Necrotizing periodontitis in which oral symptoms led to diagnosis of HIV infection, with marked improvement in gingival ulceration and periodontal status following appropriate oral management: a case report

Oral lesions can be the first clinical sign of human immunodeficiency virus (HIV) infection. We report a 29-year-old man who presented with burning oral pain, gingival bleeding, and tooth mobility after oral candidiasis, diagnosed and treated by a local otolaryngologist five months earlier, failed to resolve. At his first periodontal visit, extensive pseudomembranous candidiasis of the tongue and pharynx, necrotizing ulceration of the interdental papillae, and generalized deep periodontal pockets were observed (bleeding on probing [BOP] 86.9%, mean probing pocket depth [PPD] 3.6 mm, periodontal inflamed surface area [PISA] 2002.3 mm 2 , plaque control record [%PCR] 100%); periodontal surgery was included in the initial treatment plan given this severity. None of the three red complex pathogens tested ( Porphyromonas gingivalis , Tannerella forsythia , Treponema denticola ) were detected by PCR in subgingival plaque sampled from the deepest pocket. The severity and refractory course of the candidiasis, together with the necrotizing ulceration, raised suspicion of HIV infection; referral to hematology confirmed the diagnosis, with a CD4+ count of 36 cells/uL and a reduced CD4/CD8 ratio, meeting immunologic criteria for AIDS. A diagnosis of generalized periodontitis (Stage III, Grade B) associated with HIV infection, complicated by necrotizing periodontitis, was made. Initial periodontal therapy and antifungal treatment were started before antiretroviral therapy (ART), which was initiated once the acute oral infection was controlled; marked improvement followed (BOP 15.0%, PISA 240.9 mm 2 , %PCR 17.9%), and planned surgery was avoided in favor of supportive periodontal therapy (SPT). At 1-year follow-up, periodontal status remained stable and red complex pathogen PCR remained negative. The absence of the tested red complex pathogens throughout the disease course is consistent with a contribution from disruption of the oral commensal microbiota under HIV-associated immunosuppression, although the broader necrotizing-disease-associated flora was not evaluated and pre-existing plaque-induced periodontitis cannot be excluded.