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PubMed2004

[A new custom-made artificial articular cartilage of femoral condyle based on rapid prototyping technique: a case report].

OBJECTIVE: To design and manufacture a new custom-made artificial articular cartilage of femoral condyle based on rapid prototyping technique and explore a method to solve the necroses of allocartilage in hemi joint allotransplantation. METHODS: Design the new custom-made artificial articular cartilage of femoral condyle. The allograft and the patient distal femurs were scanned with Picker 6000 spiral computed tomography (CT) with 1.0 slice thickness and pitch of 1.5, reconstructed the distal femurs in Voxel Q image workstation with volume rendering technique. Then downloaded the transaxial 2D image data to personal computer at 0.1 mm interval and converted it into 2D digitized contour data by using image processing software developed by our team. The 3D wire frame and solid images of femoral condyle could be reconstructed when the 2D digitized contour data were input into image processing software Surfacer 9.0 (Imageware Company, USA). Subsequently based on the clinical experience and the need of design, the 3D contour image of articular cartilage was extracted from the surrounding. Based on the extracted 3D contour image, the computer-aided design (CAD) of the custom-made artificial articular cartilage was accomplished in Surfacer software, converted the CAD model into RP data format. Standard triangularization language, imported into the LPS600 rapid prototyping machine (Hengtong Company, Xi'an Jiaotong University, China), and the resin prototype was achieved. Then the resin model was used as a positive mould to build up a silica gel negative mould, the negative mould was sent to the factory to manufacture Ti-6Al-4V alloy articular cartilage through ordinary mould-melted founding process. Finally, the whole metal cartilage was completed after melting two special cages on it. A patient was selected to clinical applying. RESULTS: A new custom-made artificial articular cartilage of femoral condyle was made. It was press-fit well to the subchondral bone of the allograft bone. The patient's one and half year follow-up result was excellent. CONCLUSIONS: We design and manufacture a new custom-made artificial articular cartilage of femoral condyle based on rapid prototyping technique. The result shows that the manufacturing process has the advantage of rapidness and precision that are very important for individualized artificial implant manufacturing. The artificial articular cartilage is press-fit well and could be a good idea to solve the necroses of allocartilage in hemijoint allotransplantation.

Adolescent↗
PubMed1992

Localization of matrix metalloproteinase 3 (stromelysin) in osteoarthritic cartilage and synovium.

Degradation of proteoglycans is an initial change in osteoarthritic cartilage. Matrix metalloproteinase-3 (MMP-3; stromelysin) capable of degrading cartilage proteoglycans and type IX collagen was immunolocalized in osteoarthritic and normal cartilage. Immunohistochemical studies showed MMP-3 in chondrocytes of the superficial and transition zones in approximately 90% of osteoarthritic cartilage (60 of 67 samples) and in 31% of those of the superficial zone in some normal cartilage (4 of 13 samples). MMP-3 staining correlated directly with the histological histochemical scores of Mankin and with proteoglycan depletion, up to a certain grade of severity. Chondrocytes in the deep radial zone, clusters, and osteophytes were immunostained only when proteoglycan depletion and fissures affected them. Culture media from osteoarthritic cartilage contained significantly higher levels of metalloproteinase activity that was identified as MMP-3 by immunoblotting and lower amounts of tissue inhibitor of metalloproteinases compared with those in the control samples. MMP-3 was also immunolocalized in the lining cells of most osteoarthritic synovium (20 of 23 specimens, 87%) with a direct correlation with scores of inflammatory cell infiltration in the synovium, but it was not detected in the normal synovium. Light and electron microscopic studies demonstrated that MMP-3 digests proteoglycan aggregates in human articular cartilage. Treatment of normal and osteoarthritic cartilage slices with tumor necrosis factor-alpha and/or interleukin-1 alpha increased the number of MMP-3-immunoreactive chondrocytes and the intensity of the staining. These data suggest that MMP-3 produced by the chondrocytes and synovial lining cells under stimulation with these cytokines may be important in proteoglycan degradation in human ostoearthritic cartilage.

Cartilage Diseases↗
PubMed2005

Relationship between bone markers and knee cartilage volume in healthy men.

OBJECTIVE: To determine the relationship between biochemical bone markers and knee cartilage volume and cartilage loss over 2 years; and to investigate whether bone markers are useful to predict the cartilage loss in healthy men. METHODS: Forty healthy Caucasian men (mean age 52.3 yrs) with no symptoms of osteoarthritis (OA) were recruited. Each subject had magnetic resonance imaging (MRI) performed on his dominant knee at baseline and 2 years later. Serum level of osteocalcin (OC), urinary levels of pyridinoline (PYD) and deoxypyridinoline (DPD), and total body bone mineral content (BMC) were measured at baseline. Tibial plateau bone size was measured at baseline. Tibial cartilage volume was measured at baseline and at followup, by means of image processing. RESULTS: Twenty-eight men (70%) completed the longitudinal MRI component of the study. At baseline, no significant associations were observed between values of serum OC or urine PYD and DPD and tibial cartilage volume. Higher baseline serum OC level tended to be associated with a decreased rate of cartilage loss (p = 0.06); no significant association was shown between baseline urine PYD and DPD and tibial cartilage loss, after adjusting for age, body mass index, total body BMC, and tibial plateau bone size. CONCLUSION: Higher baseline serum OC level tended to be associated with a decreased rate of cartilage loss, suggesting that increased bone formation may protect against tibial cartilage loss over 2 years. Studies are needed to determine the role of bone metabolism in the pathogenesis of knee OA.

Adult↗
PubMed1992

[What is the effect of para-articular fractures on hyaline joint cartilage? Experimental electron optic studies of the rabbit on post-traumatic subchondral vascularization disorders].

Joint fractures can interrupt the arterial and venous blood supply to the hyaline cartilage. Previous studies revealed effects of venous engorgement and hypertension in the cartilage. In this study the influence of interruption of the blood supply on the development of osteoarthritis was analysed. In a prospective, experimental study in 40 rabbits all vessels in the patella were ligated and the cartilage was investigated after 2, 6, 12, and 24 weeks by transmission electron microscopy. After 2 weeks no degenerative signs were determined. After 6 weeks there were distinct signs of cartilage injury. The degeneration of the hyaline cartilage increased with time. The endpoint of injury was the destruction of the cartilage and necrosis of the chondrocytes, determined after an ischaemic period of 24 weeks. The stages of cartilage degeneration in our trial correspond to the changes that are well known to occur in osteoarthritis. In conclusion, interruption of the blood supply of the patella results in degenerative changes to the joint cartilage. This effects is related to the duration of ischaemia. On the basis of results we recommend early and watertight repositioning of fractured joints not only for biomechanical reasons but also to avoid irrevocable effects of interrupted blood supply on hyaline joint cartilage.

Animals↗
PubMed2006

Preliminary study of mesenchymal stem cells-seeded type I collagen-glycosaminoglycan matrices for cartilage repair.

OBJECTIVE: To investigate the possibility of repairing articular cartilage defects with the mesenchymal stem cells (MSCs)- seeded type I collagen-glycosaminoglycan(CG) matrices after being cultured with the chondrogenic differentiation medium. METHODS: The adherent population of MSCs from bone marrow of 10 adult dogs were expanded in number to the 3rd passage. MSCs were seeded into the dehydrothermal treatment (DHT) cross-linked CG matrices; 2 x 10(6) cells per 9-mm diameter samples were taken. Chondrogenic differentiation was achieved by the induction media for 3 weeks. Cell contractility was evaluated by the measurement of the cell-mediated contraction of the CG matrices with time in culture. The in vitro formation of the cartilage was assessed by an assay employing immunohistochemical identification of type II collagen and by immunohistochemistry to demonstrate smooth muscle actin (SMA). The cells seedling CGs were implanted into cartilage defects of canine knee joints. Twelve weeks after surgery, the dogs were sacrificed and results were observed. RESULTS: There was significant contraction of the MSCs-seeded DHT cross-linked CG scaffolds cultured in the cartilage induction medium. After 21 days, the MSC-seeded DHT cross-linked matrices were contracted to 64.4% +/- 0.3%; histologically, the pores were found to be compressed and the contraction coupled with the newly synthesized matrix, transforming the MSCs-seeded CG matrix into a solid tissue in most areas. The type II collagen staining was positive. The SMA staining was positive when these MSCs were seeded and the contracted CGs were implanted into the cartilage defects of the canine knee joints to repair the cartilage defects. The function of the knee joints recovered and the solid cartilaginous tissue filled the cartilage defects. Conclusion The results demonstrates that MSCs grown in the CG matrices can produce a solid cartilaginous tissue containing type II collagen after being cultured with the chondrogenic differentiation medium and implanted into cartilage defects. We hypothesize that the following steps can be performed in the chondrogenic process: (1)MSCs express SMA, resulting in matrix contraction, thus achieving a required cell density (allowing the cells to operate in a necessary society); (2)Cells interact to form a type II collagen-containing extracellular matrix (and cartilaginous tissue); (3)Other factors, such as an applied mechanical stress, may be required to form a mature cartilage with the normal architecture.

Animals↗
PubMed2006

Osteoarthritic femoral articular cartilage of knee joint in man.

Osteoarthritis is the most common of the various articular disorders affecting man. The present study was conducted to observe the microstructure of osteoarthritic human femoral articular cartilage by light microscopy. Fifteen osteoarthritic cartilage specimens obtained from patients with primary osteoarthritis (52-80 years) undergoing total knee replacement were processed for paraffin sections. 5 m thick sections were observed under light microscope. The articular surface appeared to be very irregular and fibrillated in all the specimens. The cartilage did not show the normal zonation. Various changes seen were different in all specimens and they were not related to age. Most common feature of the osteoarthritic articular cartilage was the presence of large clusters of cells in 60.0% specimens. Detached parts of the degenerating cartilage were present in the joint cavity in the form of loose bodies. The collagen fibres appeared to be coarser and irregular even near the non-fibrillated areas. Numerous tangential, oblique and vertical splits were also observed. Osteoblastic and osteoclastic activity was seen in the subchondral bone and the osteolytic cyst appeared to invade the cartilage from the subchondral bone. Blood vessels from the subchondral bone were also seen invading the cartilage in 20.0% specimens. The various changes seen in the osteoarthritic cartilage could be an effort of cartilage repair but such attempts are severely counteracted by the osteoarthritic wear process.

Aged↗
PubMed2006

[Magnetic resonance imaging of repair cartilage].

In recent years, several MR imaging techniques that enable detailed morphological and qualitative evaluations of repair cartilage have been developed. We perform fat-suppressed three-dimensional spoiled gradient-recalled (3D-SPGR) magnetic resonance (MR) imaging and delayed gadolinium-enhanced MR imaging of cartilage (dGEMRIC) for the evaluation of repair cartilage. Evaluation of the time course changes in signal intensity of repair cartilage by use of 3D-SPGR MR imaging was thought to be useful for the assessment of histological change in repair cartilage. Moreover, evaluation of the glycosaminoglycan concentration in repair cartilage by use of dGEMRIC was thought to be useful to assess the quality and function of repair cartilage. These new MR imaging techniques may be useful for evaluating repair cartilage and for assessing the treatment effect and the long-term durability of repair cartilage.

Cartilage, Articular↗
PubMedDate not supplied

Cartilage oligomeric matrix protein (COMP) is modified by intra-articular liposomal clodronate in an experimental model of arthritis.

OBJECTIVE: High-dose liposomal bisphosphonates exert apoptotic effects. This work studies the chondroprotective and anti-inflammatory properties of intra-articularly administered low-dose, non-cytotoxic liposomal clodronate. METHODS: Antigen induced arthritis in rabbits was treated with intra-articular injections of liposomal clodronate. Drug effects on cartilage oligomeric matrix protein COMP was assessed using immunohistochemistry and morphometry of synovial membrane and hyaline articular cartilage. RESULTS: COMP remained close to normal in liposomal clodronate treated superficial articular cartilage compared to a significant loss of COMP in arthritis controls treated with empty liposomes. The middle and deep layers of the hyaline articular cartilage were characterized by highly increased COMP expression in liposomal clodronate treated AIA joints compared to controls. In contrast to cartilage, synovial COMP expression was slightly decreased as a result of liposomal clodronate treatment. CONCLUSION: Low-dose, non-cytotoxic liposomal clodronate exerts a dichotomous effect on synovial membrane and articular cartilage COMP in the AIA model. COMP is a useful inflammation marker in the synovial tissue, but it also contributes to the structural integrity of the hyaline articular cartilage forming bridges between type II and IX collagens. Enhancement of COMP in clodronate treated AIA cartilage suggests a chondroprotective and anti-inflammatory effect in the inflammatorily damaged and mechanically strained cartilage.

Animals↗
PubMed1991

Degradation of cartilage matrix proteoglycan by human neutrophils involves both elastase and cathepsin G.

The granule proteases of human neutrophils are thought to be responsible for the connective tissue destruction associated with certain inflammatory diseases. Using a model system for the degradation of a macromolecular connective tissue substrate, purified neutrophil elastase and cathepsin G were both individually able to degrade cartilage matrix proteoglycan and this degradation was blocked by the appropriate specific inhibitors. Neutrophil granule lysate also produced cartilage matrix degradation but little inhibition of degradation occurred when either elastase or cathepsin G inhibitor was used alone. However, a combination of elastase and cathepsin G inhibitors each at 100 microM or each at 10 microM blocked cartilage matrix degradation by 89% +/- 1 and 65% +/- 9 (mean +/- SEM, n = 3), respectively. The magnitude of the cartilage degradation mediated by neutrophil lysate, and its sensitivity to specific inhibitors, was reproduced using purified elastase and cathepsin G at the concentrations at which they are present in neutrophil lysate. Human neutrophils stimulated with opsonized zymosan degraded cartilage matrix in a dose-dependent manner in the presence of serum antiproteases. Supernatants from stimulated neutrophils cultured in the presence of serum did not degrade cartilage matrix, indicating that neutrophil mediated degradation in the presence of serum was confined to the protected subjacent region between the inflammatory cell and the substratum. A combination of elastase and cathepsin G inhibitors each at 500 microM or each at 100 microM blocked subjacent cartilage matrix degradation by stimulated human neutrophils by 91% +/- 3 and 54% +/- 8 (mean +/- SEM, n = 5), respectively, whereas either the elastase or cathepsin G inhibitor alone was much less effective. These studies demonstrate that neutrophil-mediated cartilage matrix degradation is produced primarily by elastase and cathepsin G. Furthermore, these results support the hypothesis that inflammatory neutrophils form zones of close contact with substratum that exclude serum antiproteases and that this subjacent degradation of cartilage matrix by stimulated neutrophils can be blocked by a combination of synthetic elastase and cathepsin G inhibitors.

Cartilage↗
PubMed1990

[Degeneration of articular cartilage of the ankle in cadavers studied by gross and radiographic examinations].

Eighty-two joints out of 41 cadavers were studied grossly in order to evaluate degenerative changes in talocrural articular cartilage with age. Cartilage degeneration was seen in 97.6% of joints. Cartilage degeneration associated with cartilage defects were seen at the age of 50 years. Thereafter, the severity of degeneration became more marked with aging. This severe cartilage degeneration was mainly found in medial and anterior regions in the talocrural joints. The anterior tibiofibular, deltoid, calcaneofibular and anterior talofibular ligaments of 40 joints of out 20 cadavers were grossly studied in order to establish the relationship between the degree of degeneration of these ligaments and that of articular cartilage. Grossly severe degeneration was present only in the anterior talofibular ligaments of 2 joints. Both joints presented severe cartilage degeneration in the medial region of the talocrural joint. Severe cartilage degeneration was present in 7 out of 30 joints (23%) whose ligaments were apparently normal upon gross observation. These cartilage degenerations were present in the medial and anterior regions of the talocrural joints.

Aged↗
PubMed1990

The effect of human interleukin 1 on proteoglycan metabolism in human and porcine cartilage explants.

Human interleukin 1 (IL-1), up to 100 pg/ml, causes a decrease of the proteoglycan content of human (old and young) as well as porcine cartilage explants, without stimulating the proteoglycan release from the cartilage. The proteoglycan depletion is stronger in young than in old human cartilage and stronger in human than in porcine cartilage. The proteoglycan synthesis is considerably more inhibited by IL-1 in young than in old human cartilage. Our data suggest that an IL-1 induced inhibition of the proteoglycan synthesis, rather than a stimulation of proteoglycan breakdown causes the proteoglycan depletion of the cartilage. The data furthermore suggest a clear difference between young and old human cartilage, with respect to their sensitivity for IL-1. IL-1 in a concentration of 500 pg/ml causes in all 3 kinds of cartilage explants chondrocyte damage that might be relevant in the cartilage destruction during rheumatoid arthritis.

Aged↗
PubMed1987

Invasion of human lung carcinoma into cartilage of the bronchus.

In vivo invasion of human carcinoma of the lung into the cartilage of the bronchus was studied by light microscopy. Tumor spread into the cartilage was found in 26% (60/229). It occurred in 38/128 epidermoid carcinoma (30%) and in 14/55 adenocarcinoma (25%), but was observed in only 1/17 large cell anaplastic carcinoma (6%). Degradation of cartilage matrix was found to be limited. Destroyed area measured 9.9 +/- 1.8 mm2 on average. Tumors able to destroy bronchus cartilage were similar in size compared to tumors without detectable invasion into cartilage. Analysis of pTN stages revealed no differences between both groups. Tumor volume in extrapulmonary lymph nodes was significantly larger in case of cartilage degradation. Patients with tumors degrading bronchus cartilage showed poorer survival (median survival 360 vs. 780 days, p less than 0.10). Immunohistology differentiating inflammatory cells (B lymphocytes, T lymphocytes, monocytes, granulocytes, macrophages) revealed no participation of inflammatory cells in tumorous degradation of cartilage. The findings suggest that hyalin cartilage is highly resistant to invasion of human lung carcinoma although evidence exists for proteolytic activity of human lung carcinoma.

Adenocarcinoma↗
PubMed1989

The fate of articular cartilage after transplantation of fresh and cryopreserved tissue-antigen-matched and mismatched osteochondral allografts in dogs.

The long-term success of massive osteochondral allografts depends not only on the incorporation of the transplanted articular cartilage. Osteochondral allografts are immunogenic, and, once an immune response is stimulated by exposure to donor cellular antigens, the cartilage becomes vulnerable to direct injury by cytotoxic antibodies or by lymphocytes, or to indirect injury by inflammatory mediators and enzymes induced by the immune response. To clarify the role of histocompatibility antigen-matching on the health of transplanted articular cartilage, we orthotopically implanted canine leukocyte antigen-matched and mismatched proximal osteochondral allografts of the radius, both fresh and cryopreserved, in beagles. Four groups of dogs received: (1) canine leukocyte antigen-mismatched frozen allografts, (2) canine leukocyte antigen-mismatched fresh allografts, (3) canine leukocyte antigen-matched fresh allografts, or (4) canine leukocyte antigen-matched frozen allografts. In twelve of the dogs, the contralateral leg was subjected to a sham operation, and in ten of the dogs, the proximal part of the radius was removed and replaced as an autogenous graft control. All animals were followed for eleven months after the operation and then were killed. The cartilage of the grafts was evaluated grossly, histologically, and biochemically. The biochemical analysis consisted of measurement of dry weight, content of glycosaminoglycan and hydroxyproline, and galactosamine-to-glucosamine ratios. Analyses of variance were used to study the effect of tissue antigen-matching and freezing on degradation of cartilage. During the study, no dog had grossly obvious clinical abnormalities, all host-graft interfaces healed, and no joints dislocated. The gross appearance of the cartilage was normal for both the joints that had an autogenous graft and those that were subjected to the sham operation. The cartilage of all allografts was thinned, dull, and roughened. The synovial membrane of all of the joints that had been operated on was mildly fibrotic and hyperplastic, but only that of the dogs that had an allograft was severely fibrotic and hyperplastic and demonstrated an inflammatory response. The inflammatory response was most severe in joints that had received a fresh canine leukocyte antigen-mismatched allograft. Invasive pannus was more frequent in joints that had received a fresh graft, particularly those that had received a canine leukocyte antigen-mismatched allograft, and cartilage was sometimes eroded to subchondral bone. Freezing was harmful to the cartilage. Very few cells survived the freezing procedure, and frozen grafts received s significantly worse histological scores had significantly less glycosaminoglycans and had a lower ratio of galactosamine to glucosamine than fresh grafts.

Animals↗
PubMed1985

Osteoarthrosis. Changes of bone, cartilage and synovial membrane in relation to bone scintigraphy.

The present study was undertaken to investigate the sites at which the 99mTc phosphorous compounds bind to skeletal tissue in general, and their localization at different stages of osteoarthritis in particular, in order thereby to arrive at a better morphological basis for interpreting the scintigrams. It was endeavoured also to relate the uptake of bone-seeking agents to abnormal changes in cartilage, synovium, and subchondral bone to obtain better insight into the pathogenesis of osteoarthritis. The bone remodelling activities in subchondral bone in osteoarthritic human femoral heads were elucidated by the alkaline phosphatase activity of osteoblasts and the acid phosphatase activity of osteoclasts. The enzyme activity was measured semiquantitatively by the initial time for the histochemical reaction. The distribution of the activity of the two enzymes in different areas proved parallel, and considerable variation in enzyme activity was seen between different areas within the same femoral head. Increased osteoarthritic cartilaginous changes were associated with increased subchondral enzyme activity, highest in denuded weightbearing areas and in the osteophytes and lowest in non-weightbearing subchondral bone and centrally in the femoral head. Studies on different histochemical staining of glycosaminoglycans in the matrix of human osteoarthritic cartilage and of normal cartilage revealed a heterogeneous distribution of the different glycosaminoglycans through the cartilage. Except for superficial loss of glycosaminoglycans, no difference was found in the distribution of keratan sulphate between osteoarthritic cartilage and control cartilage. In osteoarthritis, however, a relative increase in stainability for chondroitin sulphate was found in the territorial area, especially around the cell clusters, and only chondroitin sulphate was present in the cartilage of osteophytes. These findings were interpreted as an increased GAG metabolism, its mode of production being like that of very young cartilage. In the experimental rabbit model used in studying the uptake of bone-seeking agents this GAG regeneration was able to refill demasked collagen network with glycosaminoglycans in certain areas of the joint. The height of the depleted superficial area was estimated on patellar cartilage stained for sulphated GAG with toluidine blue-0 at pH 3, visually and by optical densitometry using the wavelength corresponding to the gamma-band of toluidine blue. The time relation of the surface depletion was elucidated. A marked depletion of GAG, seen one week postoperatively, reached a maximum at 4 weeks.(ABSTRACT TRUNCATED AT 400 WORDS)

Alkaline Phosphatase↗
PubMed1987

Influence of cartilage on reactivity and on the effectiveness of verapamil in guinea pig isolated airway smooth muscle.

The authors have examined the effects of cartilage removal on smooth muscle reactivity and the action of verapamil in guinea pig trachealis. In preparations devoid of cartilage, smooth muscle reactivity to both histamine and KCl was reduced. Reactivity to methacholine was unaffected by cartilage removal. In the absence of cartilage, verapamil had a greater depressant effect on the maximum responses to histamine and methacholine than in intact tissues. Similarly, verapamil was more potent against histamine- and methacholine-induced responses in the absence of cartilage where a greater shift to the right was seen in the concentration-response curves when compared with cartilage-containing controls. The spasmolytic action of verapamil on methacholine-induced responses was greater in the absence of cartilage and was greater than its antispasmogenic activity against methacholine (whether or not cartilage was present). Thus, cartilage removal reduces muscle reactivity and increases the potency of verapamil in guinea pig trachealis.

Animals↗
PubMed1987

Nonsteroidal antiinflammatory drugs and articular cartilage.

Salicylates and some other nonsteroidal antiinflammatory drugs (NSAID) suppress proteoglycan biosynthesis in normal articular cartilage in vitro. Their effect on osteoarthritic cartilage in vitro is even greater than their effect on normal cartilage. Aspirin has a similar effect in vivo on both atrophic cartilage and osteoarthritic cartilage in the dog, although no in vivo effect of salicylate on normal joint cartilage has been observed. While the magnitude of the effects of NSAID on proteoglycan metabolism in cartilage appeared to be inversely related to the proteoglycan content of the matrix, it is possible that some drugs are selectively bound to cartilage matrix components, which could affect their action on the chondrocyte. If NSAID have similar effects in patients with arthritis, this could have implications with respect to articular cartilage lesions.

Animals↗
PubMed1979

[An experimental study on the influences of artificial socket upon articular cartilage of the femoral head (author's transl)].

In order to investigate the influences of artificial socket made of stainless-steel, pure titanium, high-density polyethylene (HDP), and polycrystal ceramics upon the articular cartilage of the femoral head, experimental artificial sockets were developed. This artificial socket was inserted into the hip joint in a dog, and the changes in the articular cartilage of the femoral head were studied at varying intervals after insertion of the socket. The results revealed that both the stainless-steel and the ceramic sockets caused slight atrophy and degeneration in the articular cartilage of the femoral head since one month after the operation, and these changes were increasingly more appreciable as time advanced. Any changes were hardly noted in the articular cartilage of the femoral head by titanium socket at the end of one month after the operation, whereas the HDP socket caused substantial changes. At the end of one year after the operation, marked degeneration was noted in the articular cartilage of the femoral head by socket made of stainless-steel, titanium, and HDP, and also the femoral head developed deformity. On the basis of the scanning electron microscopic findings on the surface of the articular cartilage of the femoral head affected by each of these artificial socket, and of the metal microscopic examinations of the surface of the artificial sockets, and furthermore on the basis of the findings of gradual deformation of femoral heads due to the artificial sockets, it was shown that articular cartilage of the femoral head was mainly influenced in the case of metallic socket and that both sides of the artificial socket and the articular cartilage of the femoral head were worn out in the case of HDP socket. The ceramic socket was found cracked, developing a loosening in some cases. In summary, it was concluded that the articular cartilage of the femoral head is affected by the artificial socket at a relatively early stage after its application despite materials of the sockets.

Animals↗
PubMed1979

[A morphological and functional analysis of the extent of cartilage coverage in the human hip joint].

The extension and the shape of the cartilage surface of 30 human femora and acetabula were measured. The results were considered and discussed as the response of the articular cartilage to the specific stress on this joint. 3 kinds of cartilage distribution were found on the femoral head; these shapes were understood as the consequence of the position and the dwelling time of the actual cartilage stimulating area. The largest extention of the cartilage was found in the ventrolateral direction and the smallest in medial direction. The cartilage margin of the "A" type was regulary curved. The "B" type has an inlet towards the fovea capitis. This inlet reaches in the "C" type to the fovea as an area free of cartilage. The acetabula could not be divided into types with different cartilage distribution because of the great similarity in shape. Therefore we computed an average acetabulum. The largest extension of the facies lunata was found 15 degrees in front of the roof of the acetabulas as seen in x-ray pictures. The cornu anterius is always narrower than the cornu posterius. The outer margin of the osseous acetabulum does not reach the equator, it lies on a latitude of 11.5 degrees. The incisura acetabuli is inclined against the vertical line with 18.3 degrees. The width of the facies lunata can be considered as a result of mechanical stress. The different extensions of the cartilage of both joint components in ventro-lateral direction seems to be the consequence of different extensions of movement. The area of movement of the caput femoris is larger than the area of the acetabulum.

Acetabulum↗