THE SPECIFIC PLAQUE HYPOTHESIS (SPH)
Most dentists think of all plaque as being identical. They are correct to the extent that plaque is an aggregation of bacteria and salivary proteins. However, the bacterial composition of plaque will vary from site to site on the tooth surfaces, and especially, between health and disease. We can recognize bacteriologically, at least three broad categories of plaque nondisease-associated plaque, caries-associated plaque and periodontal-disease-associated plaque (See Fig.l-l).
特定菌斑假說(Specific plague hypothesis SPH)
大多數的牙醫師認為所有牙菌斑都是相同的，在某種程度上這是正確的，因為牙菌斑都是細菌和唾液蛋白質的累積。然而，牙菌斑中細菌的組成差異性很大，即使是同一顆牙齒上的不同區域成分也不同，尤其是健康和患病的區域差異更大。由細菌學上，我們至少可已可以分成三大類的菌斑：非疾病相關的牙菌斑、與齲齒相關的牙菌斑以及與牙周疾病相關的牙菌斑。（見圖1-1）
Nondisease-Associated Plaque
The nondisease-associated plaque present in almost everyone's mouth is of no severe consequence, as long as it is controlled mechanically (Fig. l-2). It may be associated over a period of years with a low caries prevalence and minimal periodontal bone loss.
非疾病相關的牙菌斑
這類牙菌斑幾乎存在於每一個人的口腔，但是只要藉由機械性控制(指清潔)，並不會產生嚴重的後果(圖1-2)。它即使在口腔中存在數年以上的時間，也可能只有造成少數的齲齒以及輕微的牙周齒槽骨喪失。
Caries-Associated Plaque
A second type of plaque is associated with caries (Fig. l-3). A person who frequently ingests sucrose, especially in a sticky form, will presumably develop cariogenic plaque. Experimental verification of this statement using humans is unethical because it is the universal belief in dentistry that caries will occur on this regimen. Epidemiological evidence and general clinical observations, as well as the classic Swedish study in the Vipeholm Mental Institute, have shown this to be a reliable conclusion. Caries-associated plaques usually contain high proportions of a remarkable organism, Streptococcus mutans, that is capable of metabolizing sucrose in ways which promote demineralization and subsequent cavitation in the teeth.
與齲齒相關的牙菌斑
第二種牙菌斑是與齲齒相關的(圖1-3)。當一個人經常攝取蔗糖，尤其是較黏稠的形式，一般相信會發展出致齲性的牙菌斑。由於在牙醫界普遍相信這樣做會發生蛀牙，因此上面的敘述要經由人體實驗來驗證是不道德的。流行病學的證據及一般臨床觀察，以及瑞典Vipeholm精神病院 (Vipeholm Mental Institute)的經典研究也顯示這是一個可信的結論。這些與齲齒相關的牙菌斑中含有高比例的一種非凡的微生物，變異鏈球菌(Streptococcus mutans)，它可以代謝蔗糖助長去礦化(demineralization)及隨後牙齒上蛀洞的產生。
Periodontal-Associated Plaque
A third type of plaque (Fig. l-4) develops in the absence of oral hygiene, at the dento-gingival margin. This plaque, as it ages, undergoes a bacterial transformation in which the initial Gram-positive colonizers are replaced, in part, by a Gram-negative anaerobic flora. This Gram-negative flora produces various by-products which permeate the adjacent gingival tissue where they act as antigens and/or, as chemotoxins, thereby recruiting host defense cells to the periodontal area. Plaques associated with clinical signs of disease, such as bleeding upon probing, usually contain elevated levels or proportions of certain Gram-negative anaerobes, i.e., black-pigmented bacteroides species, such as Porphyromonas gingivalis, motile organisms, such as spirochetes, and non-motile organisms, such as Actinobacillus actinomycetemcomitans, among others.
與牙周疾病相關的牙菌斑
第三種牙菌斑 (圖1-4) 在缺乏口腔衛生時會發展於齒齦交界處的區域。這種牙菌斑，隨著時間會經歷菌種的變換，一開始的格蘭氏陽性菌漸漸一部分被格蘭氏陰性厭氧菌所取代。這些格蘭氏陰性菌會產生多種副產物，滲入到鄰近的牙齦組織成為抗原或是化學毒素，因之招來宿主的防禦細胞來到牙周區域。與臨床病徵(如牙周探測時的牙齦出血)有關的牙菌斑中常含高量或高比例的格蘭氏陰性厭氧菌，例如產黑色素菌種如Porphyromonas gingivalis，會移動的微生物比如螺旋菌，以及非移動性的微生物例如Actinobacillus actionmycetemcomitans等等。
TREATMENT ACCORDING TO THE SPECIFIC PLAQUE HYPOTHESIS
If caries and periodontal disease are due to a limited number of bacterial species, then a more realistic treatment approach would be the elimination or reduction of the pathogenic bacteria from the plaque. Treatment need be only for a short duration in those patients diagnosed as having an infection. Active infection can be diagnosed by clinical symptoms and bacteriological methods.
以特定菌斑假說（Specific plague hypothesis SPH）為根據的治療
假如齲齒及牙周病是由少數幾種細菌造成，那麼更實際的治療方式應該是針對牙菌斑中的致病菌，將之去除或減少。被診斷出有感染的病人應該只需接受短期的治療。臨床表徵及細菌學的方法可以來診斷其感染是否很活躍。
The antimicrobial treatment of dental caries according to the specific plaque hypothesis will be discussed in this monograph, while that related to periodontal disease will be described in a subsequent volume. In particular, the present monograph will present evidence that human dental decay is a treatable infection, due mainly to S. mutans and to a lesser extent, to the various lactobacilli. This does not mean that these two organisms cause all of the dental decay, but rather that they are responsible for a measurable amount of decay, with the expectation that this amount represents a significant, if not the majority, proportion.
以特定菌斑假說為根據的齲齒治療將在本書中討論，與牙周疾病相關的將會在隨後的另一本書來敘述。尤其本書將會提出證據說明人類的齲齒是一種可以治療的感染；主要來自變異鏈球菌，以及較少部分來自各種乳酸桿菌(lactobacilli)。這並不是說這兩種細菌造成所有的齲齒，只是他們必須對大部分的齲蛀負責，也期望這代表了相當大(若非主要)的比重。
This monograph is organized into three parts. PART I, which includes chapters 2-6, deals with basic information on oral bacteriology and oral microbial ecology. 0f these, Chapter 6, which describes plaque formation, is essential for the understanding of microbial specificity in dental decay. PART II, which includes chapters 7-12, presents the evidence for the role of S. mutans in animal and human decay. Chapters 9 and lO describe the relevant biochemistry, which is necessary to understand in order to appreciate how sucrose and acid are linked via S. mutans to caries etiology. PART III, which includes chapters 13-20, provides the treatment strategies and tactics that are possible, given a specific infection hypothesis. The need for these new approaches becomes apparent after a critical examination of the legacy left by treatments based upon the nonspecific plaque hypothesis (Chap. 13).
這本書共規劃成三個部分：第一部份，包括第2～6章，討論口腔細菌學和口腔微生物生態學的基礎知識，其中第6章敘述牙菌斑的形成，這對於瞭解造成齲齒的微生物專一性很重要。 第二部份，包括第7～12章，提供證據說明變異鏈球菌在動物及人類齲齒的角色。第9、10章敘述相關的生物化學，吾人才能瞭解並體會蔗糖和酸如何藉由變異鏈球菌與齲齒的成因有相關聯。第三部份，包括第13～20章，提供依據特定菌斑假說的可能治療策略。當我們中肯的檢驗依據非特定菌斑假說的治療結果後，要有這些新方法的需求就會變得相當明顯了(第13章)。
