An individual's host response plays an important role in the pathogenesis of periodontal disease. Even in a mouth where the gingiva appear healthy, there is constant low-level inflammatory response facilitated by the host to manage the constant bacterial load of plaque micro-organisms. Leukocytes and neutrophils are the main cells that phagocytose bacteria found in the gingival crevice or pocket. They migrate from the tissues in a specialised exudate called gingival crevicular fluid also known as GCF. Neutrophils are recruited to the gingival crevice area as they are signalled to by molecules released by plaque microorganisms. Damage to epithelial cells releases cytokines which attract leukocytes to assist with the inflammatory response. The balance between normal cell responses and the beginning of gingival disease is when there is too much plaque bacteria for the neutrophils to phagocytose and they degranulate, releasing toxic enzymes that cause tissue damage. This appears in the mouth as red, swollen and inflamed gingiva which may bleed when probed clinically or during tooth brushing. These changes are due to increased capillary permeability and an influx of inflammatory cells into the gingival tissues. When gingival disease remains established and the aetiology is not removed, there is further recruitment of cells such as macrophages, which assist with the phagocytic digestion of bacteria, and lymphocytes, which begin to initiate an immune response. Pro-inflammatory cytokines are produced inside the gingival tissues and further escalate inflammation, which impacts the progression of chronic systemic inflammation and disease. The result is collagen breakdown, infiltrate accumulation as well as collagen breakdown in the periodontal ligament and alveolar bone resorption. At this stage, the disease has progressed from gingivitis to periodontitis and the loss of supporting periodontium structure is irreversible.
Periodontology
Dentistry
Otology
Podiatry
Psychiatry
Rheumatology
Osteology
Orthodontics