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。
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