<unk>  is initiated by Gram-negative tooth-associated microbial biofilms that elicit a host response, which results in bone and soft tissue destruction. In response to endotoxin derived from periodontal pathogens, several osteoclast-related mediators target the destruction of alveolar bone and supporting connective tissue such as the periodontal ligament. Major drivers of this aggressive tissue destruction are matrix metalloproteinases (MMPs), cathepsins, and other osteoclast-derived enzymes. Plaque hypothesis At least two mechanisms of the microbiology of periodontitis have been described: the specific plaque hypothesis and the non-specific plaque hypothesis. Consensus is that neither view is entirely correct, but via a middle path, that damage is due to a shift in the relative populations of more and less dangerous bacteria in the plaque. This is called the ecological plaque hypothesis. The disease is associated with a variable microbial pattern. Anaerobic species of bacteria Porphyromonas gingivalis, Bacteroides forsythus, Treponema denticola, Prevotella intermedia, Fusobacterium nucleatum, Eubacterium sp. have all been implicated in<unk> . Microaerophile bacteria Actinomyces actinomycetemcomitans, Campylobacter rectus, and Eikenella corrodens also may play a role in<unk> .
Chronic periodontitis
Periodontal disease
Periodontal abscess
Denture-related stomatitis
Dental abscess
Dental fluorosis
Dental plaque
Periapical periodontitis