Histological changes were observed in a hydroxyapatite plate and hydroxyapatite granules used to repair a craniotomy defect and removed after 2 years and 9 months of use. The hydroxyapatite plates and granules had completely fused to the cranium, with new bone formation on the dural side extending in a three-dimensional matrix along the pores with the Haversian system in the center. New bone formation was less extensive under the artificial dura than under the normal dura. This finding suggests that the dura has the ability to promote bone formation. A new vessel was found along the interconnecting pores. The interconnecting pores allow osteoconduction in the hydroxyapatite plate, so new bone formation can progress. Hydroxyapatite has osteoconduction properties and is biocompatible, so gains strength in vivo through new bone formation, and is the ideal material for artificial bones. Factors important to achieving good bone formation after cranial reconstruction surgery include presence of the dura, and pore size approximate to the Haversian system (100-500 mm) and interconnecting pores in the hydroxyapatite plate.

AHC PKN (protein kinase N; also called protein kinase C-related kinase (PRK-1)), is a serine/threonine protein kinase that is ubiquitously expressed in several organs, including the brain. PKN has a molecular mass of 120 kDa and has two domains, a regulatory and a catalytic domain, in its amino-terminals and carboxyl-terminus, respectively. Although the role of PKN has not been fully elucidated, previous studies have revealed that PKN is cleaved to a constitutively active catalytic fragment of 55 kDa in response to apoptotic signals. Hydrocephalus is a pathological condition caused by insufficient cerebrospinal fluid (CSF) circulation and subsequent excess of CSF in the brain. In this study, in order to elucidate the role of PKN in the pathophysiology of hydrocephalus, we examined PKN fragmentation in hydrocephalic model rats. Hydrocephalus was induced in rats by injecting kaolin into the cisterna magna. Kaolininduced rats (n=60) were divided into three groups according to the observation period after treatment (group 1: 3-6 weeks, group 2: 7-12 weeks, and group 3: 13-18 weeks). Shamtreated control rats, injected with sterile saline (n=20), were similarly divided into three groups. Spatial learning ability was estimated by a modified water maze test. Thereafter, brains were cut into slices and ventricular dilatation was estimated. Fragmentation of PKN was observed by Western blotting in samples collected from the parietal cortex, striatum, septal nucleus, hippocampus, and periaqueductal gray matter. All kaolin-induced rats showed ventricular dilatation. Most of them showed less spatial learning ability than those of sham-treated controls. In most regions, fragmentation of PKN had occurred in a biphasic manner more frequently than that in controls. The appearance of PKN fragmentation in periaqueductal gray matter was correlated with the extent of ventricular dilation and spatial learning disability. These results revealed that PKN fragmentation was observed in rats with kaolin-induced hydrocephalus, models for chronically-damaged brain dysfunction, suggesting that persistent brain insult, such as apoptosis, had occurred in these models. PKN fragmentation could be a hallmark for evaluating morphological and functional damage of the hydrocephalus.

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