Sistema purinérgico e inflamação na doença periodontal

Abstract

Periodontal disease (PD) is characterized by the presence of a chronic inflammatory process, resulting from the accumulation of bacterial biofilm, which triggers a host response to these pathogens, leading to the destruction of the supporting tissues of dental structures. Research has demonstrated that components of the purinergic system and inflammation are closely related to the development and progression of PD. The objective of this study was to evaluate histological parameters of periodontal tissues, as well as the regulation of the purinergic system and inflammation in patients with PD, comparing them with individuals with healthy periodontium. This is a cross-sectional study of a quantitative nature, which selected 60 participants, including n= 20 healthy patients (controls), n= 20 patients with gingivitis, n= 20 patients with periodontitis, from which gingival tissue samples were collected after informed consent. Histological parameters related to tissue inflammation were analyzed, such as reactive epithelial changes, presence of inflammatory cells, fibrosis, and laboratory markers. Gene expression of purinergic system markers, with emphasis on the ectoenzymes CD39 and CD73, and on the P2X7 and A2A receptors, was performed using real-time PCR, and the presence of CD8 and CD20 markers was assessed using immunohistochemistry. Differences between groups were assessed using the chi-square test, one-way ANOVA, Kruskal-Wallis test and Student's t-test, considering a significance level of 5%. The results of the histological analysis showed that acanthosis was more frequent in both gingivitis (95% incidence - 65% mild and 30% moderate) and periodontitis (85% incidence - 60% mild and 25% moderate), compared to the control group (50% incidence) (p= 0.0121). Leukopedesis was more frequent in gingivitis (75% incidence - 30% mild, 20% moderate and 25% severe) and periodontitis (90% incidence - 20% mild, 55% moderate and 15% severe) compared to the control group (45% incidence) (p= 0.0082). Hyperkeratosis was increased in the gingivitis group (75% incidence - mild) compared to the periodontitis (30% incidence) and control (30% incidence) groups (p= 0.0043). The gingivitis (60% incidence), periodontitis (85% incidence) and control (15% incidence) groups showed monomorphonuclear cellular infiltration, becoming more evident in the periodontitis group. About that, polymorphonuclear cellular changes were more evident in the gingivitis group (40% incidence), compared to the periodontitis (10% incidence) and control (5% incidence) groups (p= 0.0001). Immunohistochemistry indicated greater immunoreactivity for CD8 in the gingivitis group compared to the control group (p= 0.0165) and for CD20 in the periodontitis group compared to the control group (p= 0.0444). The laboratory results indicated a higher expression of the CD73 gene in periodontitis compared to the control group (p = 0.0002). It is also indicated that the mean expression of the CD39 and P2X7 genes was lower in the periodontitis group compared to the control, and the mean expression of the A2A gene was higher in periodontitis compared to the healthy group (p = 0.3032; 0.2076 and 0.5144; respectively). From the histological findings, it is suggested that the greater the involvement of gingival tissue, the greater the histological and inflammatory expressions and changes. It is also indicated that periodontitis promotes a modulation of purinergic signaling components, and this modulation may be associated with ineffective bacterial clearance, promoting the maintenance of the pro-inflammatory microenvironment to benefit the disease. Therefore, this research is essential to clarify the pathophysiological aspects related to purinergic signaling and inflammation that may be involved in PD. The knowledge gained is also crucial to improving early diagnosis and expanding less invasive treatment options for this disease.