Regarding the edentulous mandible, patients benefited more from the IOD with 2 implants, as determined by OHRQoL scores. Considering the differences between each domain of the Oral Health Impact Profile (OHIP) questionnaire and the lack of long-term performance, more random control trials with sufficient sample sizes need to be designed to investigate long-term performance after treatment.

Oestrogen is essential for maintaining bone mass, and it has been demonstrated to induce osteoblast proliferation and bone formation. In this study, complementary DNA (cDNA) microarrays were used to identify and study the expression of novel genes that may be involved in MC3T3-E1 cells' response to 17-β estradiol. MC3T3-E1 cells were inoculated in minimum essential media alpha (α-MEM) cell culture supplemented with 17-β estradiol at different concentrations and for different time periods. MC3T3-E1 cells treated with 10−8 mol⋅L−1 17-β estradiol for 5 days exhibited the highest proliferation and alkaline phosphatase (ALP) activity; thus, this group was chosen for microarray analysis. The harvested RNA was used for microarray hybridisation and subsequent real-time reverse transcription polymerase chain reaction (RT-PCR) to validate the expression levels for selected genes. The microarray results were analysed using both functional and pathway analysis. In this study, microarray analysis detected 5 403 differentially expressed genes, of which 1 996 genes were upregulated and 3 407 genes were downregulated, 1 553 different functional classifications were identified by gene ontology (GO) analysis and 53 different pathways were involved based on pathway analysis. Among the differentially expressed genes, a portion not previously reported to be associated with the osteoblast response to oestrogen was identified. These findings clearly demonstrate that the expression of genes related to osteoblast proliferation, cell differentiation, collagens and transforming growth factor beta (TGF-β)-related cytokines increases, while the expression of genes related to apoptosis and osteoclast differentiation decreases, following the exposure of MC3T3-E1 cells to α-MEM supplemented with 17-β estradiol. Microarray analysis with functional gene classification is critical for a complete understanding of complementary intracellular processes. This microarray analysis provides large-scale gene expression data that require further confirmatory studies.

Background and Objective: Occlusal trauma is considered to be a contributing factor to bone loss associated with inflammatory periodontal disease. We hypothesized that pyroptosis, a recently discovered inflammation-induced programmed cell death pathway, plays a role in occlusal trauma. Materials and Methods:The occlusal trauma model was established using a cemented 1-mm elevated computer-aided design and manufacturing (CAD/CAM) metal crown.The periodontitis model was established by periodontal wire ligation with lipopolysaccharide (LPS) injection. The rats were sacrificed at 1, 2, 3, and 4 weeks. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to analyze the expression of pyroptosis-, inflammation-, and osteoclast-related markers. Micro-computed tomography (micro-CT) was used to determine bone morphology parameters. Tissue morphology was evaluated using hematoxylin and eosin staining (H&E). Osteoclasts were identified using tartrate-resistant acid phosphatase (TRAP) staining. The expression and distribution of factors related to pyroptosis and inflammation were evaluated by immunohistochemistry (IHC). The colocalization of dead cells and cysteinyl aspartatespecific proteinase-1 (caspase-1)-positive cells was analyzed by immunofluorescence. Results:Quantitative real-time polymerase chain reaction and IHC results showed that occlusal trauma induced the expression of pyroptotic factors during the early stages, while occlusal trauma with periodontitis upregulated the expression of pyroptotic factors at the later stages. The results of qRT-PCR, TRAP staining, and micro-CT showed that occlusal trauma with periodontitis increased the production of proinflammatory cytokines, leading to severe bone loss. Glyburide, an NOD-like receptor pyrin domain containing protein 3 (NLRP3)inhibitor, reduced the expression of pyroptosis markers induced by occlusal trauma with periodontitis and reversed bone resorption.Conclusions: Pyroptosis was involved in bone loss induced by occlusal trauma with or without periodontitis, while glyburide reversed inflammation and bone resorption.

These results suggested that at early phase of the occlusal trauma, osteogenesis in rat's alveolar bone was inhibited, and osteoclastogenesis was not significant.