Comparison of immediate vs. delayed guided tissue regeneration in Infrabony defect of second molars after adjacent third molar extraction: a retrospective study.

BACKGROUND: The distal aspect of the second molar (d-M2) often exhibits infrabony defects due to the adjacent third molar. Although the defects can be treated by guided tissue regeneration (GTR) after removing the third molar, the optimal timing remains uncertain following third molar removal in clinical decision-making. This study aimed to compare delayed and immediate GTR treatments to assist in clinical decision-making. METHODS: D-M2 infrabony defects with a minimum 1-year follow-up were collected and divided into three groups: Immediate GTR group, which underwent third molar extraction and received GTR simultaneously; Delayed GTR group, which underwent delayed GTR at least 3 months after third molar extraction; and Control group, which underwent only scaling and root planing during third molar extraction. The clinical and radiographic parameters related to the infrabony defect before GTR and post-surgery were evaluated using the Kruskal-Wallis test or one-way ANOVA, followed by post-hoc Dunn's test or the Bonferroni test for pairwise comparisons. RESULTS: A total of 109 d-M2 infrabony defects were assessed. No significant differences were found between the two GTR groups, although both of them showed significant reductions in infrabony defect depth: the immediate GTR group (2.77 ± 1.97 mm vs. 0.68 ± 1.03 mm, p < 0.001) and the delayed GTR group (2.98 ± 1.08 mm vs. 0.68 ± 1.03 mm, p < 0.001) compared to the control group. CONCLUSION: GTR can effectively improve d-M2 infrabony defects when the third molar is removed, whether simultaneously or delayed. Patients may experience less discomfort with immediate GTR treatment as it requires only one surgery.

Common single nucleotide polymorphisms in cyclooxygenase-2 and risk of severe chronic periodontitis in a Chinese population.

AIM: Several common single nucleotide polymorphisms (SNPs) of the cyclooxygenase-2 (COX-2) gene have been reported to be functional. The association between -1195GA, -765GC and 8473TC of COX-2, and severe chronic periodontitis (CP) in a Chinese population was investigated. MATERIAL AND METHODS: 148 cases of healthy controls (control group) and 146 cases of severe CP were recruited in this study. Genotypes of -1195GA, -765GC and 8473TC were determined by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). The distributions of genotypes and haplotypes were compared by chi(2) test and the odds ratios (ORs) were calculated by logistic regression analysis. RESULTS: The prevalence of the -1195A was more prevalent in CP group (60.62%) than control group (51.35%), and the distributions of the -765C and 8473C were higher in control group (6.76% and 21.96%) compared with CP group (3.08% and 15.07%). Only genotype distribution of -1195GA was significant when p-value was corrected for multiple testing (p(c)=0.033). The adjusted ORs for the -1195AA/GA, -765GC and 8473CC/TC were 2.49 (95% CI=1.33-4.69, p=0.005), 0.45 (95% CI=0.20-1.04, p=0.061) and 0.67 (95% CI=0.41-1.11, p=0.118). Subjects with the haplotype AGT had a significantly higher risk of periodontitis than those with the most common haplotype GGT (OR=1.91, 95% CI=1.32-2.76, p(c)<0.001). CONCLUSIONS: It suggests the -1195A variant is associated with an increased risk for severe CP.

[Impacts of periodontitis on visceral organ weight and weight percentage in obese mice].

OBJECTIVE: This study aimed to explore the impacts of periodontitis on the visceral weight and weight percentage of obese animal models. METHODS: A total of 64 C57BL/6J mice were divided into the following diet groups: high-fat diet (HFD) group (n=36), which was fed with high-fat diet to induce obesity, and low-fat diet (LFD) group (n=28), which was fed with low-fat diet as the control. After 16 weeks on diet, each diet group was divided into periodontitis (P) and control (C) groups. The P groups were induced for periodontitis by ligation with Porphyromonas gingivalis-adhered silk for 5 or 10 days, and the C groups were sham-ligated as the control. Visceral organs were resected and weighed. The organ weight percentage was calculated. RESULTS: Compared with the LFD group, the HFD group significantly upregulated the weight and weight percentage of visceral adipose tissue and spleen (P<0.05), upregulated the weight of liver and kidney (P<0.05), and downregulated the weight percentage of liver and kidney (P<0.01). In the HFD group, the weight and weight percentage of spleen were downregulated in the P group (P<0.05), but were upregulated in the 10-day group compared with the 5-day group (P<0.05). CONCLUSIONS: Periodontitis can affect the general morphology of the viscera (especially spleen) in obese animal models. Pathological indications in terms of immunometabolism might be present in the correlation between obesity and periodontitis.

[Effects of non-surgical periodontal treatment on clinical response, serum inflammatory parameters, and metabolic control of type 2 diabetes patients with moderate to severe periodontitis].

OBJECTIVE: To evaluate the effects of periodontal treatment on the clinical response, systemic inflammatory parameters, and metabolic control of type 2 diabetes patients with moderate to severe periodontitis. METHODS: A total of 56 patients with mean clinical attachment level (CAL)>3 mm were included in the subgroup analysis. A repeated-measures ANOVA (group factor: treatment group and control group; time factor: initial visit, 1.5, 3, and 6 months) was used to analyze the probing depth (PD), CAL, bleeding on probing (BOP), high-sensitivity C-reactive protein (hsCRP), glycated hemoglobin (HbA1c), and fasting plasma glucose. RESULTS: Significantly lower PD (F=62.898, P-0.000), CAL (F=51.263, P-0.000), BOP (F=75.164, P=0.000), hsCRP (F=6.391, P=0.010), HbA1c(F=4.536, P=0.011), and fasting plasma glucose level (F= 3.073, P=0.031) were observed after therapeutic periodontal improvement. The inter-group differences for PD (t=-2.050, P=0.045), BOP (t=-4.538, P=0.000), and hsCRP (t=-2.261, P=0.028) were statistically significant after therapy. CONCLUSION: Non-surgical periodontal treatment can effectively improve periodontal status, circulating inflammatory status, and metabolic control of diabetic patients with moderate to severe periodontitis.

[Differentiation characteristics of human periodontal ligament cell population in vitro].

OBJECTIVE: To explore the multi-differentiated capability of human periodontal ligament cell population (hPDLP), and provide a theoretical basis for the periodontal regeneration by tissue engineering technique. METHODS: hPDLP was cultured from periodontium of human tooth by the outgrowth method. STRO-1 and CD 146 expression were investigated by flow cytometry. hPDLP was induced to odontogenic/osteogenic-like and adipogenic-like cell. The multilineage differentiation capacities of hPDLP were evaluated by alizarin red stain, oil red O stain, anti-CD146 and STRO-1 immunocytochemistry, and reverse-transcriptase polymerase chain reaction analysis. RESULTS: hPDLP was isolated from human periodontium and most of the cells retained their fibroblastic spindle shape. hPDLP can be induced into osteoblast-like cells and adipocyte-like cells, and calcium deposition and lipid droplets were detected perspectively. And the eighth generation of hPDLP had weaker potential into adipocyte-like cells than the first passage, however, there was no difference to the aspect of calcification ability between the two passages. CONCLUSION: hPDLP cultured in vitro can differentiate into adipocytes and osteoblasts, and the first to third passage cells may have the predominance of differentiation potential.

Identification and characterization of a novel gene, Mcpr1, and its possible function in the proliferation of embryonic palatal mesenchymal cells.

We cloned a novel mouse cDNA, Mcpr1 (mouse cleft palate-related gene 1), between retinoic acid (RA)-treated murine embryonic palatal and control shelves by improved subtractive hybridization. Its transcript was identified by Northern blotting. The open reading frame encodes 132 amino acids and shows almost no identity to other genetic products. Mcpr1 expression could be detected extensively in adult mouse tissues and during murine embryonic development. It was identified to be significantly stimulated by RA in murine palatal shelves at embryonic day 12 and in palatal mesenchymal cells in vitro. We demonstrate that MCPR1 protein was localized primarily in the cytoplasm and could be synthesized and secreted by transfected COS-7 cells. Both the secretory and recombinant proteins of Mcpr1 inhibited proliferation of murine embryonic palatal mesenchymal cells and impeded the progression from the G1 to S phase in the cell cycle. The cells were prone to apoptosis after exposure to glutathione S-transferase-MCPR1. Furthermore, knockdown of MCPR1 protein levels by antisense oligodeoxynucleotides promoted progression of cells from the G1 to S phase and completely abolished the RA-induced block of the cell cycle from the G1 to S phase. These findings suggest that Mcpr1 might function as one of the RA-up-regulated genes involved in inhibiting cell proliferation during palatogenesis and RA-induced cleft palate by regulating proliferation and apoptosis of embryonic palatal mesenchymal cells and might even play a role in the development of many other organs.