Bone remodeling is a process of bone renewal accomplished by osteoclastic bone resorption and osteoblastic bone formation. These two activities are regulated by systemic hormones and by local cytokines and growth factors. Moreover, the nervous system and certain neuropeptides seem to be involved in regulation of bone remodeling. In this paper, we focus on the distribution of CGRP-containing nerve fibers and their dynamics, and discuss the role of these fibers as a possible mechanism for nervous system involvement in regulation of bone remodeling. CGRP-immunoreactive nerve fibers are widely distributed in bone tissue, such as periosteum and bone marrow, and show apparent regional distribution with different densities. They are often associated with blood vessels and show a beaded appearance. The wide distribution of CGRP-immunoreactive nerve fibers in bone tissue and the changes in distribution during bone development and regeneration suggest the involvement of these fibers in bone remodeling. The effect of CGRP on bone remodeling could partly be through its action on blood vessels, thereby regulating local blood flow. Moreover, in vitro biochemical data and the localization of CGRP-immunoreactive nerve fibers in the vicinity of bone cells suggest that they are directly involved in local regulation of bone remodeling by elevating the concentration of CGRP in the microenvironment around bone cells, especially during bone growth or repair.

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To preserve all autonomic nerves for urogenital function, optimal total mesorectal excision for rectal cancer requires dissection behind Denonvilliers' fascia.

Female perineal structures located around the perineal body were histologically examined using semiserial sections obtained from 15 elderly female cadavers. The smooth muscle content of the perineal body was greater in multiparous women. The connective tissue of the perineal body extended inferolaterally and provided a fibromuscular mass that was 10-30 mm long mediolaterally and 3-15 mm long superoinferiorly. The lateral extension (LEX) of the perineal body occupies a space that is surrounded by the vestibular bulb, internal anal sphincter, and levator ani slings. The LEX did not directly connect to the ischiopubic bony rami but did connect indirectly via the vestibular bulb and ischiocavernosus. Thus, the LEX appears to play a critical role for maintaining the topographical relationship between the vagina and the rectum. The surgical approximation of bilateral LEX instead of levator ani may be of key importance when doing a perineorrhaphy. As pudendal nerve branches run along the inferior margin of the LEX, a mediolateral episiotomy may not be the best option.

(SE) S U M M A R Y The morphology of the osteocyte changes during the cell's lifetime. Shortly after becoming buried in the matrix, an osteocyte is plump with a rich rough endoplasmic reticulum and a well-developed Golgi complex. This "immature" osteocyte reduces its number of organelles to become a "mature" osteocyte when it comes to reside deeper in the bone matrix. We hypothesized that mineralization of the surrounding matrix is the trigger for osteocyte maturation. To verify this, we prevented mineralization of newly formed matrix by administration of 1-hydroxyethylidene-1,1-bisphosphonate (HEBP) and then examined the morphological changes in the osteocytes in rats. In the HEBP group, matrix mineralization was disturbed, but matrix formation was not affected. The osteocytes found in the unmineralized matrix were immature. Mature osteocytes were seen in the corresponding mineralized matrix in the control group. The immature osteocytes in the unmineralized matrix failed to show immunoreactivity with anti-sclerostin antibody, whereas mature osteocytes in the mineralized matrix showed immunoreactivity in both control and HEBP groups. These findings suggest that mineralization of the matrix surrounding the osteocyte is the trigger for cytodifferentiation from a plump immature form to a mature osteocyte. The osteocyte appears to start secreting sclerostin only after it matures in the mineralized bone matrix. (J Histochem Cytochem 56:561-567, 2008)