Factors" in Chap. 12). Nevertheless, such noncariogenic plaques, whether from a single site (Fig. 10-3) or from many sites, displayed the characteristic pH drop following exposure to sugar solutions.
這些牙菌斑pH值的反應曲線後來就變成大家所知道的Stephan Curves. 在非活體步驟中也得到相同的曲線, 將牙菌斑從牙齒移除, 使其懸浮於一滴蒸餾水中, 讀取其pH值. 在典型實驗中, 在受試者以受試溶液漱口或攝取受試食物之前及之後測量其牙菌斑pH值.這些非活體研究可以不用用到特殊的電極且可以將牙菌斑的年紀及量做標準化. 然而, 因為需要足夠的牙菌斑作repeated samplings, 受試者需要好幾天不做口腔清潔, 且牙菌斑取得會從最容易取得之處, 例如沿著牙齦邊緣的頰側或唇側平滑面. 最多從牙菌斑培養到的細菌有S. mitis, S. samguis, 和各種不同的Actinomyces species, 這些細菌被認為是noncariogenic plaque. 不過這些noncariogenic plaques不管是從單一部位或很多部位取得, 它們在暴露於糖水後的pH drop反應特色都相同.
The pH distinctions between a noncariogenic and a cariogenic site, i.e., between Group I and Group V in Figure 10-3 were lost in these experiments with pooled plaques. Gone from consideration was the fact that Stephan separated his subjects into groups according to clinical caries status, and that these clinical diagnoses correlated with the resting pH levels of the plaques and with the magnitude of the pH depression in the plaques following the glucose rinse (Fig. 10-3). The dynamics of plaque acid production, per se, became the only parameter under investigation.
在noncariogenic處及cariogenic處的pH值差異, 例如在Figure 10-3中Group I和Group V的差異, 在pooled plaques的實驗就消失了. pH值差異的消失, 是因為它不像Stephan將其受試者依臨床蛀牙狀況分類, 這些臨床診斷和一開始牙菌斑的resting pH levels及在漱完葡萄糖水後pH depression的程度有關. 牙菌斑產酸物的動力平衡變成研究的唯一變數.
In this way Stephan's in vivo pH findings, which supported the specific plaque hypothesis, gave rise to experiments which championed the nonspecific plaque hypothesis. Subjects were studied without precisely defining their current caries status, and in some cases a salivary sediment system was substituted for a pooled plaque suspension. This latter substitution came about when it was demonstrated that noncariogenic plaque suspensions and the salivary sediments exhibited the same pH profiles after exposure in vitro to various carbohydrate and nitrogen substrates. The sediment was prepared by centrifuging whole saliva that had been collected from individuals who were instructed to neither eat nor drink and to avoid oral hygiene for finite periods prior to collection. This sediment would be composed of bacteria and epithelial cells shed primarily from the oral soft tissues and accordingly, would differ in some respects from the plaque flora. The fact that both systems produced acid in a similar manner probably reflected the dominance of the acidogenic streptococcal species, such as S. salivarius, S. mitis, and S. sanguis in the saliva and in the noncariogenic plaques. Studies employing these in vitro systems cannot describe the specific events which occur in cariogenic plaques, but provide information concerning the interactions of various substrates with a mixed oral flora.
Stephan在活體內的pH finding支持specific plaque hypothesis, 使nonspecific plaque hypothesis的擁護者開始做實驗. 受試者未明確定義其目前caries status, 在某些受試者的唾液沉澱系統被置換成pooled plaque suspension. 當noncriogenic plaque suspensions和唾液沉積在活體外接觸各種不同碳水化合物及nitrogen substrates後仍維持相同pH值, 就會出現pooled plaque suspension. 沉澱物是將每位受試者口水離心, 他們的口水在收及前一段時間不能吃或喝東西且要避免任何口腔清潔. 這樣的沉積物是由口腔軟組織的細菌及表皮細胞脫落所組成, 和plaque flora不同. 兩個系統在相同方式下都產酸很可能表示主要產酸的streptococcal species例如S. salivarius, S. mitis, 和S. sanguis會存在saliva及noncariogenic plaques中. 利用這些活體實驗的研究無法詳述在cariogenic plaques發生的事, 但提供在mixed oral flora中各種不同基質間的交互作用.
CONTINUOUS IN VIVO PLAQUE pH MEASUREMENTS
在活體中pH值的測量
Stephan had positioned a small antimony pH electrode in the plaque and measured the pH drop following a glucose rinse. An alternate approach that awaited the development of microelectronic telemetry, was the placement of a miniature glass electrode into a tooth in such a manner that the glass tip was flush with the tooth surface so that plaque would form over it.
Stephan放一個小的antimony pH electrode在牙菌斑中測量在葡萄糖水漱口後的pH drop. 另一個需要微電子遠距測量術幫忙的方式是放一個miniature glass electrode在牙齒上, glass tip會沖洗過牙齒表面, 牙菌斑就在它上面形成.
Such electrode assemblies were constructed in denture teeth by Graf and Muhlemann and are illustrated in Figure 10-4. In the upper appliance the interproximal area where the electrode was located, was bordered by the denture tooth and the abutment tooth. This arrangement was subjected to a pumping action due to the mobility of the denture saddle, which led to unexpectedly low pH values when the test substance was administered in the form of a chewable food. This was not observed when the electrode was situated in an interproximal area between two denture teeth as shown in the lower appliance in Figure 10-4. Thus a seemingly insignificant difference in the placement of the electrodes influenced the pH response, indicating how localized and specific plaque ecosystems are. The indwelling electrodes were located below the contact points of the teeth, so that they continuously monitored the pH in sites that mimicked the caries-prone interproximal surfaces in regard to salivary access and oral hygiene procedures.
這種電極裝置是由Graf和Muhlemann在denture teeth上建立出來的, 如圖10-4. 在上顎裝置, 放電極的interproximal area被denture tooth和支台齒包圍. 這樣的排列容易受到pumping action是因為denture saddle的mobility, 會導致受試者在咀嚼時會有特別低的pH值. 但是當在下顎裝置電極放在2個denture teeth的interproximal area時這種情況就不會發生, 如圖10-4. 所以似乎放電極的位置就會影響pH值的反應, 表示plaque ecosystems是很localized且specific. 在中間的電極應放在牙齒的接觸點之下, 才能追中這些在一般口水及口腔清潔活動下較容易蛀牙的鄰接面的pH值.
The discontinuous in vitro and continuous in vivo pH measuring techniques have not been directly compared in the same subjects. However, pH readings have been obtained with both methods, on different subjects, ingesting the same food items taken in the same sequence, with a fixed interval between items. In the experiment shown in Figure 10-5, six subjects per experimental group ingested one-half of a pear in 10 ml of juice, followed after one minute by the drinking of 120 ml of coffee containing 10 ml of milk and 12 g of sucrose. The dashed line reflects the pH readings obtained by the in vitro method, and the solid lines, the readings obtained by in vivo telemetry. In the in vitro experiment the acidic pear juice reduced the pH minimally, whereas the coffee decreased the pH to about 5.7. Thereafter the pH remained constant for a few minutes and then slowly increased. In the in vivo experiment, the pear juice led to an immediate drop of two pH units followed by a brief recovery which was interrupted by the ingestion of the coffee. The pH during the consumption of the coffee remained at about 4.9 and thereafter rose to about 5.2, only to drop again to about 4.5. At the 28-minute mark the in vitro method showed the pH to be about 6.0, whereas the in vivo method indicated that the pH was 4.5.
在活體外不連續的pH值和在活體內連續的pH值測量技術並沒有在相同個體內被比較. 然而這兩種方式的pH reading都用在不同個體, 以相同順序攝取相同食物且相同的interval被得知. Figure 10-5的實驗顯示, 在每一個實驗組的6個個體都攝取來自半顆洋梨10ml果汁, 接著1分鐘後喝120ml的咖啡, 內含10ml的牛奶和12g的葡萄糖. 虛線表示以非活體方式測量得到的pH 值, 實現表示以活體方式測量得到的pH 值. 在非活體實驗中, 酸性梨子汁會小小地降低pH值, 而咖啡會將pH值降到5.7. 之後pH值會維持數分鐘後再緩慢地增加. 在活體實驗中, 梨子汁會讓pH值立即下降2個單位, 之後在短暫的回覆後會再因攝取咖啡而降低. 在攝取咖啡時pH值會維持在4.9, 然後會升到5.2, 之後會再降到4.5. 在28分時非活體的方式pH值約6.0活體方式pH值為4.5.
Clearly, these methods measured the same directional movement, but differed greatly in their sensitivities. The in vivo method measures the response of plaque which formed in a caries-prone site where salivary access is limited and where acidogenic and aciduric bacteria would be selected for. The fact that the plaque pH is read on a glass surface and not on tooth surface means that there is no calcium and phosphate ions made available from the solubilized enamel to buffer the acid drop. For these reasons one would expect the pH in this location read by the continuous pH method, to be lower than the pH generated by smooth surface plaque and read either in vivo by microelectrodes applied to the enamel surface or by the in vitro method.
很明顯地這些方式測量的方向相同, 但其sensitivities差異很大. 活體方式測量的是較容易形成蛀牙處的牙菌斑, 這些地方口水流量較少且產酸性及耐酸性的細菌會選在這些地方生存. 牙菌斑pH值是在glass surface上測量而不是tooth surface, 表示沒有從溶掉enamel上calcium ions和phosphate ions來中和酸. 因為這些原因, 由continuous pH method讀出來的pH值會比在smooth surface plaque上讀出來的pH值第, 不管是活體中用microelectrode測量enamel表面或用非活體方式.
The in vivo methodology tests single site plaque samples and would yield data consistent with the specific plaque hypothesis. The in vitro method combines plaque from all accessible tooth surfaces and ignores the microbial uniqueness of cariogenic and noncariogenic plaques. The pH is read extraorally under conditions in which the metabolism of some plaque organisms could be inhibited due to the levels of atmospheric oxygen in the new environment .
活體方式側單一處牙菌斑樣本, 產生的資料和specific plaque hypothesis相符. 非活體方是測量多處牙齒表面收集來的牙菌斑, 忽略cariogenic plaques和noncariogenic plaques的microbial uniqueness.
The in vitro pH is thus measured under non-physiological conditions and reflects primarily the metabolic activity of noncariogenic plaque. Under these conditions the metabolic response is muted, but the in vitro methodology can still show differences between individuals, if the clinical caries status between them is great. Englander et al. measured the pH of pooled plaques before and after a sucrose rinse in rampant caries patients and in caries-free subjects. The initial pHs of the plaques from the caries-active patients were lower than those observed in the plaques of the caries-free subjects, which is in agreement with Stephan's findings (Fig. 10-3). Twenty minutes after the sucrose rinse, the pHs in the patients were depressed from the initial values, whereas in the caries-free subjects no changes from the baseline values were noted. Apparently the microbial differences between the plaques of the two different groups were so great, that they were able to express themselves despite the limitations of the in vitro pH methodology used.
非活體的pH值是在非生理情況下測量, 主要反應noncariogenic plaque的新陳代謝活性. 在這樣的情況下, 新陳代謝反應會被掩蓋, 但非活體方式還是可以顯示出個體差異, 如果這些個體臨床蛀牙情況差異很大的話. Englander et al.在猛爆性蛀牙和沒有蛀牙的個體分別測量其在使用葡萄糖漱口水前後pooled plaques的pH值. 一開始在caries-active病人上測到的牙菌斑pH值較caries-free病人低, 這點和Stephan的發現相符. 在以葡萄糖水漱口20分鐘後, caries-active的病人口腔內pH值較原來低, 而caries-free病人的pH值與原先相較下沒有改變. 很明顯地, 這兩組病人牙菌斑的microbial differences很大, 才能在非活體pH值測量方式的限制下, 顯現它們的差異.
THE EFFECT OF SALIVA ON PLAQUE ACID PRODUCTION
唾液對牙菌斑產酸的影響
Salivary flow, because of its volume, i.e., over one liter per day, and because of its buffering capacity, should exert an appreciable effect on plaque pH. This was established by Englander et al., who compared the changes in plaque pH in the presence and absence of saliva. Saliva was diverted away from the plaque by placing cups over the parotid duct, thereby directing the flow out of the mouth and by evacuating the submandibular saliva from the floor of the mouth by means of suction. The isolated teeth were then sprayed for 15 seconds with a 1.5 M sucrose solution (50 percent) and the pH measured in vitro at the times indicated in Table 10-6. In the absence of saliva the pHs dropped faster and attained values that were about 0.4 to 0.8 units lower than those observed in the presence of saliva.
人體的唾液, 因為一天的分泌量超過1升且有緩衝能力, 對牙菌斑pH值會有很大的影響. 這個理論是由Englander et al.建立, 他們比較在有唾液存在及無唾液存在時pH值的變化. 把小杯子放在parotid duct上將牙菌斑上的唾液導流出口外, 將吸唾管放在口底吸出submandibular saliva. 分離的牙齒以50%的葡萄糖容易沖15秒, 此時以非活體方式測量pH值, 結果紀錄在table10-6. 沒有唾液時pH值會下降較快, 比有唾液時低約0.4~0.8單位.
The in vivo experiments of Stephan (Table 10-5) indicated that the pHs of the lower anterior teeth before and after the glucose rinse were always higher than the values obtained on the upper anterior teeth. Subsequently, Kleinberg and Jenkins, with the in vitro method, showed that the resting pH of interproximal plaque taken from the lower anterior teeth was consistently higher than the pH on interproximal plaque taken from the upper anterior teeth. This was correlated with the higher pHs of the bathing submandibular and sublingual saliva about the lower teeth. In addition a correlation between salivary flow rate and pH was observed, with the faster secretors having the higher resting pH levels in their plaques.
Stephan的活體實驗(Table 10-5)指出下顎前牙的pH值不論在漱葡萄糖水之前或之後都比上顎前牙高. 接著Kleinberg和Jenkins以非活體方式淺是下顎前牙鄰接面牙菌斑的resting pH比上顎前牙鄰接面牙菌斑pH高. 這項發現符合下顎牙齒一直浸泡在在pH值較高的submandibular 和sublingual saliva. 另外也發現唾液流速和pH值間也有相關性, 流速較快的地方其牙菌斑的resting pH值較高.
There are several factors in saliva capable of restoring plaque pH towards neutrality (Table 10-7). The most obvious are the salivary fluid volume and bicarbonate content. Both of these factors are interdependent in parotid saliva in that the concentration of bicarbonate increases significantly with increased flow of saliva. As this usually occurs coincident with eating, this salivary buffer system is most suited to neutralize the pH depressions that occur during the eating of meals. This probably accounts for the fact that considerable amounts of sucrose, i.e., 3/4 pound per day, can be consumed at meal times without an obvious increase in caries activity (see "Vipeholm Study" in Chap. 11). This protective mechanism, which obviously evolved in conjunction with primitive man's pattern of eating when food was available, can be circumvented by modern man's habit of frequently ingesting high-sucrose-containing products which do not elicit a compensatory flow of saliva.
在唾液中有許多因素可以將牙菌斑pH值回復到中性(Table10-7). 效果最顯著的是唾液流量和bicarbonate content. 這兩個因素都和parotid saliva有關, 當唾液流量增加時, bicarbonate濃度就會增加. 這在吃飯時最常發生, 唾液緩衝系統最適合在此時中和pH值. 這可以用來解釋一定量的葡萄糖, 約3/4 pound, 可以在餐與餐之間食用而不會增加蛀牙活性. 人類近代的飲食習慣常攝取高葡萄糖含量製品, 會減少唾液流量, 會妨礙這個自人類攝取食物以來就有的保護機制.
Other salivary factors which neutralize plaque acidity are urea and sialin. Urea appears in the saliva in small amounts, i.e. 10mg/100ml and its levels are secondary to its levels in the serum. As such it is diet dependent and would peak in saliva a few hours after a protein food has been digested. The salivary levels of urea would be elevated in people ingesting low carbohydrate-high protein diets, and could contribute to the low caries experience associated with these diets (see "Low Carbohydrate Diets" in Chap. 16). Urea is converted by certain plaque bacteria to ammonia and carbon dioxide. At normal salivary pHs the pK of ammonia favors ammonia ion formation, thereby removing hydrogen ions from the plaque environment.
其他唾液中可以中和牙菌斑酸性的因子有urea和sialin. Urea在唾液中含量很少, 約10mg/100ml, 這個含量較血清中含量少. 它的含量和飲食有關, 在攝取含蛋白質食物數小時後在血清中會達到高峰. 攝取低碳水化合物高蛋白質飲食的人唾液中urea含量會升高, 這樣的飲食可以讓蛀牙的機會降低. 某些牙菌斑細菌會將urea轉換成ammonia和carbon dioxide. 在正常唾液pH值下, ammonia的pK值喜歡以ammonia ion的形式存在, 因此會移除牙菌斑內的hydrogen ions.
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