Knowledge of oral diseases obtained from biopsy records provides more accurate data about the diagnosis and oral health of elderly patients. These indicators thus support the development of specific health policies for the prevention and treatment of oral and maxillofacial lesions that affect this population.
Our results demonstrate differences between the expression of ECM proteins in the OCs studied. The higher tenascin and fibronectin expression in the capsule of OKCs suggests marked instability in the cystic structure and may contribute to its aggressive behavior.
Periodontal diseases are initiated primarily by Gram-negative, tooth-associated microbial biofilms that elicit a host response that causes osseous and soft tissue destruction. Carvedilol is a β-blocker used as a multifunctional neurohormonal antagonist that has been shown to act not only as an anti-oxidant but also as an anti-inflammatory drug. This study evaluated whether Carvedilol exerted a protective role against ligature-induced periodontitis in a rat model and defined how Carvedilol affected metalloproteinases and RANKL/RANK/OPG expression in the context of bone remodeling. Rats were randomly divided into 5 groups (n = 10/group): (1) non-ligated (NL), (2) ligature-only (LO), and (3) ligature plus Carvedilol (1, 5 or 10 mg/kg daily for 10 days). Periodontal tissue was analyzed for histopathlogy and using immunohistochemical analysis characterized the expression profiles of MMP-2, MMP-9, COX-2, and RANKL/RANK/OPG and determined the presence of IL-1β, IL-10 and TNF-α, myeloperoxidase (MPO), malonaldehyde (MDA) and, glutathione (GSH). MPO activity in the group with periodontal disease was significantly increased compared to the control group (p<0.05). Rats treated with 10 mg/kg Carvedilol presented with significantly reduced MPO and MDA concentrations (p<0.05) in addition to presenting with reduced levels of the pro-inflammatory cytokines IL-1 β and TNF-α (p<0.05). IL-10 levels in Carvedilol-treated rats remained unaltered. Immunohistochemical analysis demonstrated reduced expression of MMP-2, MMP-9, RANK, RANKL, COX-2, and OPG in rats treated with 10 mg/kg Carvedilol. This study demonstrated that Carvedilol affected bone formation/destruction and anti-inflammatory activity in a rat model of periodontitis.
Due to the frequent presence of inflammation in cases of carcinoma and its use as a parameter for the assessment of tumor aggressiveness, the role of inflammation in oral carcinogenesis was investigated. This was performed by evaluating the expression of cellular markers, cytokines and nuclear transcription factors that identify the cells that participate in the antitumor defense in cases of oral epithelial dysplasia (OED) and oral squamous cell carcinoma (OSCC). A semi-quantitative immunohistochemical analysis was performed for the transcription factors cluster of differentiation 8 (CD8), forkhead box P3 (FOXP3), transforming growth factor (TGF)-β, tumor necrosis factor (TNF)-α and nuclear factor κ-light chain enhancer of activated B-cells (NF-κB), in cases of OED and OSCC. CD8, TGF-β, TNF-α and NF-κB participated in the processes of tumor transformation and progression. The presence of inflammatory infiltrate in cases of OED favors the transformation and invasion process when stromal TNF-α and NF-kB are overexpressed, as NF-kB activated by TNF-α during inflammation predisposes the lesion to transformation, functioning as a link between inflammation and cancer. The control of these inflammatory mediators may prevent malignant transformation in the oral cavity.
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