02708nas a2200517 4500000000100000008004100001260001300042653001000055653000900065653002200074653002600096653003000122653002500152653001100177653001100188653001000199653002500209653002500234653000900259653001600268653002300284653001800307653002900325653001500354653003000369100001300399700001300412700001400425700001400439700001600453700001500469700001100484700001700495700001300512700001200525700001600537700001500553700001300568700001500581245009500596856004100691300001100732490000700743520142600750022001402176 2010 d c2010 Nov10aAdult10aAged10aAged, 80 and over10aAntibodies, Bacterial10aBacteroidaceae Infections10aCase-Control Studies10aFemale10aHumans10aJapan10aLeprosy, lepromatous10aLeprosy, Tuberculoid10aMale10aMiddle Aged10aPeriodontal Pocket10aPeriodontitis10aPorphyromonas gingivalis10aPrevalence10aSeverity of Illness Index1 aOhyama H1 aHongyo H1 aShimizu N1 aShimizu Y1 aNishimura F1 aNakagawa M1 aArai H1 aKato-Kogoe N1 aTerada N1 aNagai A1 aTakashiba S1 aKurihara H1 aNomura Y1 aMurayama Y00aClinical and immunological assessment of periodontal disease in Japanese leprosy patients. uhttp://www.nih.go.jp/JJID/63/427.pdf a427-320 v633 a
Periodontitis is a chronic inflammatory disease caused by the infection of periodontopathic bacteria in dental plaque. However, an individual's susceptibility to this disease appears to be associated with multiple genetic factors, as seen in the case of leprosy. In order to gain a better understanding of the pathophysiology of periodontal disease in subjects with leprosy, we investigated the clinical features of periodontitis and the immunological responses against periodontopathic bacteria in 382 subjects with a history of leprosy and 451 age-matched control subjects. The prevalence of periodontitis and the degree of periodontal pocket depth were found to be significantly higher in leprosy patients than in age-matched controls. Furthermore, a comparison of the clinical parameters of lepromatous leprosy (L-lep) and tuberculoid leprosy (T-lep) patients showed that the probing pocket depth of L-lep patients with periodontal disease was significantly higher than that for T-lep patients. In contrast, serum IgG titers against Porphyromonas gingivalis in L-lep patients were significantly lower than in T-lep patients. These results imply that L-lep patients show more severe periodontal disease than T-lep patients or age-matched control subjects, and that low humoral immunity against P. gingivalis might be one of the genetic factors determining periodontal disease susceptibility in leprosy patients.
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