{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T17:57:39Z","timestamp":1791914259043,"version":"4.3.4"},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1998,7,1]],"date-time":"1998-07-01T00:00:00Z","timestamp":899251200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Ann Periodontol"],"published-print":{"date-parts":[[1998,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:italic>Periodontal manifestations of human immunodeficiency virus (HPV) infection were first described in 1987. Initially, the lesions receiving attention were HW\u2010associated gingivitis (now known as linear gingival erythema [LGE]) and HTV\u2010associated 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 (\u2264 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\u2212 patients. Recently our laboratory has identified alterations in the host response in the gingival crevice of HIV+ patients. Comparing HIV+ and HIV\u2212 injecting drug users (IDU), levels of the proinfiammatory cytokine interleukin\u20101 \u03b2 (IL\u20101\u03b2) in gingival crevicular fluid (GCF) were slightly elevated at sites with a probing depth of 1 to 3 mm. At deeper sites (\u2265 4 mm), total IL\u20101\u03b2 in GCF was significantly greater in HIV+ individuals. Using the lysosomal acid glycohydrolase \u03b2\u2010glucuronidase (\u03b2G) as a measure of the influx of polymorphonuclear leukocytes (PMN) into the gingival crevice, our data indicated a significant correlation of total \u03b2G in GCF and probing depth in the HIV\u2013IDU (r = 76;<\/jats:italic>\n                    P\n                    <jats:italic>\n                      = .02). This result was similar to what we have observed in other studies. In contrast, for HIV+ subjects, total \u03b2G 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 to 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 Th\n                      <jats:sub>1<\/jats:sub>\n                      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\n                    <\/jats:italic>\n                    . Ann Periodontol 1998;3:62\u201375.\n                  <\/jats:p>","DOI":"10.1902\/annals.1998.3.1.62","type":"journal-article","created":{"date-parts":[[2010,10,28]],"date-time":"2010-10-28T14:01:51Z","timestamp":1288274511000},"page":"62-75","source":"Crossref","is-referenced-by-count":57,"title":["New Concepts Regarding the Pathogenesis of Periodontal Disease in HIV Infection"],"prefix":"10.1002","volume":"3","author":[{"given":"Ira B.","family":"Lamster","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John T.","family":"Grbic","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dennis A.","family":"Mitchell\u2010Lewis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melissa D.","family":"Begg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aaron","family":"Mitchell","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[1998,7]]},"container-title":["Annals of Periodontology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/aap.onlinelibrary.wiley.com\/doi\/pdf\/10.1902\/annals.1998.3.1.62","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,11,5]],"date-time":"2025-11-05T09:17:30Z","timestamp":1762334250000},"score":1,"resource":{"primary":{"URL":"https:\/\/aap.onlinelibrary.wiley.com\/doi\/10.1902\/annals.1998.3.1.62"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1998,7]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1998,7]]}},"alternative-id":["10.1902\/annals.1998.3.1.62"],"URL":"https:\/\/doi.org\/10.1902\/annals.1998.3.1.62","archive":["Portico"],"relation":{},"ISSN":["1553-0841","2162-5131"],"issn-type":[{"value":"1553-0841","type":"print"},{"value":"2162-5131","type":"electronic"}],"subject":[],"published":{"date-parts":[[1998,7]]}}}