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PubMed1999

Immunolocalisation of vascular endothelial growth factor (VEGF) in human neonatal growth plate cartilage.

Angiogenesis is essential for the replacement of cartilage by bone during growth and repair. In order to obtain a better understanding of the mechanisms regulating vascular invasion at sites of endochondral ossification we have investigated the expression of the endothelial cell-specific mitogen, vascular endothelial growth factor (VEGF), by chondrocytes in human neonatal growth plates. VEGF was absent from chondrocytes in the resting zone and only weakly expressed by occasional chondrocytes in the proliferating region. In the hypertrophic zone the number of chondrocytes stained and the intensity of staining for VEGF increased with chondrocyte hypertrophy, maximum expression of VEGF being observed in chondrocytes in the lower hypertrophic and mineralised regions of the cartilage. These observations provide the first demonstration of the presence of VEGF in situ in developing human bone and are consistent with in vitro observations demonstrating the upregulation of proangiogenic growth factor production with increasing chondrocyte hypertrophy. The presence of numerous small blood vessels and vascular structures in the subchondral region where VEGF expression was maximal indicates that VEGF produced by hypertrophic chondrocytes may play a key role in the regulation of vascular invasion of the growth plate.

Cartilage↗

PubMed2003

[An immunohistochemical study on neovascularization in TMJ during mandibular advancement].

OBJECTIVE: Neovascularization is proved to be closely correlated with ossification. This study was designed to determine the biochemical path through which the new bone formation is enhanced in TMJ during mandibular protrusion. METHODS: SD Rats were fitted with bite-jumping appliances to allow for an adequate advancement of the mandible. The animals were sacrificed 3, 7, 14, 21 and 30 days, respectively, after placement of the appliances. Slides with TMJ tissue were prepared for biochemical procedure. Immunohistochemical approaches were adopted to examine neovascularization in TMJ by immuno-localizing the newly formed endothelial cells. Computer-assisted image analysis system was applied to quantify the positive immunoreaction. RESULTS: Neovascularization in connective tissue close to the condyle was 200% higher in the experimental groups than that in the control, and, within the bony tissue of the condyle, neovascularization in experimental animals was found to be 103% higher than that of the control. CONCLUSION: Increased neovascularization triggered by mandibular protrusion might intensify new bone formation in condyle and glenoid fossa and finally lead to a growth adaptation of TMJ to bite-jumping therapy.

Animals↗

PubMed1995

Effect of therapeutic ultrasound on endochondral ossification.

The effect of therapeutic doses of ultrasound was tested on endochondral ossification of in vitro developing metatarsal long bone rudiments of 16- and 17-day-old fetal mice. Bone growth, calcification and resorption following exposure to several doses of pulse-wave (PW) or continuous-wave (CW) ultrasound were examined. PW was applied at intensities between 0.1 W cm-2 and 0.77 W cm-2 (Isatp) and CW intensities were 0.1 W cm-2 or 0.5 W cm-2 (Isata). After 1 week of culture, the metatarsal long bone rudiments were fixed and paraffin sections were prepared for histological evaluation and for measurement of the relative contribution of the various cartilage zones to the total bone length. In contrast to treatment with CW ultrasound, treatment of 16-day-old metatarsal long bone rudiments with PW ultrasound resulted after 4 days of culture in significantly increased longitudinal growth. Histology revealed a significant increased length of the proliferative zone, whereas the length of the hypertrophic cartilage zone was unaltered. This might indicate that proliferation of the cartilage cells is stimulated without influence on cell differentiation.

Animals↗

PubMed1999

Transplacental effects of bisphosphonates on fetal skeletal ossification and mineralization in rats.

Bisphosphonates are clinically used mainly to reduce bone resorption. We studied the transplacental effects of two bisphosphonates on the fetal skeleton in rats. Pregnant rats were treated during days 11-20 of pregnancy with daily subcutaneous injections of 0.1 mg/kg of alendronate or a newly synthesized bisphosphonate, VS-b6. This period of pregnancy was chosen because the active development of bones from mesenchyme through cartilaginous models occurs during that time. Histological examination of midlongitudinal sections of the 21-day-old fetuses showed an increase in the amount of diaphyseal bone trabeculae with slight shortening of the diaphysis in the experimental fetuses, in comparison to controls. Computerized histomorphometric studies similarly showed an increase in the amount of diaphyseal bone trabeculae with a concomitant decrease in bone marrow volume, but no change in cartilage volume. In addition, chemical analysis of the fetal bones showed an increase in calcium content in the treated fetuses. 14C-alendronate was shown to pass through the rat placenta and accumulate in the fetuses, most probably in their bones. This is presumed because bisphosphonates are known to accumulate in bone, being stored there for long periods of time. It is important, in light of our results, to give careful consideration to the treatment of women with bisphosphonates at childbearing age, whenever this is needed.

Alendronate↗

PubMed1985

Role of proteoglycans in endochondral ossification: inhibition of calcification.

Proteoglycans from bovine nasal septa and from the Swarm rat chondrosarcoma were isolated as aggregates (PGC) and as monomers (PGS). Portions of the PGC preparations were degraded with cathepsin D or chondroitinase AC. Chondroitin sulfates were isolated by differential precipitation from alkaline digests of the PGS from bovine nasal septa. The effects of these preparations at concentrations up to 2 mg/ml on the precipitation of tricalcium phosphate in vitro at pH 7.8 in 16 hours at 25 degrees C were ascertained. To this end, the amounts of calcium and phosphate in the precipitates and in the supernates were determined. The PGC preparations were found to be very effective inhibitors; in the presence of 2 mg/ml, precipitate did not form. The PGS preparations were less effective than the PGC preparations; in the presence of 2 mg/ml, about 20% as much calcium phosphate precipitated as in their absence. The chondroitinase AC-degraded preparations at concentrations equivalent to 2 mg/ml of the PGC preparations were approximately as effective as the PGS preparations. On the other hand, the cathepsin D-degraded PGC preparations and the chondroitin sulfate chains were relatively poor inhibitors. Although the viscosity of the solutions may have influenced the rate at which the precipitates settled to the bottom of the tubes, the amounts of the tricalcium phosphate formed were related to the composition and concentration of the proteoglycan preparations.

Animals↗

PubMed2004

Overview of bone biology in the egg-laying hen.

In young pullets, long bones elongate by endochondral growth. Growth plate chondrocytes proliferate, then hypertrophy, and are replaced by osteoblasts that form a network of trabecular bone. This bone is gradually resorbed by osteoclasts as the bone lengthens. Long bones widen, and flat bones are formed, by intramembranous ossification in which cortical bone formation by osteoblasts in the periosteal layer is accompanied by osteoclastic resorption at the inner endosteal surface. Growth of structural trabecular and cortical bone types continues up to the onset of sexual maturity in pullets. At this point, the large surge in estrogen changes the function of osteoblasts to forming medullary bone rather than structural bone. Medullary bone is a woven bone that acts as a labile source of calcium for eggshell formation. It lines structural bone and also occurs as spicules within the marrow cavity. It has little inherent strength but can contribute to fracture resistance. Osteoclasts resorb both medullary and structural bone so that during the period the hen remains in reproductive condition there is a progressive loss of structural bone throughout the skeleton, which is characteristic of osteoporosis. The increasing fragility of the bones makes them more susceptible to fractures. The dynamics of bone loss can be affected by a number of nutritional, environmental, and genetic factors. If the hen goes out of reproductive condition, estrogen levels fall, osteoblasts resume structural bone formation, and skeletal regeneration can take place.

Animal Feed↗

PubMed1982

[Monitoring of the spinal cord function using evoked spinal cord potentials].

Monitoring of the spinal cord function by evoked spinal cord potentials (ESP) has come to be used widely with the establishment of a safe technique using an epidural electrode and the great improvement in medical electronic devices. According to other investigations ESP has been recorded through an electrode placed in the posterior epidural space, it is well known that residual ESP can be actually recorded after transection of the posterior half of the spinal cord and that ESP shows no change after a small transection of the anterior column. If ESP originating from the anterior half of the spinal cord is recorded, it is very useful for monitoring during anterior decompression surgery for myelopathy such as ossification of the posterior longitudinal ligament and cervical spondylosis. The purpose of this report is to analyse ESP originating from the anterior half of the spinal cord experimentally and further investigate the ESP monitoring clinically. Sixty cats were used in this study. ESP recording principally consisted of stimulation to the spinal cord at the level of thoracic or lumbar region and recording of ESP with a monopolar electrode placed in the cervical epidural space. Changes in the ESP after transection and compression of the spinal cord were analysed. Anterior vertebrectomy and laminectomy at C2 and C6 were performed for the purpose of placing an electrode correctly and facilitating transection or compression of the spinal cord. Recording electrodes were placed on both the anterior and posterior surfaces of the dura mater at C2. As the result of this study, it is apparent that there exists the ESP originating from the anterior half of the spinal cord. Such ESPs are more accurately recorded through an anterior placed electrode rather than through that placed posteriorly.

Animals↗

PubMed1993

BMPs induce direct bone formation in ectopic sites independent of the endochondral ossification in vivo.

Bone formation in vivo occurs via two major processes, one of which depends on pre-existing cartilage, and the other does not. Bone morphogenetic proteins (BMPs) have been suggested to induce cartilage formation from non-skeletogenic mesenchymal cell population, which results in osteogenesis through the endochondral sequence. In the present study we examined if BMPs could cause direct bone formation independent of pre-existing cartilage using bovine fibrous collagen membrane (FCM) as a carrier for BMPs. Bovine metatarsal bone was extracted in 4 M guanidine HC1 and BMPs were partially purified through the hydroxyapatite chromatography and the Heparin-Sepharose CL6B chromatography. The carrier was loaded with BMPs and then implanted in Wistar rats subcutaneously. The implants were fixed together with surrounding tissue every week after implantation and processed for von Kossa stain, immunohistochemistry, and electron microscopy. The phenotypes of bone and cartilage were identified histologically and immunohistochemically using antibodies against type I and type II collagen. Cartilage and bone were independently induced by 2 weeks. The bone formed directly on the collagen substrate of FCM without pre-existing cartilage. Calcification occurred in the carrier as well as the cartilage and bone matrix. The present study suggests that the BMPs induce osteogenesis in vivo independent of the endochondral sequence.

Animals↗

PubMed1998

Type X collagen is not localized in hypertrophic or calcified cartilage in the developing rat trachea.

Our previous studies have shown that rat tracheal chondrocytes become larger and hypertrophic, and that the cartilage matrix calcifies during development. Type X collagen is a short collagen molecule identified in hypertrophic and calcified cartilage in the growth plate of long bones during endochondral ossification. The present study was designed to investigate the distribution of type X collagen in rat tracheal cartilage during development before and after hypertrophization and calcification. Tracheas from postnatal Wistar rats, newborn, and at 4, 8 and 10 weeks were fixed along with hind limbs from newborn rats. Serial sections were made and adjacent sections were processed for von Kossa staining or immunohistochemistry for type X collagen. In addition, the immunoreactivity to type II collagen was examined as a control. The anti-type X collagen antibody stained hypertrophic and/or calcified cartilage in the newborn rat tibia. The immunoreaction for type X collagen was localized in the uncalcified peripheral region of tracheal cartilage in 4, 8 and 10-week-old rats. In contrast, the anti-type X collagen antibody did not show immunoreactivity to hypertrophic or calcified cartilage in the central region of the 10-week-old rat tracheal cartilage. The present study has suggested that type X collagen is not involved in hypertrophization of chondrocytes or calcification of the matrix in developing rat tracheal cartilage.

Animals↗

PubMed1991

Cyproterone acetate in the treatment of sexual disorders: pharmacological base and clinical experience.

Cyproterone acetate (CPA) has been discovered more than 25 years ago and it was the first antiandrogen suitable for clinical use. CPA inhibits the action of endogenous and exogenous androgens at all androgen target organs; these include the prostate, seminal vesicles, testes, and the vas deferens. However, this antiandrogen also antagonizes less sex-specific effects of androgens, for example ossification of the epiphyseal cartilage, sebaceous gland function and skin thickness. Indications for CPA: Prostate cancer, androgen induced disorders of the skin (acne, seborrhoea, hirsutism, alopecia), precocious puberty and sexual disorders in men. Concerning sexual deviations clinical trials started in 1966. CPA leads to loss of libido and the ability to achieve erection, followed by the inability to achieve orgasm, after about 14 days of treatment (100-200 mg daily orally or 300 mg weekly i.m.). These effects are reversed in the same order as the onset. About 75 to 80% of patients respond to this therapy. CPA is generally well tolerated. Tiredness, lack of drive, listlessness and depressive moods have been reported as non-specific side-effects. Slight gynecomastia occurs in about 20% of patients. There are no good alternatives in this indication. Pure antiandrogens are unsuitable, because these are unable to inhibit libido sufficiently. Tranquilizers are not very effective, high doses of estrogens are associated with severe (cardiovascular) side effects. Orchidectomy is an irreversible intervention, LHRH analogues are associated with hot flushes and the initial increase in testosterone (flare phenomenon).

Androgen Antagonists↗

PubMed1998

Frontal sinus fractures: principles of treatment and long-term results after sinus obliteration with the use of lyophilized cartilage.

The most commonly used techniques for frontal sinus obliteration involve the implantation of an autogenous tissue graft: either fat, muscle or bone. Lyophilized allogenic cartilage due to its unique properties, such as the tendency to ossification and resistance to volume reduction, can be used as the material of choice for sinus obliteration. A clinical and radiological study of 66 patients operated on for frontal sinus fractures, between January 1 1988 through December 31 1995 was undertaken. Variables recorded included the aetiological factors, the clinical and radiological fracture features with the corresponding treatment modality, the association of frontal sinus fractures with intracranial involvement, the early and late postsurgical complications and the correlation between pre- and postoperative radiological findings. Obliteration of the frontal sinus with lyophilized cartilage chips was performed in 51 (77.3%) patients. The postsurgical evaluation showed no major complications. Revision of the frontal sinus was only required in one patient. The radiological findings verified the progressive calcification of the obliterated sinus. Allogenic lyophilized cartilage implantation offers distinct advantages in cases of severe frontal sinus trauma: 1. There is nearly unlimited availability of the material. 2. There is no need for a second operation field with the associated potential donor site morbidity. 3. The operation time is reduced due to the avoidance of a second operation on the donor site.

Adolescent↗

PubMed1996

Cartilage-bone replacement in endochondral ossification of mandibular condylar heads in young beagle dogs.

The cellular mechanisms of cartilage-bone replacement in endochondral bone formation, in mandibular condylar heads, are poorly understood. In particular, there is no definitive evidence indicating whether cartilage is resorbed by so-called chondroclasts. Using 3-week-old male beagle dogs, we examined the cartilage-bone replacement processes in mandibular condylar heads by means of light and electron microscopy. Calcification of the cartilage matrix occurred in the central area of the longitudinal septa but not in thin transverse septa. Chondrocytic lacunae were opened by the removal of transverse septa by perivascular rough-surfaced endoplasmic reticulum (RER)-rich mononuclear cells. These cells also phagocytosed calcified cartilage fragments in the surface layer of longitudinal septa. Shortly thereafter, a thin bone layer was deposited on the remaining longitudinal septa by invading osteoblasts. Preosteoclastic multinucleated cells in lacunar canals developed neither ruffled borders nor clear zones in the cartilage matrix, but once the bone layer had been deposited on the remaining cartilage, these structures formed. Our results suggest that the cartilage-bone replacement in mandibular condylar heads involves four sequential processes: 1) degradation of the transverse septal cartilage by RER-rich mononuclear cells, 2) phagocytosis of calcified cartilage fragments in the longitudinal septa by these cells, 3) bone deposition of the remaining longitudinal septa, and 4) degradation of both bone and calcified cartilage by differentiated osteoclasts.

Animals↗

PubMed2000

Matrix vesicles mediate mineralization of human thyroid cartilage.

Mineralization and ossification of human thyroid cartilage first starts after the end of adolescence when the previously cartilaginous human skeleton has become ossified and the epiphyseal discs are in the process of closing. However, the mechanisms involved in mineralization and ossification of human thyroid cartilage are not well understood. Ultrastructural analysis of human thyroid cartilage revealed that mineralization started close to cartilage canals in a matrix containing gigantic collagen fibers (asbestoid fibers). Matrix vesicles were detected in mineralized areas and were often associated with needle-like crystals. For the first time we were able to isolate matrix vesicles from human thyroid cartilage by mild enzymatic digestions and ultracentrifugation. These particles were oval and varied in size; some were heavily calcified. They were enriched in alkaline phosphatase, calcium, and inorganic phosphate, suggesting that the particles contain Ca2+-Pi complexes. Immunoblot analysis of these vesicles revealed the presence of annexins II, V, and VI, membrane-associated, channel-forming proteins, which allow influx of Ca2+ into the vesicles and intralumenal crystal growth. In addition, the vesicles were associated with types II and X collagen, suggesting that this association not only anchors the vesicles to the extracellular matrix, but, as shown previously, also stimulates Ca2+ influx into these particles. In conclusion, matrix vesicles isolated from human thyroid cartilage contain all the components, enabling them to initiate and mediate the mineralization process in human thyroid cartilage.

Adult↗

PubMed2002

1Alpha,25-dihydroxyvitamin D3 promotes vascularization of the chondro-osseous junction by stimulating expression of vascular endothelial growth factor and matrix metalloproteinase 9.

Vitamin D deficiency results in defects in endochondral bone development characteristic of rickets, which include elongation of the cartilaginous growth plates and disorganization of the primary spongiosa. These defects are caused in part by impaired cartilage mineralization and vascularization of the chondro-osseous junction. Blood vessel invasion of mineralized cartilage is an essential step in endochondral ossification, providing access for cells that degrade cartilage as well as those that form bone. Vascular endothelial growth factor (VEGF) was shown to be a key regulator of this process when infusion of a dominant negative VEGF receptor effectively blocked vascular invasion and endochondral ossification in the growth plates of juvenile mice. Here, we show that the active metabolite of vitamin D 1alpha,25-dihydroxyvitamin D3 [1alpha,25(OH)2D3] directly stimulates transcription of mRNAs encoding VEGF121 and -165 isoforms in the CFK2 chondrogenic cell line. Enhanced VEGF expression also was evident in growth plate chondrocytes and osteoblasts in the tibia of juvenile mice treated systemically with 1alpha,25(OH)2D3. This was seen in conjunction with enhanced expression of matrix metalloproteinase (MMP) 9, which activates VEGF stored in the cartilage matrix, in osteoclastic cells adjacent to the chondro-osseous junction. The alterations in VEGF and MMP-9 expression were accompanied by enhanced vascular invasion of mineralized cartilage, as assessed by CD31 immunoreactivity. These results provide evidence that 1alpha,25(OH)2D3 signaling stimulates VEGF and MMP-9 gene expression and promotes neovascularization of the epiphyseal growth plate in vivo through increased availability of active growth factor.

Animals↗

PubMed2004

VEGFA is necessary for chondrocyte survival during bone development.

To directly examine the role of vascular endothelial growth factor (VEGFA) in cartilage development, we conditionally knocked out Vegfa in chondrocytes, using the Col2a1 promoter to drive expression of Cre recombinase. Our study of Vegfa conditional knockout (CKO) mice provides new in-vivo evidence for two important functions of VEGFA in bone formation. First, VEGFA plays a significant role in both early and late stages of cartilage vascularization, since Vegfa CKO mice showed delayed invasion of blood vessels into primary ossification centers and delayed removal of terminal hypertrophic chondrocytes. Second, VEGFA is crucial for chondrocyte survival, since massive cell death was seen in joint and epiphyseal regions of Vegfa CKO endochondral bones. Chondrocytes in these regions were found to upregulate expression of Vegfa in wild-type mice at the time when massive cell death occurred in the Vegfa CKO mice. The expression of the VEGFA receptors Npr1 and Npr2 in epiphyseal chondrocytes and lack of blood vessel reduction in the vicinity of the cartilaginous elements in the Vegfa CKO mice raise the possibility that the observed cell death is the result of a direct involvement of VEGFA in chondrocyte survival. Interestingly, the extensive cell death seen in Vegfa CKO null bones had a striking similarity to the cell death phenotype observed when hypoxia-inducible factor 1 alpha (Hif1a) expression was abolished in developing cartilage. This similarity of cell death phenotypes and the deficient VEGFA production in Hif1a null epiphyseal chondrocytes demonstrate that HIF1 alpha and VEGFA are components of a key pathway to support chondrocyte survival during embryonic bone development.

Animals↗

PubMed2004

Matrix metalloproteinase-9 expression, tartrate-resistant acid phosphatase activity, and DNA fragmentation in vascular and cellular invasion into cartilage preceding primary endochondral ossification in long bones.

Vascular and cellular invasion into cartilage are essential for endochondral ossification. Recently it has been shown that matrix metalloproteinase-9 (MMP-9)/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes. To study vascular and cellular invasion into cartilage preceding primary endochondral ossification in long bones, precursor femurs from 13- to 16-day-old murine embryos were sectioned. Tartrate-resistant acid phosphatase (TRAP) activity, in situ hybridization for matrix metalloproteinase-9 (MMP-9), immunostaining for CD31, and in situ detection of apoptosis (TUNEL) were studied. TRAP activity, MMP-9 mRNA, and CD31 expression were initially detected in the intertrabecular spaces of the perichondral collar, and then in cells migrating into the cartilage. The first cells involved in the primary invasion into cartilage were CD31-positive vascular endothelial cells and MMP-9-positive cells, followed by TRAP-positive cells. At the cartilage-marrow interface, CD31-positive vascular endothelial cells and MMP-9-positive cells were predominant. These results suggest that MMP-9-positive cells cooperate with vascular endothelial cells in cartilage angiogenesis. TUNEL-positive staining was detected on chondrocytes attached to the inner surface of the perichondral collar, and also detected in the area where cartilage was removed. These results suggest that chondrocytes separated from the cartilage matrix may undergo apoptosis.

Acid Phosphatase↗

PubMed1994

Hormonal regulation of longitudinal bone growth.

The regulation of postnatal somatic growth is complex. Genetic, nutritional factors and hormones exert regulatory functions. Hormones that have an established role in the regulation include growth hormone (GH), thyroid hormone and sex steroids. GH promotes mainly the growth of the long bones in terms of final height, while the action of the sex steroids and thyroid hormone is less well known. Longitudinal bone growth is the result of chondrocyte proliferation and subsequent endochondral ossification in the epiphyseal growth-plates. The growth-plate is a cartilaginous template that is located between the epiphysis and the metaphysis of the long bones. GH and insulin-like growth factor-I (IGF-I) have different target cells in the epiphyseal growth-plate. GH stimulates the slowly dividing prechondrocytes in the germinative cell layer while IGF-I promotes the clonal expansion in the proliferative cell layer of a GH primed cell. Thyroid hormone blocks the clonal expansion and stimulates chondrocyte maturation. IGF-I mRNA is primarily regulated by GH, and IGF-I is produced in several tissues such as the liver, muscle, fat and epiphyseal growth plates. However, IGF-I mRNA is also increased during compensatory growth of heart and kidneys and by estrogen in the Fallopian tube in the rat. Nutrition, i.e. energy from fat and carbohydrates and proteins, also influences the final height, but the cellular mechanism of action is not known. The aim of this article is to review hormonal action on longitudinal bone growth.

Animals↗

PubMed2006

Differences in biomarkers of type II collagen in atrophic and hypertrophic osteoarthritis of the hip: implications for the differing pathobiologies.

BACKGROUND: Cartilage destruction in osteoarthritis (OA) involves the excessive degradation and increased synthesis of cartilage matrix macromolecules including type II collagen (CII) and proteoglycans. The lack of osteophytes (atrophic form of OA) has been shown to be a disease severity factor in hip OA. Since osteophyte formation involves endochondral ossification and a cartilage intermediate, atrophic OA may also exhibit differences in cartilage turnover compared to hypertrophic OA. Cartilage serum biomarkers may offer an opportunity to identify such differences in patients. AIM: To determine whether serum levels of cartilage biomarkers can distinguish between the presence and absence of osteophyte formation in patients with atrophic and hypertrophic hip OA. PATIENTS AND METHODS: Fifty-six patients (mean age/standard deviation (SD): 62/11; mean body mass index (BMI)/SD: 27/11) with symptomatic hip OA (American College of Rheumatology criteria; mean Lequesne index/SD: 8.3/4) were classified as having an atrophic or hypertrophic form of OA, according to the absence or presence, respectively, of any osteophyte on a standard radiograph of the pelvis. Minimum joint space width (minJSW) and angles of dysplasia [centre-edge (CE) and head-neck-shaft (HNS)] were determined by computerized measurements. The following serum markers were used which are commercial kits from Ibex Diagnostics (Montreal, QC): proteoglycan aggrecans turnover: CS 846; CII synthesis: C-propeptide (CPII), cleavage by collagenase of type II (C2C) and type I and II (C1,2C) collagens. STATISTICS: Patients with atrophic and hypertrophic OA were compared for each variable and step to step logistic regression was used to determine the effect of variables on the belonging to each group. Correlations were examined using linear regression or Spearman test. RESULTS: CPII serum levels were significantly lower in the atrophic OA patients (77.3 vs 117.4 ng/mL). There were no significant differences between groups for C2C, C1,2C and CS 846 . CPII and C2C concentrations were highly correlated in hypertrophic OA (P=0.002) but not in atrophic OA (P=0.8). CONCLUSION: Atrophic hip OA is characterized by reduced synthetic activity involving type II collagen synthesis. This could account in part for the absence of osteophyte formation. The highly significant correlation between CPII and C2C in hypertrophic but not in atrophic OA suggests that the physiological coupling between CII formation and degradation may be lost in atrophic OA. These differences may therefore help explain the absence of osteophyte in atrophic OA and its association with more rapid disease progression.

Adult↗