Rat Mandibular Condyle Research Articles

Influence of food consistency and dental extractions on the rat mandibular condyle: a morphological, histological and immunohistochemical study

The purpose of this study was to investigate the relationship between food consistency and the growth of the mandibular condyle in rats. Secondly, the effect of dental extractions on cartilage of the mandibular condyle was examined in young adult rats fed foods of varying consistency. Thirty-six male Wistar rats were divided into four groups: (A) Solid diet--non-Extraction (non-Ext.) group; (B) Solid diet--Extraction (Ext.) group; (C) Powder diet--non-Ext. group; and (D) Powder diet--Ext. group. Extractions were performed at 12 weeks of age. The mandibular condyles were removed at 1, 4, and 8 weeks after the extractions. The shape of the mandibular condyles in the powder diet groups (C and D) was significantly narrower. In the Ext. groups (B and D), the thickness of the hypertrophic zone was reduced one week after the extractions. In the powder diet groups (C and D), the intensity of the staining of fibronectin decreased in the proliferative zone regardless of the extractions. In group B, a decreased intensity of this reaction was observed one week after the extractions. From these results, it appeared that food consistency and/or dental extractions affected the morphology of the mandibular condyle and the histological characteristics of the mandibular condylar cartilage.

Endochondral ossification in the rat mandibular condyle and changes in intramedullary blood vessels with growth

Endochondral ossification in the rat mandibular condyle and changes in intramedullary blood vessels with growth

Age-related histological changes in rat mandibular condyle

The effect of aging on rat mandibular condyle was histologically assessed using 1-, 4-, 9-, and 16-month-old male Fischer rats (Eight rats of each group). The medial and anterior portions of the condyle protruded with age. The hypertrophic cell layer of the condylar cartilage occurring up to 4 months was no longer observable at 9 months, after which calcification of the cartilage layer with a tidemark was featured. The chondrocytes in the calcified cartilage layer were reduced in size and intensely stained by toluidine blue. A mineralizing front was formed parallel to, and migrated toward, the condyle surface. At 9 months, osteon-like osteogenesis occurred around blood vessels on the border between the calcified cartilage and the subchondral bone. Condyles of 16-month-old rats exhibited osteosclerotic changes. The calcified cartilage of the middle portion of the condyle formed a remarkably thick layer. The increased volume of the trabecular bone appears to lead to enhanced osteosclerotic changes of the condyle. The aging-related protrusion of the anterior and medial portions of the condyle could be the result of a combination of mechanical forces, e.g., occlusion and mastication. Further, our study revealed that the turnover from cartilage to bone occurring in rat condyle through the process of aging involved an osteon-like bone formation around the blood vessels on the border between the calcified cartilage layer and the bone. This process differs from the endochondral ossification process observed in younger rats.

ラット下顎頭の軟骨細胞・骨芽細胞におけるコラーゲン合成能の日内変動

ラット下顎頭の軟骨細胞・骨芽細胞におけるコラーゲン合成能の日内変動

Three-Dimensional Ultrastructural Study on Age-Related Alteration of Articular Surface in the Rat Mandibular Condyle

Three-Dimensional Ultrastructural Study on Age-Related Alteration of Articular Surface in the Rat Mandibular Condyle

A comparative ultrastructural study of the mitotic chondrogenic cells in the mandibular condyle and tibial growth plate of the rat

Mitotic cells in the rat mandibular condyle (proliferative mandibular cells) were compared with mitotic cells in the rat tibial growth plate (proliferative tibial cells). In the tibial proliferative cells, the rough endoplasmic reticulum mostly became vacuolated during the latter stage of mitosis, whereas the rough endoplasmic reticulum of the proliferative mandibular cells rarely underwent disorganization. Further, a wide area remained outside of the mitotic spindle in the proliferative tibial cells at the metaphase, while only a narrow area remained in the proliferative mandibular cells. This finding might account for the difference of disorganization of the rough endoplasmic reticulum.

An ultrastructural study of the mitotic preosteoblasts in the primary spongiosa of the rat mandibular condyle

In this study, we observed mitotic preosteoblasts that have the structural features of osteoblasts in the primary spongiosa of the rat mandibular condyle. The rough endoplasmic reticulum and the Golgi apparatus showed remarkable disorganization during mitosis. The Golgi saccules were replaced by groups of large vacuoles and small vesicles. The cisternae of the rough endoplasmic reticulum also were vacuolized. Since this disorganization occurred in conjunction with the formation of the mitotic spindle, it is probably related to the changes of the microtubular cytoskeleton. Further, secretory granules were arrayed along the mitotic spindle microtubules at the metaphase, and concentrated around the midbody at the telophase. These findings indicate a close relationship exists between secretory granules and microtubules.

Ultrastructural alteration of cartilaginous fibril arrangement in the rat mandibular condyle as revealed by high-resolution scanning electron microscopy.

Three-dimensional alteration of fibrillar matrix in the rat mandibular condylar cartilage was investigated with a high-resolution scanning electron microscope (SEM) and it was determined whether alterations correlate with developing occlusion and advancing age. Two important SEM techniques of DMSO freeze-cracking and treatment with trypsin and hyaluronidase were employed to remove interfibrillar proteoglycans and disclose fibril arrangement. Our SEM investigation demonstrated that collagen fibrils in the fibrous zone covering hyaline-cartilaginous area in the condyle are thicker (50 to 80 nm in diameter) than the fibrils (30 to 50 nm in diameter) that predominantly constituted an interterritorial fibrillar matrix (IFM) in the area. While the thick fibrils had a distinct striation of about 55 nm periodicity, the thin fibrils had no distinguishable striation. The thick fibrils having a periodic striation of about 60 nm was found along with the thin fibrils, also in the IFM in the aged rats and in the deep IFM, but were considerably less than the thin fibrils. The fibrils in the fibrous zone and IFM were disorderly arranged at 19-day-insemination age. In 1-week-old rats whose incisors erupted, the fibrils constituting the fibrous zone altered from disordered to ordered arrangement. The IFM in these rats took the form of a network. Incorporation of small fibrillar bundles into the fibrillar network was seen in 2-week-old rats whose upper and lower first molars erupted. In 8-week-old rats whose molars had erupted completely, the IFM completely occupied by regularly oriented fibrils appeared additionally.(ABSTRACT TRUNCATED AT 250 WORDS)

In vivo effects of tunicamycin on chondrocytes of rat mandibular condyles as revealed by lectin cytochemistry.

The in vivo effects of tunicamycin on the glycosylation of proteoglycans and link protein in rat mandibular condylar chondrocytes were studied by ultrastructural lectin histochemistry. The binding of wheat-germ agglutinin was shown by using anti-lectin antibody followed by protein A-gold complex. In normal rats, wheat-germ agglutinin labeling was restricted to trans cisternae and vacuoles of the Golgi complex, whereas it was observed in neither the cis region of the Golgi complex nor in the rough endoplasmic reticulum. By 3 h after the drug administration, wheat-germ agglutinin binding sites on the disorganized Golgi vacuoles were dramatically reduced in number. At 6 h after the drug administration, the lectin binding sites on the Golgi vacuoles were restored. These results demonstrate that the in vivo use of tunicamycin in combination with histochemical analysis using lectin probes is of significant value for the study of protein glycosylation in chondrocytes of the rat mandibular condyle.

Bromodeoxyuridine immunohistochemistry for evaluating age-related changes in the rat mandibular condyle decalcified by intravenous infusion.

Age-related changes in cell proliferation kinetics of the mandibular condyle were studied in Sprague-Dawley rats using bromodeoxyuridine (BrdUrd) immunohistochemistry in decalcified, paraffin-embedded tissues. Intraperitoneal injection of 40 mg/kg BrdUrd was given 1 hr before animal sacrifice. Continuous perfusion of EDTA solution via the left ventricle shortened the decalcification time. Immunohistochemical staining was performed with monoclonal anti-BrdUrd antibody. BrdUrd labeled cells, i.e., the S-phase cells, were clearly visible with well-preserved cytological detail. Their nuclei exhibited homogeneously stained granules. The labeling index in the intermediate zone of the condyle decreased with increasing age of the animals. This method is useful for evaluating physiological and pathological changes of the rat mandibular condyle as well as other bones and joints.

Mitotic activity of cells in the fibrous zone of the rat mandibular condyle

To investigate cell renewal in this fibrous zone, Wistar rats at 3 and 6 weeks of age were injected intraperitoneally with colchicine (1 mg/kg) three times, at 10:00, 13:00 and 16:00 h, and mitotic cells were examined after killing the rats at 18:00 h. Colchicine induced a significant increase in the number of arrested meta.phases in the fibrous and the proliferating cell zone. The mitotic rates (per 1000 cells per h) in the fibrous zone at 3 weeks of age were 0.426 for the superficial layer and 0.266 for the deeper layer. These findings suggest that the fibrous zone of young rats grew with the proliferation of the cells within this zone. Age-associated histological changes in the fibrous zone were related to changes in mitotic rates within that zone.

Histological observation of large light cells that seem to be surviving hypertrophic chondrocytes in the rat mandibular condyle

Large light cells (more than 20 μm dia), including some with mitotic figures, appeared to be surviving hypertrophic chondrocytes. Thus at least a few hypertrophic chondrocytes in the rat mandibular condyle may survive, be released into the primary spongiosa, and divide.

Growth potential of the rat mandibular condyle as an isogeneic transplant traversing the interparietal suture

The mandibular condyle of 5-, 10- or 20-day inbred male rats was transplanted across the interparietal suture of male litter-mates and the transverse dimension of the neurocranium was measured from dry skulls at 25 or 35 days. The width of the neurocranium had increased significantly from days 5 or 10 to 25 in the rats with the transplants, whereas the difference from controls was small or non-existent by 35 days. Histological examination showed that the cartilaginous zone was reduced in the transplants at 25 days but that there were still layers of chondrocytes at 35 days. It is suggested that the rat mandibular condyle is endowed with a tissue-separating, interstitial growth potential that, to some extent, is unrelated to mobility, and essentially effected by chondrocyte hypertrophy.

Ultrastructural observation on matrix fibers in the condylar cartilage of the adult rat mandible.

In this study, ultrastructural and immunohistochemical studies were performed on the adult rat (15 weeks old) mandibular condyle, with particular attention to the matrix fibers in the condylar cartilage. The fibrous zone had thick collagen fibrils which formed fibril bundles. These collagen fibrils consisted mainly of Type I collagen. From the proliferative zone to the mature zone, the density of the collagen fibrils became higher. In the hypertrophic zone, thick collagen fibrils were formed around the chondrocytes. Immunohistochemical study indicated that these collagen fibrils consisted mainly of Type I collagen. Therefore, it was confirmed that the hypertrophic chondrocytes in this tissue had one of the osteoblastic phenotypes.

成長期虚弱骨に対する高カルシウム食, カルシトニンの併用療法に関する実験的研究 : 下顎頭の変化

Three-week-old male rats of Wistar strain were given a calcium-free diet for three weeks and the state of bone debility was induced in them. The rats were then given a high-calcium diet and eel calcitonin (ECT) for three weeks and the effect on the mandibular condyle was investigated. The results were as follows : 1. Histopathological findings As compared with the control group, the Ca-free diet group showed marked increase of the cartilage layer due to increase of the hypertrophic zone. Most of the trabecular were in the state of low calcification and were narrow in width and were running disorderly. The Ca-deficient diet + high-Ca diet group, as compared with the Ca-free diet group, had a narrower cartilage layer in the hypertrophic zone and findings of active erosion by chondroclast was observed. Trabeculae were more orderly but their widths were narrower as compared with those of the control group. The Ca-free diet + high-Ca diet + ECT group showed even narrower width of the cartilage layer. Although trabeculae became thicker, they were running irregularly as compared with the control group. 2. Scanning electron microscopic findings Calcospherites were observed on the cartilage lacuna wall in each group, but in the Ca-free diet group, its state of fusion was weakest and longitudinal matrices were ruptured in many parts. The Ca-free diet + high-Ca diet group and Ca-free diet + high-Ca diet + ECT group both showed strong fusion among calcospherites as compared with the Ca-deficient diet group but incomplete fusion as compared with the control group, and ruptures of longitudinal matrices were seen in part. Trabeculae were observed in both resorption sites and bone formation sites in the control group and collagenous fibers were running regularly. In the Ca-free diet group, bone resorption sites increased and many collagenus fibril networks were scattered. In the Ca-deficient diet + high-Ca diet group, bone matrices increased and collagenus fibrils were running regularly. In the Ca-free diet + high-Ca diet + ECT group, many osteocyte lacunae were observed and matrices aroud them were formed by collagenus fibers. On the matrices surfaces collagenous fiber networks were scatterd. Openings of bone canaliculi were observed, and some of them were distinct and the others were indistinct. On the basis of the foregoing findings, combined administration of high-calcium diet and ECT to the rat mandibular condyle showing experimental bone debility proved to accelerate formation of calcified cartilages and also to have an acceleration effect on bone construction in bone growth thereafter.

Regenerating Marrow Induces Systemic Increase in Osteo- and Chondrogenesis

Marrow ablation in long bones induces an increase in osteogenesis in distant skeletal sites. To test the role of marrow regeneration in this phenomenon, rat mandibular condyles were evaluated histomorphometrically during postablation healing of tibial marrow and after inhibition of healing. Ten days after removal of tibial marrow all bone formation parameters in the condylar subchondral bone were markedly elevated, indicating an enhanced osteoblastic activity. The thickness of the cartilaginous zone of calcification was also augmented. These changes were absent when postablation healing was inhibited in the tibia and after massive liver injury. Extensive periosteal injury induced only a slight increase in osteoblast activity. Except for a fall on day 7, the [methyl-3H]thymidine labeling index in the condylar cartilage and oral mucosa remained at control levels 3-18 days after ablation. These findings imply that stimulation of cell proliferation has only a secondary role in the skeletal response to marrow ablation. It is concluded that the systemic increase in osteogenesis occurs preferentially during marrow regeneration and is not a nonspecific skeletal reaction to tissue injury. Apparently, the systemic osteogenic response is mediated by circulating factors produced by the healing marrow; conceptually it is related to other instances where local repair in extraskeletal sites is accompanied by generalized alterations in respective tissues.

The fine structure of the fibrous zone of articular cartilage in the rat mandibular condyle.

The ultrastructure of the articular fibrous zone of the rat mandibular condyle was observed at 3 and 6 weeks of age in order to investigate the histological changes that occur during the establishment of mastication after suckling. We divided the articular fibrous zone into two layers (F1 layer and F2 layer). The F1 layer was composed of fibroblast-like cells, macrophage-like cells, and the matrix which consisted of granular or fibrillar material, loosely arranged small bundles of collagen fibrils with uniform thickness of 30-50 nm, and independent microfibrils. The F1 layer was continuous with the synovial membrane without any distinct boundary in its peripheral area. Mitotic figures could infrequently be observed in the fibroblast-like cells. The cells in the F2 layer closely resembled fibroblasts. The matrix in the F2 layer mostly consisted of densely arranged bundles of collagen fibrils which are not of uniform diameter ranging 40-100 nm. Elastic fibers occurred among the collagen fibrils. The F1 layer which was observed clearly at 3 weeks almost disappeared at 6 weeks of age. It is confirmed that the F1 layer resembling the synovial membrane exists over the condyle up to the weaning period about 3 weeks of age but it degenerates before 6 weeks of age when the masticatory function is established.

Removal of tibial marrow induces increased formation of bone and cartilage in rat mandibular condyle: I. Dab, D. Gazit, A. Massarawa, and J. SelaCalcif. Tissue Int. 1985;35:551–555

Removal of tibial marrow induces increased formation of bone and cartilage in rat mandibular condyle: I. Dab, D. Gazit, A. Massarawa, and J. SelaCalcif. Tissue Int. 1985;35:551–555

The fate of hypertrophic chondrocytes of the rat mandibular condyle in strontium rickets.

In the mandibular condyle of young rats, strontium rickets was induced by a diet in which 2.2% SrCO3 was substituted for calcium salt in a standard diet. The main morphological changes which were characteristic of strontium rickets were a small condyle, an enlarged ramus, an expansion of the hypertrophic cell zone, and the formation of osteoid tissue. By light and electron microscopy, mitotic figures were often observed in the hypertrophic chondrocytes located in the transitional area between the hypertrophic cell zone and osteoid tissue. In addition, the cells within the lacunae in the same area, showed a series of cytological features suggesting a transition of hypertrophic cells to osteoblast-like cells and further to osteocyte-like cells, which were involved in the formation of osteoid tissue. These findings strongly suggest that in strontium rickets the hypertrophic chondrocytes do not degenerate, but can transform into osteogenic cells directly or after mitotic division. In the mandibular condyle of control rats which were given a standard diet containing 1.5% CaCO3, many hypertrophic chondrocytes showed their activity until their lacunae were eroded by the invasion of capillaries. Although the further fate of these surviving chondrocytes has not been confirmed yet, our findings contradict the generally accepted concept that hypertrophic chondrocytes ultimately die during the process of endochondral ossification.

Removal of tibial marrow induces increased formation of bone and cartilage in rat mandibular condyle.

The present paper reports alterations in osteogenesis recorded in mandibular condyles 3-18 days after the removal of marrow tissue from tibial bones. Computerized histomorphometric evaluation of undecalcified condyles revealed a considerable increase in the thickness of condylar cartilage, in particular, the zone of provisional calcification. Measurements of the subcartilaginous trabecular bone suggested an increase in the number of osteoblasts and in their activity. The systemic enhancement of osteogenesis may be initiated by circulating factors released at the affected limb during regeneration of the marrow.