Nobumitsu Oka

The effect of ovariectomy on the temporomandibular joints of growing rats

PURPOSE This investigation studied the effects of ovariectomy, on the temporomandibular joints (TMJ) of young rats. MATERIALS AND METHODS Four-week-old female Wistar rats were ovariectomized and killed at the intervals of 1, 2, 4, and 8 weeks postoperatively. Histomorphometric study of the TMJ was performed in a synchronous manner with an age-matched sham-operated control group. The serum levels of estrogen, calcitonin, and C-terminus parathyroid hormone were also determined. RESULTS In the sham-operated control group, the serum levels of estrogen and calcitonin increased with age. An increase of the bone volume, with a concomitant increase of the osteoid surface, was observed at 12 weeks. Thickness of the articular soft tissue was decreased with increasing age. In the ovariectomized animals, serum estrogen was not detected during the experiment. A biphasic change in the parathyroid hormone level, with decreases at 1 and 2 weeks after the ovariectomy and increases at 4 and 8 weeks postoperatively, was observed, whereas a constant value was noted in the calcitonin level. Thickness of the articular soft tissue was increased in the anterior and central portions of the condyle at 1, 2, and 4 weeks after the ovariectomy, whereas no appreciable changes were observed in the posterior portion. The bone volume was decreased during the experiment, particularly in the posterior portion. An osteophyte in the anterior region was also observed 8 weeks postoperatively. CONCLUSIONS Estrogen deficiency in rats during puberty predisposes to alterations of the TMJ through changes in serum calcitonin and parathyroid hormone levels.

Different protein kinase C isozymes could modulate bradykinin-induced extracellular calcium-dependent and -independent increases in osteoblast-like MC3T3-E1 cells

Effects of protein kinase C (PKC) on bradykinin (BK)-induced intracellular calcium mobilization, consisting of rapid Ca2+ release from internal stores and a subsequent sustained Ca2+ inflow, were examined in Fura-2-loaded osteoblast-like MC3T3-E1 cells. The sustained Ca2+ inflow as inferred with Mn2+ quench method was blocked by Ni2+ and a receptor-operated Ca2+ channel blocker SK&F 96365, but not by nifedipine. The short-term pretreatment with phorbol 12-myristate 13-acetate (PMA), inhibited BK-stimulated Ca2+ inflow, and the prior treatment with PKC inhibitors, H-7 or staurosporine, enhanced the initial internal release and reversed the PMA effect. Moreover, 6 h pretreatment with PMA caused similar effect on the BK-induced inflow to that obtained with PKC inhibitors, whereas 24 h pretreatment was necessary to affect the internal release. On the other hand, the translocation and down-regulation of PKC isozymes were examined after PMA treatment of MC3T3-E1 cells by immunoblot analyses of PKCs with the isozyme-specific antibodies. 6 h treatment with PMA induced down-regulation of PKC beta, whereas longer treatment was needed for down-regulation of PKC alpha. Taken together, it was suggested that the BK-induced initial Ca2+ peak and the sustained Ca2+ inflow through the activation of a receptor-operated Ca2+ channel, are differentially regulated by PKC isozymes alpha and beta, respectively, in osteoblast-like MC3T3-E1 cells.

Kabuki make-up syndrome (Niikawa-Kuroki syndrome) with cleft lip and palate

Kabuki make-up syndrome (Niikawa-Kuroki syndrome), recognized in Japan in 1981, is characterized by mental and growth retardation with specific craniofacial malformation such as lower palpebral eversion and depressed nasal tip. In this paper we describe a case associated with cleft lip and palate. Attention should be paid by maxillofacial surgeons to this syndrome, since 41% of the cases have been associated with cleft lip and palate (Niikawa et al., 1988; Tonoki and Niikawa, 1988).

Histomorphometric study of trabecular bone remodeling during condylar process fracture healing in the growing period: Experimental study

Trabecular bone remodeling during condylar fracture healing in the growing period was analyzed by histomorphometry with a synchronous system. Data from the study showed displacement of the fractured condyle was compensated by the changes in remodeling ascribed to the pubertal spurt of growth, and that such remodeling still continued even after clinical healing. The regional acceleratory phenomenon, evolved to potentiate tissue healing, was observed 1 week after induction of the fracture. Mesenchymal cells were presumably modulated into chondroblasts that promoted endochondral ossification. It was concluded that trabecular bone remodeling plays an important role in healing of condylar fractures during the growth period.

Chondroma of the tongue. Report of a case.

A case of chondroma which occurred in the midline of the dorsum of the tongue in a 40-year-old Japanese male is reported together with a review of the literature. Histological investigation revealed that this lingual chondroma had the characteristics of hyaline cartilage. We regard the metaplastic transformation theory as the best explanation of histogenesis of lingual chondroma at the lateral margin, while cartilaginous rests are the origin of lingual chondroma on the dorsum of the tongue.

Myeloperoxidase deficiency as a predisposing factor for deep mucocutaneous candidiasis: A case report

Abstract Myeloperoxidase deficiency (MPD) is an immunosuppressive condition; the bactericidal ability of neutrophils is reduced in spite of their normal phagocytic activity. 1,2 Susceptibility to candidal and staphylococcal infection has been the chief problem resulting from MPD. 1 Candidiasis is not a rare condition in the oral cavity. Deep candidiasis, however, is uncommon compared with the superficial form, and seldom is seen in the oral cavity. 3 The following report describes a case of alveolar pyogenic granuloma in the right maxillary anterior region accompanied by an external fistula to the infraorbital area, which was caused by infection with Candida albicans in a patient with MPD.

Factor XIIIa-containing cells and fibrosis in oral and maxillofacial lesions: an immunohistochemical study.

The distribution of subunit A of blood coagulation factor XIII (FXIIIa) was investigated by the avidin-biotin-peroxidase complex (ABC) method in various oral and maxillofacial tissues. These tissues were from normal tongue, gingiva, lip, and submandibular gland, and from Dilantin gingival hyperplasia (one case), pyogenic granuloma (three cases), peripheral fibroma (four cases), squamous cell carcinoma (seven cases), chronic sclerosing submandibular adenitis (two cases), and fibrous dysplasia of the mandibular bone (one case). The distribution of collagenous components was examined in the same tissues by means of the Sirius red F3BA method. By means of the ABC method, FXIIIa was detected in the cytoplasm of certain connective tissue cells in each of the tissues examined. These FXIIIa-containing cells were sparse in the normal tissues but evidently abundant in the fibrous connective tissue of inflammatory and neoplastic lesions. In the present study, the close relationship between the distribution of FXIIIa-containing cells and that of collagenous components is demonstrated. The role that FXIIIa-containing cells play in the process of fibrosis is discussed.

Characterization of cells containing factor XIII subunit a in benign and malignant buccal lesions

SummaryIn the present study, the distribution pattern and characteristics of cells containing Factor XIII subunit a (FXIII A) have been studied in benign and malignant lesions of human buccal mucosa. Tissues from four irritation fibromas and three squamous cell carcinomas were studied by means of double immunofluorescent staining techniques in which the detection of FXIII A was combined with a reaction with CD14 (recognizing a monocyte/macrophage differentiation marker antigen), Mac 387 (reacting with a special subset of macrophages), anti-HLA-DR, Ki-M7 (labelling phagocytosing macrophages) or Ki-67 (visualizing a nuclear antigen associated with cell proliferation) monoclonal antibodies. FXIII A was detected in cells of the connective tissue stroma in both benign and malignant buccal lesions. The number of these FXIII A-reactive cells (FXIII A+ cells) increased considerably in the tumour tissues, in particular in those surrounding tumour cell clusters. FXIII A+ cells scattered in the fibromatous tissues were spindle-shaped, whereas in the tumour stroma, large stellate cells predominated, and round cells were likewise labelled around blood vessels. FXIII A+ cells were labelled with CD14 and Ki-M7 in both fibromatous and tumoural buccal mucosa; however, they failed to show any reaction with Ki-67. FXIII A+ cells accumulated in the tumour stroma reacted for HLA-DR as well. These results indicate that in both the benign and malignant buccal lesions FXIII A is contained in a subpopulation of tissue macrophages, which represents a monocyte-derived (CD14+) and phagocytosing (KiM7+) cell population. The accumulation of the FXIII A+ cells in the tumour stroma is believed to be a result of direct migration from the circulating blood. The FXIII A+ cells of the tumour stroma may be actively involved in both antigen presentation and matrix remodelling during tumour progression.

The platysma myocutaneous flap for oral reconstruction: Experience with MacFee's cervical incision

The present study was performed to demonstrate and evaluate the effectiveness of the Platysma Myocutaneous Flap in conjunction with MacFees cervical incision (MacFee, 1960) for reconstruction after oral cancer excision. Ten squamous cell carcinoma cases were provided for postoperative evaluation of tongue movement and aesthetic problems of the cervical skin. It was found that the thickness of the skin island was adequate for covering the oral defects and was not a hindrance to proper postoperative function. MacFees incision improved the condition of the scar caused by flap elevation. The procedure for preparing the muscle pedicle beneath the cervical skin tunnel was carried out without much difficulty by carefully preparing the surgical field.

Accumulation of cells containing factor XIII subunit a around the foci of intense fibrosis in human epulides.

SummaryOn the basis of clinical and biochemical findings, Factor XIII subunit a (FXIII A) has been conjectured to play an important role in fibrotic processes. Epulis samples at different stages of fibrotic tissue formation were used as a model system for studying the localization and tissue distribution of FXIII A during the course of connective tissue generation. Marker characteristics of cells containing FXIII A (FXIII A+ cells) were determined as well. In double immunofluorescent labelling systems, FXIII A was localized in monocyte-derived (CD-14+), activated (HLA-DR+), and phagocytosing (Ki-M7+) tissue macrophages, which are widely distributed homogeneously in granulation tissues, but start to accumulate around foci of fibrosis as soon as the foci appear. During the relatively long process of fibrosis, FXIII A+ macrophages continuously decrease in number, and their morphological appearance changes from stellate to spindle-shaped. The nuclei of these cells were not labelled by Ki-67 monoclonal antibody; this indicating that they represent a non-proliferating cell population in the connective tissue stroma. The present findings may help to link theories concerning the role of FXIII A and those of macrophages in the connective tissue formation so far found separately in the literature.