Involvement of sensory neurons in bone defect repair in rats

Abstract

We investigated bone repair in sensory-denervated rats, compared with controls, to elucidate the involvement of sensory neurons. Nine-week-old male Wistar rats received subcutaneous injections of capsaicin to denervate sensory neurons. Rats treated with the same amount of vehicle served as controls. A standardized bone defect was created on the parietal bone. We measured the amount of repaired bone with quantitative radiographic analysis and the mRNA expressions of osteocalcin and cathepsin K with real-time polymerase chain reaction (PCR). Quantitative radiographic analysis showed that the standard deviations and coefficients of variation for the amount of repaired bone were much higher in the capsaicin-treated group than in the control group at any time point, which means that larger individual differences in the amount of repaired bone were found in capsaicin-treated rats than controls. Furthermore, radiographs showed radiolucency in pre-existing bone surrounding the standardized defect only in the capsaicin-treated group, and histological observation demonstrated some multinuclear cells corresponding to the radiolucent area. Real-time PCR indicated that there was no significant difference in the mRNA expression levels of osteocalcin and cathepsin K between the control group and the capsaicin-treated group. These results suggest that capsaicin-induced sensory denervation affects the bone defect repair.

Calcification during bone healing in a standardised rat calvarial defect assessed by micro‐CTandSEM‐EDX

“…The twelve‐week‐old rats in the control group were fixed and the physiological parietal bone was compared with the healing bone in weeks 1, 2, 4 and 8. The juvenile bone growth of rats ceases in 12 weeks after birth, which gives us the premise that new bone formation observed in the experimental model with these rats is due to bone healing, but not bone growth (Honma et al , ; Henmi et al , ).…”

“…The drill was carefully performed to avoid injury to the dura mater. The periosteal and skin flaps were returned and sutured (Honma et al , ; Henmi et al , ).…”

“…Therefore, we hypothesise that increase in mineral density is coupled with the increase in volume in healing bone as in developing bone. To test the hypothesis, our study was designed to investigate the process of calcification during bone healing using a standardised rat calvarial bone defect model (Honma et al , ; Henmi et al , ). Calcification was evaluated by measuring the bone mineral density with microcomputed tomography (micro‐CT), and the concentration and distribution of elements that constitute the bone matrix, such as calcium (Ca), phosphorus (P) and carbon (C), were analysed using energy‐dispersive X‐ray spectroscopy (SEM‐EDX).…”

Sensory neurons from dorsal root ganglia regulate endothelial cell function in extracellular matrix remodelling

“…Numerous evidence from animal studies that began in the 1980's, suggest a relationship between sensory nerve damage and joint diseases [7][8][9]. The focus on skeletal neurobiology emerged with a series of sensory denervation experimental models performed mainly in rats [10,11] and confirmed the role of peripheral innervation in the regulation of bone tissue development and regeneration. Nerve fibres exist throughout bone but are more abundant in the periosteum, as well as in the mineralized and vascularized parts of bone tissue, and are predominantly located at metabolically active regions of bone [12][13][14][15][16][17][18].…”

Effects of inferior alveolar nerve rupture on bone remodeling of the mandible

“…[7,9,10,12,14,16,17] The related results of immunohistochemical analysis revealed that IAN injury altered the expression level of several IAN-secreted neuropeptides, such as calcitonin gene-related peptide (CGRP) and substance P (SP), and subsequently impaired bone remodeling by affecting osteoclast and osteoblast activities. [6,9,10,13,17]…”