The focal infection theory, which for almost half a century justified indiscriminate extraction of teeth to cure focal infections, since the end of the 1940s has become progressively a discarded concept. In parallel with the declining importance assigned to pulp and periapical infections in the pathogenesis of focal diseases, over the last decade there has been increasing interest in the possible relationship between periodontal infection and systemic diseases. Periodontal pathogens and their products, as well as inflammatory mediators produced in gingival tissue, might enter the bloodstream through ulcerated pocket epithelium, causing systemic effects (focal diseases). On the basis of this mechanism, chronic periodontitis has been implicated as risk factor for cardiovascular diseases associated to atherosclerosis, bacterial endocarditis, diabetes mellitus, respiratory disease preterm delivery, rheumatoid arthritis, and more recently osteoporosis, pancreatic cancer, metabolic syndrome, renal diseases and neurodegenerative diseases such as Alzheimer‘s disease. Numerous hypotheses, including common susceptibility, systemic inflammation, direct bacterial infection and cross-reactivity, or molecular mimicry, between bacterial antigens and self-antigens, have been postulated to explain these relationships. In this context, the association of periodontal disease with systemic diseases has introduced the concept of periodontal medicine, which ultimately guides the medical community in therapeutic approaches to improve not only the patient oral health but also systemic health.
|Title of host publication||Periodontal Disease: Symptoms, Treatment and Prevention|
|Number of pages||32|
|Publication status||Published - 2011|
|Name||DENTAL SCIENCE, MATERIALS AND TECHNOLOGY|