Periodontics. Fernando Suarez

Чтение книги онлайн.

СКАЧАТЬ bacterial plaque. Supragingival calculus will be located coronal to the gingival margin and is usually whitish to dark yellow or brown, hard, with a claylike consistency and easily detachable from the tooth surface. Its rate of formation will depend on the bacterial plaque present and on the quality and quantity of the secretions of the salivary glands. Subgingival calculus is located apical to the gingival margin, so it is not visible on routine clinical examination. Occasionally, subgingival calculus may be visible in dental radiographs. Both sub- and supragingival calculus provide perfect environments for bacterial adhesion, growth, and maturation, as well as increase the surface for bacterial colonization. It is important to mention that sterilized³⁸ or disinfected³⁹ calculus does not trigger a marked inflammatory reaction, but the bacterial plaque attached to it will. For this, calculus is considered a secondary factor for periodontal disease, as it provides an ideal surface topography for plaque accumulation.

      Theories of Pathogenesis

      Different theories have emerged throughout the years trying to relate dental plaque and the transition from health to disease. Most of the theories have evolved and adapted based on the microbial and host response knowledge at the time.

      NONSPECIFIC PLAQUE THEORY

      Initially, the most common hypothesis was that periodontal infections were caused by a nonspecific overgrowth of bacteria.^40–42 Regardless of the specific types of microorganisms present, the most important factor was the increased amount of bacterial load in the periodontal tissues. Based on this hypothesis, the host would have a defined threshold, and periodontal disease would develop if that threshold became surpassed by increased amounts of bacteria, bacterial byproducts, and virulence factors.⁴³ This theory supports the notion that the most effective method to prevent and arrest disease progression is by the mechanical removal of plaque.

      SPECIFIC PLAQUE THEORY

      In 1976, Walter J. Loesche⁴¹ described the specific plaque hypothesis, postulating that dental caries was a bacteria-specific infection, particularly originated by Streptococcus mutans, and that acute necrotizing ulcerative gingivitis was caused by specific intermediate-sized spirochetes, as well as Bacteroides melaninogenicus (known today as Prevotella melaninogenica).

      The specific plaque hypothesis was further developed in the 1970s and 1980s, when more advanced culture and bacterial identification techniques were developed.^44,45 Key periodontal pathogens related to severe and aggressive periodontal diseases were identified, such as Aggregatibacter actinomycetemcomitans, P gingivalis, T forsythia, or T denticola.^32,46,47 In light of the increased microbiologic understanding, it became evident that periodontal destruction was not only influenced by quantity, but also by the qualitative composition of bacterial plaque.⁴¹

      ECOLOGICAL PLAQUE HYPOTHESIS

      In 1994, Marsh⁴⁸ described the ecological plaque hypothesis, which encompasses the previous plaque theories relating bacterial plaque and the host response. Thus, specific bacteria as well as the total amount of bacterial plaque contribute to the development and progression of periodontal disease. Changes in the environment (eg, ecological stress) increase the competitiveness of putative pathogens at the expense of species associated with oral health, resulting in an upregulation of the expression of virulence factors. Therefore, there is a link between local environmental conditions and the activity and composition of the biofilm.⁴⁹

      In conclusion, the different dental plaque and bacteria hypotheses are dynamic theories that continue to evolve as new evidence and pathogenic mechanisms are unveiled.

      Gingivitis

      Plaque-induced or dental biofilm–induced gingivitis refers to an inflammatory response of the gingival tissues occurring secondary to bacterial plaque accumulation around the gingival margin.^40,50 In order to understand the initiation and progression of this inflammatory condition, Löe et al⁴⁰ performed an experimental gingivitis study. For this investigation, patients with healthy gingiva were asked to withdraw from all oral hygiene methods until the inflammatory changes were observed. Gingivitis developed within 10 days for three subjects, while for the remaining nine subjects it took between 15 and 21 days. Once these inflammatory changes were observed, patients were instructed to resume oral hygiene methods, and gingival health was regained within a week, also reestablishing the original bacterial flora. While simple in design, this study proved several concepts: (1) the bacterial plaque is the etiology of the disease, (2) the differences in the response suggest different progressions models and susceptibility of patients, and (3) gingivitis is reversible.⁴⁰

      In addition, bacteriologic changes were also evaluated. Healthy gingiva presented with small groups of bacteria mainly composed of gram-positive cocci and short rods. The initial stages of plaque accumulation (ie, 1 to 2 days) yielded an increase in rods and cocci followed by an accumulation of filamentous forms and fusobacteria (2 to 4 days) accompanied by further leukocyte accumulation. During the last phase, the predominant bacterial flora was characterized by Vibrio spp and spirochetes with still a large number of cocci, rods, and filamentous organisms as well as a heavy leukocyte accumulation. One year later, the same group performed a follow-up investigation demonstrating the increase in complexity of the microbial flora when gingivitis was established.⁵¹ During the next decades, several other investigations focused on the progression and the different stages of gingivitis.^52–54 It is important to mention the methodologic differences among these studies. Page and Schroeder⁵² reviewed the progression of gingivitis based on animal and human studies. Seymour et al⁵⁴ carried out experimental gingivitis in dental students. Last, Kornman et al⁵³ reviewed the relationship between bacterial challenge and host immunity during the progression of gingivitis.

      Clinical signs and symptoms of plaque-induced gingivitis include edema, bleeding, erythema, tenderness, gingival enlargement, and halitosis.^55,56 In addition, the severity of these symptoms can vary among individuals and can be influenced by a variety of anatomical and restorative factors.^57,58 While gingivitis does not directly cause tooth loss, the prevention and early treatment of this condition represents a key component of the prevention of periodontitis.⁵⁹

      Dental plaque–induced gingivitis can also be associated with dental biofilm alone, or on the other hand, it can be potentially modified or mediated by a variety of local and systemic factors including sex steroid hormones, hyperglycemia, leukemia, smoking, malnutrition, certain subgingival restorations, and hyposalivation.⁵⁰ Moreover, drug-influenced gingival enlargements can also occur secondary to antiepileptic drugs, certain calcium channel blockers, immunoregulators, and high-dose oral contraceptives.⁵⁰ It is important to bear in mind that while bacteria are necessary to develop gingivitis in conjunction with these medications, not all patients taking these drugs will experience gingival enlargement.

      Non-Plaque-Induced Gingival Diseases

      While dental biofilm–induced gingivitis is the most common form of periodontal disease, several other non-plaque-induced gingival diseases are described. Based on the 2017 World Workshop, these non-plaque-induced gingival diseases include⁶⁰:

       Genetic/developmental disorders

       Specific infections

       Inflammatory and immune conditions

       Reactive СКАЧАТЬ