Review Note

The injurious agent in periodontal disease is thought to be a {{c1::dysbiotic biofilm}} containing increased numbers of certain pathogenic {{c1::gram-negative bacteria}}. This infection induces local inflammation with many {{c1::macrophages}} infiltrating the underlying gingival tissues. {{c1::Bacterial LPS}} ({{c1::lipopolysaccharide}}) (only found on gram-negative bacteria) and {{c1::cytokines}} (e.g., IFN-g) from T cells cause the macrophages to become '{{c1::super-macs}}.' These super-macs engulf any bacteria and bacterial products that may have entered the gingival tissues.

These activated super macrophages also 'drool' (i.e., {{c2::exocytose}}) destructive {{c2::enzymes}} and {{c2::oxygen radicals}} onto the surrounding tissues. All good, to a limited extent anyway! However, if this goes on for long, the supporting structures that adhere the gingival tissues to the tooth begin to fail, and {{c2::attachment loss}} occurs. The super-macs also secrete many inflammatory mediators and CKs. These can cause de-coupling of the {{c3::osteoblast}} - {{c3::osteoclast}} activities, by up regulating {{c3::osteoclasts}}. If this goes on for long the bone structure that ‘cradles’ the tooth is lost. Left untreated the ultimate result is tooth loss, (which does work to eliminate the insult and keep the infection from becoming systemic - remember this is the ultimate goal of inflammation). Attachment and bone loss are clinical signs of the ongoing inflammatory response that the clinician can see and treat by aiding the body’s attempt to eliminate/reduce the plaque bacterial infection.