In 2002 in the U.S. alone, approximately 20 million people were estimated to be affected by both diagnosed Perhapsmoresignificantly,however,theulceratedpock-and undiagnosed DM, representing over 9% of the adult et epithelium may serve as an entry portal for these bac-population. 11, 12 Type 2 DM is by far more common than teria, their byproducts, and host-derived cytokines into Type 1, constituting approximately 85%-90% of cases the systemic circulation, from where they have the po-and may currently affect over 150 million people world- tential to exert effects throughout the body. In untreated wide. 13 The U.S. prevalence of type 2 DM is greatest in severe periodontal disease, the cumulative surface area the Native American, Hispanic-American, and African- of ulcerated pocket epithelium has been estimated to be American populations.14 In contrast to the improving from 8 to 20 cm2 (approximately 3 in2 or about the size gingival health trends in the U.S., diabetes incidence has of the palm of a hand). 19, 20 In these patients with severe increased at an alarming rate of nearly 500,000 new disease, bacteremia can be induced by dental procedures cases every year from 1998 through 2002, and the rate as well as by normal daily activities like chewing. 21 In one continues to climb at a staggering pace. 15 Coupled with study, chewing was shown to cause systemic endotox-the estimate that over 6 million people in the U.S. with emia in 40% of patients with periodontitis compared with diabetes are undiagnosed, this is a public health crisis of only 12% of periodontally healthy patients, and the con-massive proportions. 15 The documented increase in DM centration of endotoxin in the bloodstream was 5 times incidence parallels enhanced diabetes screening meth- higher in those with periodontitis. 22 Thus, the effects of ods but also is very much coincident with the increasing inflammation can spread from the localized periodontal incidence of obesity in the American population. lesion into the systemic circulation.
The Periodontal Disease–Inflammation Connection Serum inflammatory markers are elevated in the periph-Periodontal diseases are initiated by biofilm infections eral blood of patients with periodontitis. Periodontal in-of the gingival sulcus at the interface of the gingival tis- flammation may directly increase the concentrations of sues and the tooth. Over 400 different species of bacteria these substances in the blood or indirectly stimulate their reside in these plaque biofilms, many of which are gram- formation as part of the acute-phase response. 23 Acute-negative and anaerobic. 16 With disease onset, the sulcus phase reactants are proteins produced in the liver during transforms into a pathologically deepened pocket, where the innate immune response to bacterial challenge and a delicate balance is struck between the bacteria and the serve a variety of proinflammatory functions, including host’s immune system, which attempts to destroy them. complement activation, bacterial phagocytosis, and stim-The bacteria directly invade the soft tissues or release ulation of tissue repair and regeneration. 24 Acute-phase their toxic products, including endotoxins from the cell proteins such as C-reactive protein (CRP), serum amyloid walls of gram-negative bacteria, chemotactic peptides, A, and fibrinogen appear not only in acute disease pro-organic acids, and protein toxins, into the pocket, caus- cesses but also in chronic diseases. These proteins also ing inflammation. 17 As the pocket epithelium proliferates may have deleterious effects on end organs. CRP, which in response to the ongoing inflammation and becomes along with fibrinogen is an accepted risk factor for ma-ulcerated, the compounds released from the biofilm jor cardiovascular events, may exert its effects by modu-readily enter the gingival tissues and further stimulate lating coagulation and atherosclerosis. 25, 26 Studies have the host’s immune response. Significantly, the majority of further suggested that periodontitis patients harboring the destruction seen in periodontal disease results from Porphyromonas gingivalis (P. gingivalis), Tannerella this stimulation of the immune system and the exuber- forsythia, and Prevotella intermedia, all highly virulent ant host inflammatory response, which leads to the ac- gram-negative bacteria, have significantly higher serum tivation of host enzymes. 17 These compounds, produced levels of CRP, IL- 6, and fibrinogen than patients with-
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