New concepts regarding the pathogenesis of periodontal disease in HIV infection.

Periodontal manifestations of human immunodeficiency virus (HIV) infection were first described in 1987. Initially, the lesions receiving attention were HIV-associated gingivitis (now known as linear gingival erythema [LGE]) and HIV-associated periodontitis (now known as necrotizing ulcerative periodontitis [NUP]). The true prevalence of LGE was difficult to determine due to variable diagnostic criteria. Recently, LGE has been associated with intraoral Candida infection. The prevalence of NUP is low (< or = 5%), and this lesion is associated with pronounced immunosuppression. Current focus on the periodontal manifestations of HIV infection centers on rapid progression of chronic adult periodontitis in HIV+ patients. Attempts to identify the pathogenesis of the increased progression of periodontitis have not proven successful. For example, analysis of subgingival plaque for the presence of bacterial pathogens has failed to detect differences between HIV+ and HIV- patients. Recently our laboratory has identified alterations in the host response in the gingival crevice of HIV+ patients. Comparing HIV+ and HIV- injecting drug users (IDU), levels of the proinflammatory cytokine interleukin-1 beta (IL-1 beta) in gingival crevicular fluid (GCF) were slightly elevated at sites with a probing depth of 1 to 3 mm. At deeper sites (> or = 4 mm), total IL-1 beta in GCF was significantly greater in HIV+ individuals. Using the lysosomal acid glycohydrolase beta-glucuronidase (beta G) as a measure of the influx of polymorphonuclear leukocytes (PMN) into the gingival crevice, our data indicated a significant correlation of total beta G in GCF and probing depth in the HIV-IDU (r = 76; P = .02). This result was similar to what we have observed in other studies. In contrast, for HIV+ subjects, total beta G was not associated with probing depth (r = .20; NS). These data suggest that HIV+ patients have altered regulation of PMN recruitment into the gingival crevice. We have begun to investigate the conditions under which subgingival Candida may contribute total periodontal lesions in HIV+ individuals. Candida from subgingival sites has been cultured in HIV+ individuals. Subgingival Candida was distinct from Candida isolated from tongue and buccal mucosal surfaces (as indicated by genomic fingerprinting). We hypothesize the absence of adequate priming of PMN by HIV+ patients. This may be due to a reduced Th1 lymphocyte response. The inability of HIV+ individuals to adequately prime PMN may allow Candida to colonize the subgingival environment. In that milieu, it may act directly or in concert with subgingival bacterial pathogens, or as a cofactor (by inducing production of proinflammatory cytokines) to increase the occurrence of periodontal attachment loss.

The relationship of candidiasis to linear gingival erythema in HIV-infected homosexual men and parenteral drug users.

Periodontal status was evaluated in two cohorts participating in a study of the natural history of human immunodeficiency virus (HIV) infection. One cohort consisted of 77 seropositive and 44 seronegative homosexual men, and the other cohort was comprised of 44 seropositive and 39 seronegative parenteral drug users (PDU). No differences were observed between seropositive and seronegative individuals within a cohort in terms of clinical periodontal parameters (percent of sites with > or = 4 mm probing depth, percent of sites exhibiting bleeding on probing, mean oral hygiene index). The PDU displayed more existing periodontal disease than the homosexual men. Periodontal disease in the seropositive individuals in both cohorts was not strictly related to the number of CD4+ lymphocytes. Linear gingival erythema (LGE), defined as an erythematous band of at least 2 mm extending between adjacent papilla, was observed in all 4 groups. Seropositive homosexual men displayed more LGE than seronegative homosexual men (16.6% vs. 11.4%) and seronegative PDU displayed more LGE than seropositive PDU (38.5% vs. 29.5%), but neither difference was significant. LGE tended to be related to reduced numbers of CD4+ lymphocytes, but this relationship did not reach statistical significance. A statistically-significant relationship was found between the presence of intraoral candidiasis and LGE in seropositive homosexual men: 42.9% of these subjects with candidiasis had LGE, while only 12.7% of the subjects without candidiasis had LGE (P < .05). For the seropositive PDU, 35.3% of the individuals with candidiasis had LGE and 25.9% of the subjects without candidiasis displayed LGE, but the difference was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Identifying oral lesions associated with crack cocaine use.

Dental patients who smoke crack cocaine are at higher risk for HIV infection and other medical concerns including stroke, heart failure and pulmonary hemorrhage. Four cases are reported which illustrate oral ulcers caused by crack cocaine usage.