Periodontitis

Periodontitis is a chronic inflammatory disease of the tissues supporting the teeth — the gingiva, periodontal ligament, cementum, and alveolar bone. It begins as gingivitis, a reversible inflammation of the gums driven by accumulated bacterial plaque, but when the host response becomes dysregulated the attachment between tooth and bone breaks down, forming periodontal pockets that harbour further bacteria and drive progressive alveolar bone loss. Clinical signs include bleeding gums, persistent halitosis, gingival recession, sensitivity, tooth mobility, and eventual tooth loss; pain is frequently absent until late in the disease. It is among the most prevalent chronic inflammatory conditions worldwide and is consistently associated with cardiovascular disease, diabetes, adverse pregnancy outcomes, rheumatoid arthritis, and cognitive decline.

The disease arises from microbial dysbiosis rather than infection by any single organism. Keystone pathogens including Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola remodel the subgingival community and subvert host defences. Bacterial lipopolysaccharide activates TLR2 and TLR4, driving NF-κB signalling and release of IL-1β, IL-6, TNF-α, and prostaglandin E2. Neutrophils release matrix metalloproteinases, particularly MMP-8 and MMP-9, degrading connective tissue, while an elevated RANKL to osteoprotegerin ratio activates osteoclasts and resorbs alveolar bone. Th17 responses, complement activation, and oxidative stress sustain the cycle.