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PubMed1995

Localization of the Ca(2+)-binding alpha-parvalbumin and its mRNA in epiphyseal plate cartilage and bone of growing rats.

This study describes the localization of alpha-parvalbumin, in undecalcified tibial epiphyseal cartilage and bone of growing rats by immunocytochemistry in the light microscope, and of parvalbumin mRNA by in situ hybridization. They were compared to the distribution of the calbindin-D9K and its mRNA in rat epiphyseal cartilage. All the chondrocytes of the epiphyseal cartilage were parvalbumin-immunopositive, but there was no parvalbumin immunoreactivity in the uncalcified or calcified extracellular cartilage matrix. The intensity of the immunostaining increased from the resting and proliferative to the mature and hypertrophic chondrocytes, with the greatest intensity in the terminal hypertrophic chondrocytes in the calcifying zone. The parvalbumin immunostaining was located in the cytoplasm, but no immunoreactivity was detected in any chondrocyte processes. The parvalbumin mRNA distribution and levels, as revealed by in situ hybridization, exactly mirrored those of the parvalbumin protein. In contrast to parvalbumin, calbindin-D9K and its mRNA appeared in mature chondrocytes and decreased in hypertrophic up to calcifying chondrocytes. Calbindin-D9K was located in the cytoplasm and all along the cell processes. In bone, the osteoblasts and the osteocytes of trabecular and compact cortical bones were immunoreactive for parvalbumin and contained parvalbumin mRNA. Parvalbumin lay in their cytoplasm, but there was no parvalbumin immunostaining in the extracellular uncalcified or mineralized bone matrix. The long processes of osteocytes, in compact bone only, were parvalbumin immunoreactive. Osteoclasts contained cytoplasmic parvalbumin immunoreactivity. Thus, the pattern of immunoreactive parvalbumin distribution indicates that the protein is not involved in the extracellular mineralization of cartilage and bone matrix. It appears to be associated with specific calcium-related intracellular functions in chondrocytes and in osteoblasts, osteocytes, and osteoclasts. As the highest cytoplasmic concentration of parvalbumin is in the terminal hypertrophic chondrocytes, parvalbumin could act as a calcium buffer to delay the death of chondrocytes. In compact bone, parvalbumin could also have a role throughout the osteocyte processes in regulating the fluxes of calcium ions for mineral homeostatis.

Animals↗
PubMed1988

Morphologic and growth alterations of epiphyseal plate after isohistogeneic transfer of young rat limb to adult rat.

The hind limbs of young rats were transferred to adult rats to clarify the morphologic and growth changes of a young epiphyseal plate in an adult hormonal environment. The transplanted femur and tibia achieved about 70 percent of normal growth in length, or significantly less than normal control (p less than 0.001). Histologically, the thickness of the epiphyseal plate in the transplanted bone was significantly thinner than that of normal control (p less than 0.001), and earlier epiphyseal union was also noted. Hormonal alterations during adolescence are believed to have a marked effect on these findings. However, the circumferential growth of the femur and tibia was greatly affected by the loss of biomechanical stress, precluding an evaluation of the influence exerted by hormonal alterations.

Aging↗
PubMed1992

[Epiphyseal dysplasia of the hip joint, its diagnosis and differential diagnosis with MRT].

Sixteen hip joints of eight patients with multiple epiphyseal dysplasia were examined by clinical investigation, plain films and by magnetic resonance imaging (MRI), using T1- and T2-weighted images and gradient echoes. MRI is useful in demonstrating the congruity of the joint, in the changes of the epiphyseal signal intensities and the epiphyseal line. Individual changes of the signal intensity patterns on T1- and T2-weighted scans are described. Although MRI exhibits a variety of patterns in different patients, a clearcut differentiation from Legg-Calvé-Perthes' disease is possible.

Adolescent↗
PubMedDate not supplied

[Etiology and pathogenesis of epiphyseal necrosis in childhood as exemplified with the hip].

In many cases the etiology of juvenile necrosis of the femoral head has not been unequivocally explained. Essentially, however, it is due to reduced arterial blood flow, although venous congestion also has to be considered. Epiphyseal necrosis is frequently a result of known underlying diseases. These include, for example, both specific and nonspecific forms of coxitis and rheumatic coxitis, hormonal dysfunctions, metabolic disorders such as mucopolysaccharidosis, blood diseases (e.g. hemophilia, sickle cell anemia), leukosis, and tumors and necrosis following cortisone and cytostatic therapy. The following four factors may directly or indirectly cause arterial vascular damage and thus necrosis: 1) primarily exogenous and 2) primarily endogenous factors, 3) genetic, and 4) skeletal maturation factors. These etiological factors are described in detail and discussed. Epiphyseal deformation occurs in a strict sequence of five phases, which are described. It should be emphasized that while necrotic bone tissue is being gradually resorbed, deposits of new bone matrix are already accumulating on dead trabecula and will subsequently form new bone fibre. In other word, a gradual substitution takes place. Two important clinical facts derive from this. First, epiphyseal crash is not due to the load of the body's weight. Since active resorption takes place, there is no justification for weight-relieving therapy in the basic therapeutic concept for Perthes' disease. Second, in light of our studies, surgical containment therapy appears to be the most suitable form of treatment if performed at the right time, i.e. in the golden period of remodelling, depending on the patient's age, the extent of necrosis and the degree of dislocation. Where stringent criteria are fulfilled we perform a three-dimensional intertrochanteric osteotomy, i.e. an extension-derotation reduction osteotomy.

Child↗
PubMedDate not supplied

[Morphometric measurements in the area of the epiphyseal groove of the parietal vertebra in experimentally-induced scoliosis in rabbits].

In 3 rabbits we provoked a short-curved dorsolumbal scoliosis by costo-lumbal cerclage. In order to quantify with morphometric methods the morphologically by various authors described effect of pressure parallel to the axis of epiphyseal growth under Hueter-Volkmann's law, we measured the height and area of different parts of the epiphyseal plate in frontal semi-thin sections (Alcian-blue) by means of a pictoral analysis system based on a mini-computer. On the concave side, the side of increased pressure, we found a relative atrophy of the epiphyseal plate of 40% and a diminished area of 49%.

Animals↗
PubMed1956

Electron microscopy of cartilage and bone matrix at the distal epiphyseal line of the femur in the newborn infant.

An examination of the fine structure of cartilage and bone matrix at the distal epiphyseal line of the femur of a newborn infant has revealed the following information. Cartilage matrix is composed of a network of widely spaced fibers without obvious periodic banding. Calcification is first seen about the level of the third chondrocyte capsule distal to the furthest penetration of the capillaries. It starts as a haphazard deposition of crystals which have no obvious relationship to the location of the fibers. The process of calcification is completed before ossification commences but the central zone of matrix remains only partly mineralized. Bone matrix is formed over a bar of calcified cartilage. Fibers, recognizable as collagen, are deposited in a loose network in a narrow zone between the osteoblasts and cartilage. These fibers are 2 to 5 times as wide as the fibers in epiphyseal cartilage. Calcification then begins in the osteoid, crystals being first laid down irregularly on or close to the fibers. As they increase in number, the crystals tend to line up along the fibers and eventually are arranged so that the periodicity of the underlying collagen is emphasized. In such an area the fibers are more tightly packed than when uncalcified. There is no change observed in the calcified cartilage at this level. The extracellular matrices of this epiphyseal cartilage and bone can be distinguished from one another in the electron microscope.

Bone Matrix↗
PubMed1987

Role of epiphyseal cartilage in endochondral bone formation.

The avian epiphyseal growth plate plays an important role in skeletal development. Compared with the mammalian species, the avian growth plate contains more cells, is less well organized and appears more susceptible to malformation. Abnormal cartilage development is associated with chondrodystrophy, tibial dyschondroplasia and rickets. Many nutrient deficiencies result in chondrodystrophy, which is characterized by shortened, thickened bones and a narrowing of the epiphyseal growth plate. Manganese, the most extensively studied of these deficiencies, is necessary for proteoglycan biosynthesis. Tibial dyschondroplasia is a condition in which the prehypertrophic cells fail to hypertrophy and vascularization is aborted. This abnormality is found in genetically predisposed animals and its occurrence is altered by subtle changes in calcium, phosphorus and electrolyte content of the diet. Calcium and vitamin D deficiencies cause rickets, which is characterized by an increase in the width of the prehypertrophic zone of the epiphyseal growth plate. Most of the biochemical and histological changes can be related to the need for calcium for chondrocyte hypertrophy and maturation, although there is some evidence that chondrocytes require specific vitamin D metabolites. Phosphorus deficiency increases the zones of hypertrophy and metaphyseal primary spongiosa.

Animal Nutritional Physiological Phenomena↗
PubMed1996

PTH/PTHrP receptor mRNA is down-regulated in epiphyseal cartilage growth plate of uraemic rats.

PTH/PTHrP receptor mRNA is down-regulated in epiphyseal cartilage growth plate of uraemic rats. Growth retardation, hypocalcaemia, hyperphosphataemia, and skeletal resistance to the action of PTH are well known features of advanced chronic renal failure (CRF). It has been suggested that the downregulation of renal and skeletal PTH receptors (PTH/PTHrP-R) could play an important role in the occurrence of these abnormalities. In the present study, four uraemic (4 weeks after 5/6 nephrectomy) and four control (sham-operated) rats were analysed for PTH/PTHrP-R mRNA expression at the proximal femoral and tibial growth plates by in situ hybridization. Uraemic rats had plasma biochemical abnormalities of advanced CRF including high creatinine, phosphate, and PTH, and low calcium and calcitriol levels. The femoral and tibial bones of uraemic animals were shorter in length than those of control rats, and had reduced width and cellularity of the epiphyseal cartilage growth plate. Mean (+/- SD) tibia growth plate width was 152 +/- 30 microns in uraemic rats, compared with 170 +/- 35 microns in control rats. The difference was mostly due to a marked reduction of the zone expressing PTH/PTHrP-R (mature chondrocytes) which was 30 +/- 5 microns in tibias from uraemic versus 44 +/- 10 microns in tibias from control rats. The hybridization signals of PTH/PTHrP-R per individual cell were quantified on dark field images using a computer-assisted image analysis system. The number of grains in PTH/PTHrP-R positive cells was also decreased in uraemic rats, 103 +/- 13 compared with 123 +/- 14 arbitrary units (dark pixel density)/cell in control rats (P < 0.005). In conclusion, these data indicate that rats with severe CRF and secondary hyperparathyroidism have reduced epiphyseal cartilage PTH/PTHrP-R mRNA expression. This alteration may be relevant in the pathogenesis of growth retardation in uraemia.

Animals↗
PubMed2000

Epiphyseal plate involvement in osteosarcoma.

Fourteen boys (56%) and 11 girls (44%) 4 to 17 years of age (mean, 12.2 years) who had osteosarcoma and open epiphyseal plates were studied. A possible correlation between transepiphyseal spread of osteosarcoma and radiologic and histopathologic findings was investigated. Epiphyseal plate invasion was detected radiologically in only 11 patients (44%), whereas histopathologic examination showed transepiphyseal extension in 21 patients (84%). The authors conclude that the epiphyseal plate is not a barrier against tumor growth and strongly recommend that limb salvage surgery preserving the epiphysis be planned carefully.

Adolescent↗
PubMedDate not supplied

Micromechanical properties of epiphyseal trabecular bone and primary spongiosa around the physis: an in situ nanoindentation study.

The elastic modulus and hardness of the mineralized bone around the growth plate was measured to determine its regional micromechanical properties. Multiple nanoindentation tests, >10 sessions, with depths ranging from 100 to 1,000 nm at loading rates of 12.5 and 750 microN/s, were performed on the trabecular bone in the epiphysis, trabecular bone at the junction of the physis and epiphysis, primary spongiosa in the metaphysis, and surrounding cortical bone of the distal femur of 300-gm Sprague-Dawley rats. The indentation load-displacement data obtained in these tests were analyzed to determine the elastic modulus and hardness of the tissues. The nanoindentation results highlighted the regional variations in the material properties of the mineralized tissues around the growth plate. The primary spongiosa had a lower elastic modulus and hardness than both epiphyseal trabecular and cortical bone (p < 0.01). A relatively well-defined thick trabecular band at the physeal-epiphyseal junction had modulus and hardness values comparable to those of cortical bone (p > 0.05). These findings support the hypothesis that the primary spongiosa has micromechanical properties that are significantly lower than the epiphyseal trabecular bone. On this basis, it is speculated that the fracture patterns commonly seen in patients with physeal injuries are influenced by the micromechanical properties of these tissues, as well as by the nature and direction of the applied force.

Analysis of Variance↗
PubMed2000

Distal tibial and fibular epiphyseal fractures in children: prognostic criteria and long-term results in 158 patients.

From 1974 to 1993, 158 injuries of the ankle joint were treated at the Department of Orthopedics and Traumatology of Santobono Children's Hospital. One hundred thirty-two patients were treated conservatively; 26 patients underwent surgical treatment. Fibular fractures of the malleolus without epiphyseal separation or dislocation (68 patients) were excluded from this review. Of the 158 patients, 113 (70%) were available for follow-up. The mean age of patients was 11 years. The mean follow-up was 6 years (range 3-15 years). In this review, the authors compare, based on the degree of epiphyseal separation or dislocation, the Carothers-Crenshaw classification, which is based on the mechanism of trauma, with the Salter-Harris classification, which is based on anatomical-radiographic criteria. The aim is to review the authors' patients based on these classifications, to verify the prognostic ability of these criteria and thus to establish a better and more viable treatment for these injuries. Therefore, two fundamental factors should be considered for the prognosis: the mechanism of trauma and damage to the epiphyseal plate. Compressive trauma and adduction-supination trauma are the most dangerous types of injury, and any damage or gap in the physis should be perfectly reduced, by open means if necessary, to prevent a bone bridge from forming.

Ankle Injuries↗
PubMed1981

Bilateral femoral head collapse in an adolescent with brachydactyly (multiple epiphyseal dysplasia tarda type 1c).

Children with femoral head radiographic changes suggestive of bilateral avascular necrosis require a careful differential diagnosis. Although the child may be found to have an epiphyseal dysplasia, the course may not be benign. At adolescence, in certain of the multiple epiphyseal dysplasia tarda forms, rapid destruction of the femoral head occurs with clinical and radiographic features indistinguishable from avascular necrosis. A possible interrelationship between epiphyseal dysplasia and avascular necrosis is considered.

Adolescent↗
PubMed1981

The longitudinal epiphyseal bracket: implications for surgical correction.

Surgical approaches to the correction of deformities in the skeletally immature hand or foot require adequate comprehension of the specific and changing chondro-osseous anatomy of each lesion. Detailed macroscopic and microscopic examination of an abnormal metatarsal showed a trapezoid-shaped diaphyseal/metaphyseal osseous unit that was longitudinally bracketed by a functioning physis and epiphysis along the lateral side. Only the medial side of the diaphysis had a normal periosteum. The arcuate physis extended from the medial, proximal side toward and along the lateral side and then back to the medial side distally. The epiphyseal ossification center was a composite of initially separate proximal and distal secondary centers that had a extended toward each other within the laterally placed epiphyseal cartilage. We have termed this deformity a "longitudinal epiphyseal bracket." We suggest that in the skeletally immature patient, opening wedge chondro-osteotomy should not routinely be accompanied by interposed bone graft extending to either the split ossification center or the physeal cartilage. Such a procedure may induce a partial surgical epiphyseodesis with subsequent progressive recurrence of the angular deformity or cessation of longitudinal growth. Instead, based on our anatomical findings, and preliminary surgical cases, we recommend osteotomy accompanied by fat interposition comparable to the Langenskiöld procedure for traumatic epiphyseodesis.

Bone Diseases, Developmental↗
PubMedDate not supplied

Biodegradation of polydioxanone in bone tissue: effect on the epiphyseal plate in immature rabbits.

Implants of polydioxanone (PDS), 1.3 mm in diameter, were operatively fixed in the juxta-epiphyseal area of the right proximal tibial metaphysis in six rabbits and were driven into a drill hole of equal bore through the right proximal tibial epiphyseal plate in ten rabbits. The PDS implants had biodegraded almost completely in cortical bone at 16 weeks without any significant sign of inflammation or foreign body reaction. The PDS implants did not cause any growth disturbance. Histologic studies, however, showed that seven of 10 rabbits demonstrated significant osseous bridge formation across the epiphyseal plate.

Animals↗
PubMed1989

Distribution of protein disulfide isomerase in rat epiphyseal chondrocytes.

We investigated the intracellular distribution of protein disulfide isomerase (PDI) in rat epiphyseal chondrocytes by immunocytochemistry, using a post-embedding protein A-gold technique. Gold particles were localized primarily in the cisternal space of the rough endoplasmic reticulum (ER) and nuclear envelopes. The ER cisternae of the chondrocytes in all the differentiating epiphyseal zones--resting, proliferative, pre-hypertrophic, and hypertrophic--were equally and highly labeled. The labeling density of the cisternal space of the dilated ER, probably reflecting marked accumulation of secretory proteins such as procollagen, was always higher than that of the non-dilated ER. In the dilated cisternal space, gold particles were freely and evenly distributed, without preferential binding to the luminal surface of the ER membranes. We suggest that PDI catalyzes the formation of disulfide bonds of various secretory proteins, perhaps type II procollagen, in the cisternal space of the ER in epiphyseal chondrocytes. The exclusive localization of gold particles in the cisternal space of the ER and nuclear envelopes and the lack of gold particles in the Golgi apparatus, including cis-Golgi cisternae, indicate that PDI is an ER-soluble protein in the chondrocytes and is presumably sorted out in some pre-Golgi compartment and not transported to the Golgi apparatus.

Aging↗
PubMed1985

Morphologic and metabolic development of human fetal epiphyseal chondrocytes in primary culture.

Primary chondrocyte culture was carried out after enzymatic digestion of femoral and tibial epiphyseal cartilage of human fetuses, collected with informed parental consent within 12 h postmortem. Chondrocytes were cultured in HAM F-12 medium with penicillin and 15% serum. Three types of serum were used: human placental cord serum (HPS), fetal calf serum, and human male adult serum. Chondrocytes cultured with HPS grew as monolayers, formed abundant colony groups with a highly metachromatic pericellular matrix, and floating round cells were observed in the culture medium. By the 10th day of culture the great majority of proteoglycans present in the culture medium were found as aggregates. Chondrocytes cultured with fetal calf serum or human male adult serum grew as monolayers, were polygonal in shape, and the pericellular matrix was far less developed than in HPS cultures. By the confluent phase of growth, only approximately a third of the proteoglycans present in the culture medium were found as aggregates. Chondrocytes cultured with HPS proliferated significantly more rapidly than those cultured with fetal calf serum or human male adult serum. The results suggest that certain, as yet unidentified, factors are present in sufficient amount in HPS to allow chondrocytes in culture to retain phenotypic morphological and biochemical characteristics. HPS also facilitates growth of human fetal epiphyseal chondrocytes in culture. Primary human fetal epiphyseal chondrocyte culture could be a suitable experimental tool for the in vitro study of biochemical characteristics of cartilage and factors involved in fetal cartilage metabolism.

Blood↗
PubMed1992

Morphological changes of epiphyseal plate in the long bone of chondrodysplastic dwarfism in Japanese brown cattle.

A total of 20 cases of disproportionate calves on Japanese Brown cattle were examined morphologically. Investigation of 5 affected calves revealed that the insufficiency of endochondral ossification was confined only to the long bones of the limbs and was not accompanied by other associated changes. On the basis of the histological changes of epiphyseal plate and the affected site, this condition may be called chondrodysplasia of the rhizomelic type. Therefore, this disorder was defined as a bovine dwarfism. From three dimensional image analysis and histological changes of the tibial proximal portion in the other 15 cases, deformity and shortness of the tibia were related to the state of distribution and the degree of damages of the epiphyseal plate. In the affected cartilage matrix, cystoid degeneration, fibrous striation, bone spicule, necrotic foci and rent were found. Inadequate metachromasia suggests the abnormal staining of sulfated glycosaminoglycans and alcian blue stainability may be attributable to the abnormal interactions between proteoglycan and other matrix components. At the interface of cartilage and bone, irregular calcification, fibrotic scar and sealing by osseous tissue with relation to vascularity were found. These changes in this study indicated the failure of modeling on the epiphyseal plate, showing disturbance of chondrocytic differentiation and abnormal formation of the matrix.

Animals↗
PubMed1999

Immunohistochemical observations on the initial disorders of the epiphyseal growth plate in rats induced by high dose of vitamin A.

The initial disorders of the epiphyseal growth plate cartilage were immunohistochemically examined in the proximal tibia of rats administered a high dose of vitamin A. Male Wistar rats were given 100,000 IU/100 g body weight/day of vitamin A for administration periods of 1 to 5 days (Day 1 to 5) from 4 weeks after birth or were given deionized water and used as control. They were sacrificed after 5-bromo-2'-deoxyuridine (BrdU) injection on Day 1 to Day 5 to remove the tibiae. The tibiae were processed for immunohistochemical examinations using antibodies against type I, II, X collagens and BrdU. BrdU-incorporated chondrocytes and type X collagen-negative area were reduced since Day 2 and type X collagen-positive area was reduced since Day 4. The cartilage matrix partially lost type II collagen and deposited type I collagen in the epiphyseal growth plate near the periosteum on Day 5. These findings suggest that a high dose of vitamin A initially disturbed the differentiation from resting to proliferating chondrocytes, subsequently inhibited the differentiation from proliferating to hypertrophic chondrocytes, caused the chondrocytes to deviate from the process of normal differentiation, and finally resulted in the deformation of the epiphyseal growth plate.

Animals↗