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 processes
Neoplasms
Endocrine, nutritional, and metabolic diseases
Traumatic lesions
Gingival pigmentation
Chronic Periodontitis
Based on the 2017 World Workshop on the classification of periodontal and peri-implant diseases and conditions, three forms of periodontitis are recognized: necrotizing periodontitis; periodontitis (formerly known as chronic and aggressive periodontitis); and periodontitis as a manifestation of systemic diseases.61 However, for the purpose of this chapter, both chronic and aggressive periodontitis are discussed separately.
Periodontitis was recently defined by the 2017 World Workshop as a “chronic multifactorial inflammatory disease associated with dysbiotic plaque biofilms and characterized by progressive destruction of the tooth-supporting apparatus.”1 The main features of this disease include the presence of periodontal pockets, gingival bleeding, clinical attachment loss, and alveolar bone loss (Fig 3-3). If left untreated, periodontitis could lead to tooth mobility and ultimately tooth loss. In addition, chronic periodontitis is influenced by a great variety of local and systemic factors that can significantly exacerbate disease progression. These factors are discussed in the following chapters.
Fig 3-3 Periodontitis (formerly referred to as chronic periodontitis.) (a) Initial presentation of maxillary and mandibular anterior dentition prior to nonsurgical therapy. (b) Radiographic evaluation prior to nonsurgical therapy. (c) Reevaluation 3 months after nonsurgical therapy.
As mentioned previously, periodontitis is caused by an exaggerated inflammatory response from the host caused by a dysbiosis. This process is the result of a transition from the symbiotic microbial and immune state of a healthy individual (or nonprogressive gingivitis) to an abnormal and exacerbated host response accompanied by a dysbiotic microbiome.62 It is important to mention that while gingivitis may or may not advance to periodontitis, attachment loss and the development of periodontitis are always preceded by gingival inflammation.63 Consequently, many authors have studied the changes and progression from gingivitis to periodontitis. In 1985, Listgarten et al64 longitudinally followed 61 adults with varying degrees of gingivitis. Results from this investigation revealed that only 1 out of 1,000 tooth surfaces increased in probing depths by 3 mm or more from baseline regardless of the protocol for recall maintenance intervals. Therefore, the authors concluded that despite the high prevalence of gingivitis, most individuals were relatively resistant to periodontitis. Subsequently, other investigations aimed at studying disease development, disease progression, and several other parameters related to periodontitis, such as attachment loss or changes in bone level.
Löe et al65,66 conducted a series of landmark investigations aimed at studying the natural development and progression of periodontal disease. One of the first investigations was published by this group in 1978 and compared two populations with different geographic, cultural, socioeconomic, and educational differences. Both groups were chosen due to the extreme differences with regard to health care systems and dental care. The study population from Oslo, Norway, had access to programs for dental care while the population from Sri Lanka never had access