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.

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Background: Periodontitis (PDT) has gained attention in the literature with the increase in life expectancy of people living with HIV on combined antiretroviral therapy (cART). Thus, the search for inflammatory biomarkers could be useful to understand the pathophysiology of chronic oral diseases in the cART era. Objective: The aim of this study was to evaluate the impact of non-surgical periodontal therapy (NSPT) on clinical parameters of PDT, Candida spp. count and expression of LF and HST in saliva and CGF of HIV-infected patients. Methods: Bleeding index (BI), probing depth (PD), clinical attachment level (CAL), colony-forming units (CFUs) of Candida spp, and lactoferrin (LF) and histatin (HST) levels were measured in saliva and GCF of both groups at three different times: baseline (before treatment), and 30 and 90 days after the NSPT. Clinical, mycological and immunoenzymatic analyses were also performed. Results: Twenty-two HIV-infected patients and 25 non-HIV-infected patients with PDT participated in the study. NSPT was effective in improving periodontal clinical parameters, including ≤ 4 sites with PD ≤ 5mm and BI ≤ 10%. No significant change in oral Candida spp. count occurred neither between the two groups nor during the time after the periodontal treatment. And the salivary and GCF levels of LF and HST seems not to be influenced by the NSPT. By contrast, except for salivary LF, HST and LF were shown to exhibit significantly higher levels in HIV-infected than in non-HIV-infected patients. Conclusions: NSPT was effective in improving periodontal disease parameters in HIV-infected patients, but do not affect lactoferrin and histatin-5 expression in saliva and ginvival crevicular fluid of HIV-infected patients.

À Deus, pois se eu cheguei até aqui foi através de ti. Foi o meu sustento e minha força nos momentos mais fracos, mesmo sem muitas vezes eu merecer nunca me abandonou. Muito obrigada Senhor por me amar e cuidar de mim, que a cruz sagrada seja a minha luz por todos meus caminhos. Até quando eu viver, vou te honrar. Posso perder tudo, mas nunca a minha fé em ti. À Nossa Senhora, por me amar como filha, cuidar de mim, pude sentir sua presença em todos os momentos dessa jornada, o terço foi meu alimento e minha força para seguir em frente e não desistir diante das dificuldades. Obrigada minha mãe. À minha mãe Carmem, minha grande guerreira e amiga. Por todos momentos difíceis que passamos, conseguimos mais uma conquista. Mãe, você é meu alicerce. Enquanto houver você do outro lado, eu estarei aqui, de pé, forte, pois eu sei que independente do que aconteça eu sempre vou ter o seu abraço e seu amor. Obrigada por seu meu porto seguro, minha paz, minha vida. Essa vitória é sua, minha rainha e minha inspiração. Ao meu irmão Raony, por ser meu anjo enviado por Deus, grande amigo e parceiro da vida. Agradeço pelo incentivo constante e por sempre acreditar no meu potencial. À minha mestre Profa. Fabiana de Freitas Bombarda Nunes, por ter sido uma grande incentivadora dos meus sonhos acadêmicos. Eu agradeço seu carinho, amizade, profissionalismo e por ter semeado em mim o amor pela estomatologia. Aos participantes do estudo, que diante da fragilidade em conviver com a infecção por HIV e sofrer todo o preconceito, que ainda existe em torno da doença, transmitiram-me grandes lições de vida, mostraram-me o verdadeiro valor da vida, e depositaram toda a confiança em nossa equipe de trabalho na esperança de uma possível melhoria na qualidade de vida. Sem o "sim" de vocês não seria possível a concretização deste estudo. AGRADECIMENTOS À Profa. Dra. Ana Carolina Fragoso Motta, por ter me acolhido como orientada, por ter me incentivado a não desistir do meu ingresso no mestrado, quando todas as possibilidades pareciam esgotadas. Pelo incentivo e confiança depositados em todas as atividades que me propus. Por me inspirar a ser uma profissional dedicada, prudente, e sobretudo sensível para com os alunos e pacientes. Trabalhar contigo durante o mestrado me fez evoluir bastante como dentista e ser humano! Não existem palavras para expressar a minha gratidão! À Profa. Dra. Marilena Chinali Komesu, por ter me aberto a primeira porta da USP, proporcionando o meu estágio no DAPE, sem mesmo me conhecer, investindo grandemente na minha carreira acadêmica. Pelos conhecimentos compartilhados durante todo este período em que ficamos juntas. Além das inúmeras oportunidades que me proporcionou. Muito obrigada é muito pouco para manifestar minha gratidão! Ao Prof. Dr. Alan Grupioni Lourenço, por toda a paciência, amizade e por confiar parte do seu trabalho, a mim. Agradeço por ser grande colaborador para a minha vida profissional. Desejo todo o sucesso ao longo da sua vida como professor.

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.