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Patients infected with the human immunodeficiency virus (HIV) are highly susceptible to chronic marginal periodontitis (CMP) and the lesion is generally characterized by abundant plasma cell infiltration. HIV-induced reduction of CD4+ T cells may indirectly affect local production of immunoglobulins (Ig). Gingival biopsies taken from 10 HIV+ and 12 HIV- control patients with CMP were washed, fixed in ethanol and embedded in paraffin. Sections were examined after immunohistochemical staining with monoclonal antibodies against IgA, IgA1-2, IgG, IgG1-4, IgM and IgE. Ig-containing cells were counted in 3 separate connective tissue zones (subjacent to pocket epithelium, central zone and subjacent to oral epithelium). HIV+ patients showed a remarkably increased density of all Ig-containing cells in the connective tissue zone subjacent to the oral epithelium (p<0.05) and a lower % of IgG2+ cells in the entire gingival section (p<0.05). In HIV+ patients, the density of IgG-containing cells in the gingiva was strongly correlated with the serum IgG concentration. The altered topical distribution might imply impaired restriction of the inflammatory lesion, additional antigenic challenges by unusual microorganisms in the oral cavity, or be secondary to HIV-induced dysregulation of the B-cell system.

Levels of total IgA and specific IgA reactive with Streptococcus mutans, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Prevotella nigrescens and Fusobacterium nucleatum were measured by ELISA in parotid saliva from HIV+ and HIV- persons with healthy gingiva (HG), chronic gingivitis, chronic marginal periodontitis (CMP), or necrotizing ulcerative periodontitis (NUP). When the HIV+ group was compared with the HIV- group regardless of periodontal status, total salivary IgA concentration was higher in HIV+ patients, but no such difference was observed for total IgA output. HIV+ CMP displayed higher total IgA concentration as compared with HIV- CMP. No significant differences in specific IgA outputs and ratios were detected between HIV+ and HIV- subgroups with similar periodontal status. HIV+ NUP displayed increased specific IgA output towards S. mutans and increased specific IgA ratio values towards S. mutans, P. gingivalis and P. nigrescens as compared with HIV+ CMP, and increased specific IgA ratio values towards S. mutans and P. nigrescens as compared with HIV+ HG. No such differences were observed between the HIV- subgroups. In sum, salivary IgA responses to bacteria in dental plaque seem not to be related to chronic periodontal disease and HIV infection, but are possibly influenced by acute periodontal infection.

Serum samples were obtained from 44 HIV-seropositive (HIV+) and 37 HIV-seronegative (HIV-) persons that were grouped according to periodontal status. Serum IgG and IgA reactivities towards Streptococcus mutans, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis. Prevotella intermedia, Prevotella nigrescens and Fusobacterium nucleatum were measured by means of ELISA. HIV+ persons with chronic marginal periodontitis showed significantly lower IgG reactivities to the periodontal pathogens A. actinomycetemcomitans, P. gingivalis, P. intermedia and F. nucleatum as compared with their HIV- counterparts (p < 0.05). Specific serum IgA reactivities were similar in the two periodontitis groups, except for P. nigrescens where the HIV+ group with chronic marginal periodontitis had lower values than their systemically healthy counterparts (p < 0.05). The results indicate that HIV infection affects the humoral serum immune responses against bacteria in dental plaque; the depressed antibody responses may contribute to the increased susceptibility for periodontal infections in HIV-infected patients.

A quantitative, immunohistologic evaluation of CD3+, CD4+ and CD8+ cells was carried out on gingival biopsies from 25 HIV-infected persons with gingivitis or periodontitis and 13 HIV-seronegative persons with periodontitis. CD3+ T cells were found in all biopsies. CD8+ cells were significantly more numerous and the CD4+/CD8+ ratio was significantly decreased in the gingival connective tissue of the HIV+ patients (p < 0.05). The number of CD4+ lymphocytes subjacent to the pocket epithelium was moderately lower in the HIV+ patients as compared to the HIV patients (p < 0.05). HIV+ patients with a history of necrotizing periodontal disease had fewer CD4+ cells subjacent to the oral gingival epithelium than patients without such disease (p < 0.05). The general HIV-related changes in T lymphocyte numbers were therefore reflected in inflamed gingival tissues. HIV+ patients had, however, significantly higher CD4+/CD8+ ratios in gingiva than in peripheral blood (p < 0.05), indicating that CD4+ T cells are actively recruited to gingiva, even in cases of extreme CD4+ T lymphocytopenia.

Gingival biopsies were taken from 27 HIV (human immunodeficiency virus)-seropositive persons with gingivitis or periodontitis and 16 HIV-seronegative persons with periodontitis. Sections were stained with hematoxylin and eosin or periodic acid-Schiff. Candidal hyphae and pseudohyphae were found in the parakeratinized oral epithelium in 7 specimens from the HIV-infected patient group such specimen. No fungal invasion was found in any of the biopsies from the HIV-seronegative persons. Candidal invasion was significantly more frequent (P < 0.05) in patients with a confirmed history of necrotizing periodontal diseases (5/9) than in patients without known episodes of such diseases (3/18). The most prominent histopathologic changes observed in connection with candidal invasion comprised polymorphonuclear leucocyte infiltration of the oral gingival epithelium and numerous mitoses, some of which were located suprabasally. It is suggested that Candida albicans may contribute to the development of necrotizing periodontal diseases in HIV-infected persons.

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