RESUMO
Peri-implant diseases, characterized by inflammatory conditions affecting peri-implant tissues, encompass peri-implant mucositis and peri-implantitis. Peri-implant mucositis is an inflammatory lesion limited to the mucosa around an implant, while peri-implantitis extends from the mucosa to the supporting bone, causing a loss of osseointegration. For non-surgical treatments, we tested the null hypothesis that the presence or absence of air-polishing made no difference. The study focused on randomized controlled trials (RCTs) comparing air-polishing with mechanical or ultrasonic debridement, evaluating outcomes such as bleeding on probing (BOP), probing depth (PD), plaque index/plaque score (PI/PS), clinical attachment level (CAL), bone loss, and mucosal recession (MR). Two independent reviewers conducted data extraction and quality assessments, considering short-term (<6 months) and long-term (≥6 months) follow-up periods. After screening, ten articles were included in the meta-analysis. In nonsurgical peri-implant disease management, air-polishing moderately mitigated short-term PI/PS for peri-implant mucositis and showed a similar improvement in long-term BOP and bone loss for peri-implantitis compared to the control group. The Egger test found no evidence of publication bias except for the long-term PI/PS of peri-implant mucositis. Leave-one-out analysis confirmed the stability of the results. The findings highlight the need for future research with longer-term follow-up and high-quality, multi-center, large-sample RCTs.
RESUMO
Chondrocytes, known for their metabolic adaptability in response to varying stimuli, play a significant role in osteoarthritis (OA) progression. Glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme of the pentose phosphate pathway, has recently been found to upregulate in OA chondrocyte. However, the exact role of G6PD in temporomandibular joint osteoarthritis (TMJOA) and its effect on chondrocyte function remains unclear. In present study, we induced OA-like conditions in the rat temporomandibular joint via occlusal disharmony (OD), noting a marked increase in G6PD expression in the condylar cartilage. Our data show that G6PD knockdown in mandibular condylar chondrocytes (MCCs) reduces the expression of catabolic enzymes (e.g., MMP3, MMP13) and inflammatory cytokines (e.g., IL6) induced by IL-1ß. G6PD knockdown also mitigates IL-1ß-induced upregulation of ERK, JNK, and p38 phosphorylation and reduces reactive oxygen species (ROS) levels by decreasing the nicotinamide adenine dinucleotide phosphate (NADPH) and NADPH oxidases 4 (NOX4) mRNA expression. In summary, G6PD appears to regulate the inflammatory state of condylar chondrocytes via the NOX-ROS-MAPK axis, highlighting its potential as a therapeutic target for TMJOA.