Assessment and management of periodontal infections: a medical-surgical approach.
Over the last 30 years, significant advances have been achieved in elucidating the etiology, pathogenesis, and treatment of periodontal diseases. A new paradigm has emerged that includes the initiation of disease by specific bacteria within a biofilm that stimulate an immunoinflammatory host response, resulting in host tissue destruction. Disease modifiers, which may be of genetic, environmental, or acquired origin, have been recognized as major determinants of disease severity and progression. Current treatment protocols include an assessment of risk factors to identify an individual's degree of susceptibility and therapeutic responsiveness. Basic and clinical research has resulted in the development of several strategies to identify specific bacteria and host-derived markers associated with disease progression. Preventive and therapeutic antimicrobial therapies, which use various delivery systems, have been devised to target drug placement to the infection site. More recently, host modulatory therapies have been created that inhibit disease progression through the reduction of inflammatory mediators. Finally, biological mediators, including growth and differentiation factors, have been used to enhance an individual's healing potential to achieve periodontal and bone regeneration. A combined medical-surgical approach is indicated for these new methods of diagnosis, prevention, and treatment of periodontal diseases, which will allow for earlier treatment interventions and improved patient outcomes.
Oringer
R J
RJ
Department of Periodontics, School of Dental Medicine, State University of New York at Stony Brook, Stony Brook, New York, USA.
Williams
R C
RC
D000891:Anti-Infective Agents, Local / Q000627:therapeutic use; D001424:Bacterial Infections / Q000382:microbiology / Q000628:therapy; D001439:Bacteroides / Q000472:pathogenicity; D024042:Collagen Type I / Q000737:chemistry; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use; D004269:DNA, Bacterial / Q000032:analysis; D003773:Dental Plaque / Q000628:therapy; D005883:Gingival Crevicular Fluid / Q000737:chemistry; D006801:Humans; D018836:Inflammation Mediators; D007527:Isoenzymes / Q000037:antagonists & inhibitors; D008565:Membrane Proteins; D010518:Periodontitis / Q000382:microbiology* / Q000628:therapy*; D016966:Porphyromonas gingivalis / Q000472:pathogenicity; D011451:Prostaglandin-Endoperoxide Synthases; D014208:Treponema / Q000502:physiology
D000891:Anti-Infective Agents, Local; D024042:Collagen Type I; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D004269:DNA, Bacterial; D018836:Inflammation Mediators; D007527:Isoenzymes; D008565:Membrane Proteins; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases