Effects of neonatal sympathectomy and capsaicin treatment on bone remodeling in rats.
Bone metabolism may be influenced by the innervation of skeletal tissues. Neuropeptides such as vasoactive intestinal peptide, from sympathetic nerves, and calcitonin gene-related peptide, from sensory nerves, have been implicated as local modulators of bone metabolism. The effect of neonatal sympathectomy and of capsaicin-induced sensory denervation in rats was studied on the following: (i) the radial bone growth and apposition rate in tibiae (normal growth and modeling) and (ii) the percentage of periosteal surface of the mandible occupied by osteoclasts during induced remodeling. Neonate rats were treated with guanethidine, capsaicin, or appropriate vehicle. At seven weeks, maxillary molars were removed to induce remodeling on the buccal surface of the mandible. Animals were killed four days after surgery. Cross-sectional cortical area, medullary area, and periosteal apposition rate were measured by histomorphometry in ground sections of tibiae. The percentage of periosteal surface at the remodeling site occupied by osteoclasts (stained for acid phosphatase) was measured in frozen, undecalcified sections. There was no significant difference in cortical or medullary area or periosteal apposition rate in tibiae between each drug treatment and its control. However, the mandibular bone surface occupied by osteoclasts was increased 45.5% (P less than or equal to 0.005) in animals treated neonatally with guanethidine compared to controls. In contrast, the mandibular surface occupied by osteoclasts was decreased 21.2% (P less than or equal to 0.04) in animals treated neonatally with capsaicin compared to controls. The alteration of bone remodeling (osteoclast surface) by both treatments indicates that sensory and sympathetic nerves play a role in focal metabolism of bone.
Hill
E L
EL
Department of Cell Biology and Neuroanatomy, University of Minnesota, MN.
Turner
R
R
Elde
R
R
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D016723:Bone Remodeling / Q000187:drug effects* / Q000502:physiology; D015740:Calcitonin Gene-Related Peptide / Q000032:analysis / Q000502:physiology*; D002211:Capsaicin; D004299:Dopamine beta-Hydroxylase / Q000032:analysis; D006145:Guanethidine; D008297:Male; D008334:Mandible / Q000294:innervation; D009412:Nerve Fibers / Q000187:drug effects / Q000502:physiology; D009413:Nerve Fibers, Myelinated / Q000187:drug effects / Q000502:physiology; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology; D010010:Osteoclasts / Q000473:pathology; D051381:Rats; D011919:Rats, Inbred Strains; D013373:Substance P / Q000032:analysis; D013563:Sympathectomy, Chemical; D013977:Tibia / Q000294:innervation / Q000473:pathology; D014660:Vasoactive Intestinal Peptide / Q000032:analysis / Q000502:physiology*
D013373:Substance P; D014660:Vasoactive Intestinal Peptide; D004299:Dopamine beta-Hydroxylase; D015740:Calcitonin Gene-Related Peptide; D002211:Capsaicin; D006145:Guanethidine