Concentrated growth factor and collagen as barrier materials in alveolar ridge preservation for posterior teeth: a prospective cohort study with one-year follow-up.

OBJECTIVES: This study aims to evaluate the efficacy of concentrated growth factor (CGF) membrane and collagen as barrier materials in sealing the alveolar socket in alveolar ridge preservation (ARP) in the posterior region during a one-year follow-up. METHODS: A total of 24 patients who underwent ARP in the posterior region were selected for inclusion and randomly assigned to the CGF group (12 cases) and Collagen group (12 cases). The patients in both groups underwent extraction of posterior teeth. The extraction sockets were filled with a bone substitute to the level of the pre-extraction buccal and lingual or palatal alveolar bone plates. The wounds in the CGF group were closed with a fabricated CGF overlaying the upper edge of the bone substitute material, whereas those in the Collagen group were closed with Bio-Oss Collagen. The implants were placed after 6 months. The evaluation was based on implant retention, re-grafting rate, and vertical and horizontal alveolar ridge bone volume changes measured by cone beam computed tomography (CBCT). Data were statistically analyzed using SPSS 28.0 software. RESULTS: No patient withdrew throughout the follow-up period. No implant failure and no severe peri-implant or mucosal soft tissue complications were observed. Six months after the operation, the degree of vertical alveolar ridge height resorption in the CGF group was lower than that in the Collagen group (P<0.05). There were no statistically difference between the groups at 1 year after the operation (P>0.05). The amount of bone reduction in horizontal alveolar ridge width showed no difference between the groups at 6 months and 1 year after surgery (P>0.05). CONCLUSIONS: CGF membrane and Bio-Oss Collagen as barrier materials for posterior ARP inhibited reduction in alveolar ridge bone mass.

Sensory neuron transient receptor potential vanilloid-1 channel regulates angiogenesis through CGRP in vivo.

Angiogenesis plays a key role in bone regeneration. The role of neurons of peripheral nerves involved in angiogenesis of bone defects needs to be explored. The transient receptor potential vanilloid 1 (TRPV1), a nociceptor of noxious stimuli, is expressed on sensory neurons. Apart from nociception, little is known about the role of sensory innervation in angiogenesis. Calcitonin gene-related peptide (CGRP), a neuropeptide secreted by sensory nerve terminals, has been associated with vascular regeneration. We characterized the reinnervation of vessels in bone repair and assessed the impact of TRPV1-CGRP signaling on early vascularization. We investigated the pro-angiogenic effect of neuronal TRPV1 in the mouse model of femur defect. Micro-CT analysis with Microfil® reagent perfusion demonstrated neuronal TRPV1 activation enhanced angiogenesis by increasing vessel volume, number, and thickness. Meanwhile, TRPV1 activation upregulated the mRNA and protein expression of vascular endothelial growth factor A (VEGF-A), cell adhesion molecule-1 (CD31), and CGRP. Immunostaining revealed the co-localization of TRPV1 and CGRP in dorsal root ganglia (DRG) sensory neurons. By affecting neuronal TRPV1 channels, the release of neuronal and local CGRP was controlled. We demonstrated that TRPV1 influenced on blood vessel development by promoting CGRP release from sensory nerve terminals. Our results showed that neuronal TRPV1 played a crucial role in regulating angiogenesis during bone repair and provided important clinical implications for the development of novel therapeutic approaches for angiogenesis.

Neuronal TRPV1-CGRP axis regulates bone defect repair through Hippo signaling pathway.

Transient receptor potential vanilloid type 1 (TRPV1) is highly expressed on sensory neurons where it serves as a polymodal receptor for detecting physical and chemical stimuli. However, the role of TRPV1 in bone metabolism remains largely unclear. This study aimed to investigate the underlying mechanism of neuronal TRPV1 in regulating bone defect repair. In vivo experiment verified that TRPV1 activation could trigger dorsal root ganglion (DRG) producing the neuropeptide calcitonin gene-related peptide (CGRP) in mice. The accelerated bone healing of femoral defect in this process was observed compared to the control group (p < 0.05). Conversely, Trpv1 knockdown led to reduced CGRP expression in DRG and nerves innervating femur bone tissue, following impaired bone formation and osteogenic capability in the defect region (p < 0.05), which could be rescued by local CGRP treatment. In vitro, results revealed that TRPV1 function in DRG neurons contributed essentially to the regulation of osteoblast physiology through affecting the production and secretion of CGRP. The capsaicin-activated neuronal TRPV1-CGRP axis could enhance the proliferation, migration and differentiation of osteoblasts (p < 0.05). Furthermore, we found that the promoting role of neuronal TRPV1 in osteogenesis was associated with Hippo signaling pathway, reflected by the phosphorylation protein level of large tumor suppressor 1 (LATS1), MOB kinase activator 1 (MOB1) and Yes-associated protein (YAP), as well as the subcellular location of YAP. Our study clarified the effects and intrinsic mechanisms of neuronal TRPV1 on bone defect repair, which might offer us a therapeutic implication for bone disorders.