ABSTRACT
BACKGROUND: The aim of the study was to clinically evaluate the healing of intrabony defects after treatment with a new generation of platelet-rich fibrin (A-PRF+) respect to enamel matrix derivative (EMD). METHODS: Thirty (30) intrabony defects of 18 patients (9 males, 9 females) were randomly treated with A-PRF+ (test, n = 15) or EMD (control, n = 15). The following clinical parameters were recorded at baseline and 6 months after surgery: pocket depth (PD), gingival recession (GR) and clinical attachment level (CAL). After debridement the intrabony defects were filled with A-PRF+ in the test group, respectively with EMD in the control group, and fixed with sutures to ensure wound closure and stability. RESULTS: Both treatment methods resulted in statistically significant PD reductions, respectively CAL gains six months post-operatively. No statistically significant differences were found between the two groups as the mean CAL gain was 2.33 ± 1.58 mm in the A-PRF+ group, respectively 2.60 ± 1.18 mm in the EMD group (p < 0.001). CONCLUSION: Within the limits of this study the new-generation platelet-rich fibrin seems to be as clinically effective as EMD during surgical treatment of intrabony defects. Treatment with A-PRF+ or EMD resulted in reliable clinical outcomes. The use of A-PRF+ as a human autologous product can give a positive impact on periodontal healing. Clinical Relevance A-PRF+ may be suitable for the treatment of intrabony periodontal defects. Trial registration number (TRN) NCT04404374 (ClinicalTrials.gov ID).
Subject(s)
Alveolar Bone Loss , Dental Enamel Proteins , Gingival Recession , Platelet-Rich Fibrin , Alveolar Bone Loss/surgery , Dental Enamel Proteins/therapeutic use , Female , Gingival Recession/surgery , Guided Tissue Regeneration, Periodontal , Humans , Male , Periodontal Attachment Loss/surgery , Treatment OutcomeABSTRACT
The adipose-derived hormone leptin maintains energy balance in part through central nervous system-mediated increases in sympathetic outflow that enhance fat burning. Triggering of ß-adrenergic receptors in adipocytes stimulates energy expenditure by cyclic AMP (cAMP)-dependent increases in lipolysis and fatty-acid oxidation. Although the mechanism is unclear, catecholamine signalling is thought to be disrupted in obesity, leading to the development of insulin resistance. Here we show that the cAMP response element binding (CREB) coactivator Crtc3 promotes obesity by attenuating ß-adrenergic receptor signalling in adipose tissue. Crtc3 was activated in response to catecholamine signals, when it reduced adenyl cyclase activity by upregulating the expression of Rgs2, a GTPase-activating protein that also inhibits adenyl cyclase activity. As a common human CRTC3 variant with increased transcriptional activity is associated with adiposity in two distinct Mexican-American cohorts, these results suggest that adipocyte CRTC3 may play a role in the development of obesity in humans.