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1.
J Clin Periodontol ; 51(6): 733-741, 2024 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-38449337

RESUMO

AIM: This study aimed to investigate the effects of diabetes care on periodontal inflammation. MATERIALS AND METHODS: This prospective cohort study included 51 Japanese patients with type 2 diabetes who underwent intensive diabetes care including educational hospitalization and regular outpatient treatment for 6 months. Dental prophylaxis without subgingival scaling was provided three times during the observational period. Associations between changes in periodontal parameters and glycaemic control levels were evaluated using multiple regression analysis. RESULTS: Overall, 33 participants (mean age: 58.7 ± 12.9) were followed up for 6 months. At baseline examination, 82% were diagnosed with Stage III or IV periodontitis. Haemoglobin A1c (HbA1c) level changed from 9.6 ± 1.8% at baseline to 7.4 ± 1.3% at 6 months. The ratio of probing pocket depth (PPD) ≥4 mm, bleeding on probing (BOP), full-mouth plaque control record (PCR), periodontal epithelial surface area (PESA) and periodontal inflamed surface area (PISA) also significantly improved. The reduction in PPD and PESA was significantly associated with changes in both HbA1c and fasting plasma glucose (FPG) levels, and the reduction in PISA was significantly associated with an improvement in FPG after adjusting for smoking, change in body mass index and full-mouth PCR. CONCLUSIONS: This is the first study to report a significant improvement in PPD and BOP after intensive diabetes care and dental prophylaxis without subgingival scaling. CLINICAL TRIAL REGISTRATION NUMBER: UMIN000040218.


Assuntos
Profilaxia Dentária , Diabetes Mellitus Tipo 2 , Hemoglobinas Glicadas , Índice Periodontal , Humanos , Diabetes Mellitus Tipo 2/complicações , Pessoa de Meia-Idade , Estudos Prospectivos , Masculino , Feminino , Hemoglobinas Glicadas/análise , Idoso , Profilaxia Dentária/métodos , Glicemia/análise , Periodontite/prevenção & controle , Periodontite/complicações , Estudos de Coortes , Bolsa Periodontal/prevenção & controle , Seguimentos
2.
J Periodontol ; 2023 Nov 27.
Artigo em Inglês | MEDLINE | ID: mdl-38009257

RESUMO

BACKGROUND: This study aimed to investigate the effects of low-level erbium-doped: yttrium, aluminum, and garnet (Er:YAG) laser irradiation on periodontal tissue healing and regeneration through angiogenesis in vivo and in vitro studies. METHODS: Intrabony defects were surgically created in the bilateral maxilla molar of rats. The defects were treated by open flap debridement (OFD) with Er:YAG laser, including low-level laser irradiation (LLLI) to bone and blood clot surfaces, or conventional procedures. The mRNA expression of vascular endothelial growth factor (VEGF) in the surgical sites was quantified using real-time polymerase chain reaction. The decalcified specimens were prepared for histometric analysis. Also, LLLI was performed on human umbilical vein endothelial cells to evaluate the effects on angiogenesis. Cell proliferation, VEGF expression, and tube formation were assessed. In addition, capsazepine (CPZ), a selective inhibitor of transient receptor potential vanilloid 1 (TRPV1), treatment was performed before LLLI for the same assays. RESULTS: OFD using Er:YAG laser did not generate thermal damage on bone or root surfaces. LLLI accelerated hemostasis by coagulation of the superficial layers of blood clots in the laser-treated group. Postoperative healing was sound in all animals in both groups. VEGF expression and bone formation were significantly increased in the laser-treated group compared to those in the conventional treatment group. In vitro, cell proliferation and VEGF expression were significantly increased in the LLLI group compared to the control group. Tube-formation assays showed that LLLI significantly promoted angiogenesis. CPZ treatment significantly suppressed VEGF expression and tube formation following LLLI. CONCLUSIONS: This study suggests that Er:YAG laser irradiation may promote periodontal tissue healing by enhancing angiogenetic effect of endothelial cells via TRPV1.

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