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.
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