Evidence that diabetes mellitus aggravates periodontal diseases and modifies the response to an oral pathogen in animal models.
Bacterial plaque has been shown to initiate periodontal diseases. Most studies indicate that the host response, rather than the direct effect of bacteria, is responsible for much of the destruction associated with periodontitis. Bacteria or their products have an indirect role by stimulating inflammation, which is associated with the excessive production of inflammatory mediators, such as prostaglandins, or cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1. These mediators, in turn, induce the production and activation of enzymes that destroy gingival connective tissue and stimulate the formation of osteoclasts to resorb bone. Based on results in animal models and studies in humans showing that similar responses occur, the initial steps in the breakdown of connective tissue attachment to the tooth surface and bone resorption involve the production of inflammatory cytokines. Moreover, the risk and severity of periodontal diseases is affected by systemic factors, such as diabetes. Diabetes in particular seems to impair the ability to produce new bone formation after bone loss by preventing the formation of new bone that normally occurs after bone is resorbed, a process called coupling. In addition, the cytokines that stimulate loss of tissue, particularly TNF-alpha, may kill the cells that repair damaged connective tissue or bone. In diabetes there may be more TNF-alpha produced, leading to an even more limited capacity to repair tissue. The diminished capacity to form new bone may make it more difficult for diabetics in particular to repair the loss of tissue that occurs in periodontal diseases.
Graves
Dana T
DT
Department of Periodontology and Oral Biology, Goldman School of Dental Medicine, Boston University, Boston, Massachusetts, USA.
Al-Mashat
Hesham
H
Liu
Rongkun
R
D016301:Alveolar Bone Loss / Q000209:etiology; D000818:Animals; D003238:Connective Tissue / Q000473:pathology; D003773:Dental Plaque / Q000150:complications / Q000276:immunology / Q000382:microbiology; D048909:Diabetes Complications / Q000503:physiopathology*; D003920:Diabetes Mellitus / Q000503:physiopathology*; D004195:Disease Models, Animal; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology; D018836:Inflammation Mediators / Q000502:physiology*; D007375:Interleukin-1 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000378:metabolism; D051379:Mice; D010518:Periodontitis / Q000150:complications* / Q000209:etiology / Q000276:immunology / Q000378:metabolism; D011453:Prostaglandins / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D014945:Wound Healing / Q000502:physiology
D018836:Inflammation Mediators; D007375:Interleukin-1; D008070:Lipopolysaccharides; D011453:Prostaglandins; D014409:Tumor Necrosis Factor-alpha