Current studies show that, even in the era of antiretroviral therapies, HIV-1 infection is associated with more severe and frequent refractory chronic periodontitis. Areas covered: This review, based on a systematic analysis of the literature, intends to provide an update on factors that may be involved in the pathogenesis of periodontal disease in HIV-1-infected patients, including local immunosuppression, oral microbial factors, systemic inflammation, salivary markers, and the role of gingival tissue as a possible reservoir of HIV-1. Expert commentary: The therapeutic revolution of ART made HIV-1 infection a chronic controllable disease, reduced HIV-1 mortality rate, restored at least partially the immune response and dramatically increased life expectancy of HIV-1-infected patients. Despite all these positive aspects, chronic periodontitis assumes an important role in the HIV-1 infection status for activating systemic inflammation favoring viral replication and influencing HIV-1 status, and also acting as a possible reservoir of HIV-1. All these issues still need to be clarified and validated, but have important clinical implications that certainly will benefit the diagnosis and management of chronic periodontitis in HIV-1-infected patients, and also contributes to HIV-1 eradication.

NSPT had a beneficial impact on clinical and immunological parameters of CP, reduction of oral Candida counts, and improvement of HIV-infection status.

Background Despite combined antiretroviral therapy (cART), total cure of immunodeficiency virus type 1 (HIV‐1) infection remains elusive. Chronic periodontitis (CP) is strongly associated with HIV‐1 infection. This condition is characterized by an intense inflammatory infiltrate mainly constituted of immune cells which in turn may be a valuable source of HIV‐1 reactivation. This study aimed to determine if gingival tissue could act as a reservoir for HIV‐1. Methods Twelve patients with HIV‐1 and CP and 12 controls (no HIV‐1‐infection and no CP) were evaluated in a cross‐sectional study. RNA viral load and interleukin (IL) levels were determined in blood plasma and saliva. Histological sections of gingival tissue were stained with fluorescent antibodies against p24 antigen and different cellular biomarkers. Results In six of the 12 patients, HIV RNA load was detected, despite cART; in three of them, expression of viral RNA was also detected in saliva. The levels of IL‐2, IL‐6, and IL‐12 were higher in blood and saliva of patients with HIVand CP than controls. HIV‐1 p24 antigen was detected by immunostaining in gingival biopsies of 10 of the 12 patients but in no controls. Immune markers for T cells and antigen‐presenting cells were also identified in most patients and some controls. Conclusion These preliminary data showing the detection of HIV‐1 p24 antigen in the gingival biopsies of a significant part of patients with HIV‐1 and CP under cART together with the presence of immune cells, plead for the existence of a HIV‐1 reservoir in the gingival tissue of this population.

Background Following human immunodeficiency virus‐1 (HIV‐1) infection and antiretroviral therapy, the development of periodontal disease was shown to be favored. However, the influence of HIV‐1 infection on the periodontal microbiota after non‐surgical periodontal debridement (NSPD) needs a broad comprehension. This work aimed to compare the subgingival microbiological content of patients infected with HIV‐1 and controls (non‐infected) with periodontitis undergoing NSPD. Methods The bacterial profile of subgingival biofilm samples of patients with HIV‐1 (n = 18) and controls (n = 14) with periodontitis was assessed using 16S rRNA gene sequencing. The samples were collected at baseline, 30, and 90 days after NSPD. The taxonomic analysis of gingival microbiota was performed using a ribosomal RNA database. The microbiota content was evaluated in the light of CD4 cell count and viral load. Results Both HIV and control groups showed similar stages and grades of periodontitis. At baseline, the HIV group showed higher alpha diversity for both healthy and periodontal sites. Streptococcus, Fusobacterium, Veillonella and Prevotella were the predominant bacterial genera. A low abundance of periodontopathogenic bacteria was observed, and the NSPD induced shifts in the subgingival biofilm of patients with HIV‐1, leading to a microbiota similar to that of controls. Conclusions Different subgingival microbiota profiles were identified—a less diverse microbiota was found in patients infected with HIV‐1, in contrast to a more diverse microbiota in controls. NSPD caused changes in the microbiota of both groups, with a greater impact on the HIV group, leading to a decrease in alpha diversity, and produced a positive impact on the serological immune markers in patients infected with HIV‐1. Control of periodontitis should be included as part of an oral primary care, providing the oral health benefits and better control of HIV‐1 infection.

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