Immunolocalization of matrix metalloproteinase-13 on bone surface under osteoclasts in rat tibia

Nakamura, Hiroaki; Sato, Ginga; Hirata, Azumi; Yamamoto, Tetsuro

doi:10.1016/j.bone.2003.09.001

Cited by 65 publications

(59 citation statements)

References 51 publications

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“…Some reports demonstrated that MMP-13 is expressed in the hypertrophic zone, and it is highly effective for cleaving type II collagen (8,13,16). Others have showed MMP-13 synthesis also by osteoclasts (18). In this study, MMP-13 was overexpressed in the most inferior region of the MMP-9 −/− hypertrophic zone at the third postnatal day, which strongly indicates that it partially compensates for MMP-9 deficiency.…”

Section: Discussionsupporting

confidence: 64%

Histochemical aspects of the vascular invasion at the erosion zone of the epiphyseal cartilage in MMP-9-deficient mice

et al. 2013

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We have histologically examined vascular invasion and calcification of the hypertrophic zone during endochondral ossification in matrix metalloproteinase (MMP)-9 deficient (MMP-9 −/− ) mice and in their littermates at 3 days, 3 weeks and 6 weeks after birth. Capillaries and osteoclasts at the chondro-osseous junction showed an intense MMP-9 immunopositivity, suggesting that they recognize chemical properties of cartilaginous matrices, and then release MMP-9 for cartilage degradation. CD31-positive capillaries and tartrate-resistant acid phosphatase-reactive osteoclasts could be found in the close proximity in the region of chondro-osseous junction in MMP-9 −/− mice, while in wild-type mice, vascular invasion preceded osteoclastic migration into the epiphyseal cartilage. Although MMP-9 −/− mice revealed larger hypertrophic zones, the index of calcified area was significantly smaller in MMP-9 −/− mice. Interestingly, the lower layer of the MMP-9 −/− hypertrophic zone showed intense MMP-13 staining, which could not be observed in wild-type mice. This indicates that MMP-13 may compensate for MMP-9 deficiency at that specific region, but not to a point at which the deficiency could be completely rescued. In conclusion, it seems that MMP-9 is the optimal enzyme for cartilage degradation during endochondral ossification by controlling vascular invasion and subsequent osteoclastic migration.Endochondral ossification enables the longitudinal growth of long bones, keeping the balance between chondrocyte proliferation and differentiation (i.e., appositional and interstitial growth) and vascular invasion into cartilage prior to bone deposition (12,27). The length of the hypertrophic zone appears to be maintained by two mechanisms: 1) the rate at which chondrocytes enter the hypertrophic phenotype and 2) the pace at which vascular endothelial cells invade the hypertrophic zone of the cartilage. After the formation of calcified cartilage matrices, the process of endochondral ossification involves a well-defined series of events in which osteogenic and osteoclastic cells replace calcified cartilage for bone (2). At an erosion zone, vascular endothelial cells invade and collapse incompletely-calcified transverse partitions of cartilage matrix, making a way for osteoclastic and osteoblastic migration. On the other hand, the longitudinal intercolumnar septae are

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Section: Discussionsupporting

confidence: 64%

Histochemical aspects of the vascular invasion at the erosion zone of the epiphyseal cartilage in MMP-9-deficient mice

et al. 2013

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“…Biologic factors related to the bone loss may have triggered a response in the tendon substance, directly leading to deterioration of the tendon and decreased suture grasping strength. Although there were no clear differences when examining inflammation in the two groups, it is possible that matrix metalloproteinase levels may have been significantly higher in the delayed group [15]. Further study is necessary to elucidate the link between the bone loss and the decreased mechanical properties of the repair.…”

Section: Discussionmentioning

confidence: 89%

Delayed repair of tendon to bone injuries leads to decreased biomechanical properties and bone loss

et al. 2005

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Introduction. Repair of the torn rotator cuff tendon is a common procedure performed in the shoulder. In the clinical setting, a significant delay between rotator cuff tear and subsequent repair often exists. The purpose of this study was to investigate the biomechanical properties and bone density of the tendon to bone repair site after acute and delayed repair.Methods. The supraspinatus tendons in bilateral shoulders of 60 rats were transected from the bone. In the acute group, the tendons were immediately repaired with suture. In the delayed group, the tendons were allowed to retract and repaired in a second procedure after a 3-week delay. Cross sectional area and biomechanical properties were evaluated. Bone density of the humeral head was assessed using peripheral quantitative computed tomography. Histologic sections were obtained and examined.Results. At 10 days the repair tissue displayed vascular and fibroblast proliferation accompanied by predominantly mononuclear infiltrate. At 28 days the inflammatory process gradually decreased. No significant histologic differences were noted between the acute and delayed repair specimens. Cross-sectional area was higher in the delayed group at the early time points (44% at 10 days and 3 1% at 28 days). Viscoelastic properties were greater in the acute group at the early time points and significantly less at the latest time point, compared to the delayed group. Bone density was markedly decreased (8% and 12%, 28 and 56 days respectively) in the delay group.Discussion. Inferior rotator cuff healing was demonstrated when there was a delay between injury and repair. Viscoelastic properties of the acute repairs were increased compared to the delayed group at 10 days, indicating tendon stiffening during the 3-week delay before repair. Viscoelastic properties of the acute repairs were decreased compared to the delayed group at 56 days indicating deterioration of properties over time in the delayed group. The deterioration in properties in the delayed group coincide with bone density decreases in the greater tuberosity. These results indicate that bone loss may a significant factor in poor healing.

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“…The matrix structure varies in transverse and longitudinal cartilage septa [28] and, worthy of note, matrix mineralization does occur in longitudinal septa of the lower hypertrophic zone, whereas transverse septa are rarely mineralized [29]. Recent studies indicate that perivascular cells degrade unmineralized matrix and transverse septa, whereas osteoclasts are involved in degradation of longitudinal septa and mineralized cartilage [30]. Our data support that degradation of cartilage matrix by both the action of osteoclasts and that of invading capillary sprouts is compromised in rapamycin-treated animals.…”

Section: Discussionmentioning

confidence: 99%

Rapamycin retards growth and causes marked alterations in the growth plate of young rats

et al. 2007

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Rapamycin is a potent immunosuppressant with antitumoral properties widely used in the field of renal transplantation. To test the hypothesis that the antiproliferative and antiangiogenic activity of rapamycin interferes with the normal structure and function of growth plate and impairs longitudinal growth, 4-week-old male rats (n=10/ group) receiving 2 mg/kg per day of intraperitoneal rapamycin (RAPA) or vehicle (C) for 14 days were compared. Rapamycin markedly decreased bone longitudinal growth rate (94±3 vs. 182±3 μm/day), body weight gain (60.2±1.4 vs. 113.6±1.9 g), food intake (227.8±2.6 vs. 287.5±3.4 g), and food efficiency (0.26±0.00 vs. 0.40± 0.01 g/g). Signs of altered cartilage formation such as reduced chondrocyte proliferation (bromodeoxiuridine-labeled cells 32.9±1.4 vs. 45.2±1.1%), disturbed maturation and hypertrophy (height of terminal chondrocytes 26±0 vs. 29±0 μm), and decreased cartilage resorption (18.7±0.5 vs. 31.0±0.8 tartrate-resistant phosphatase alkaline reactive cells per 100 terminal chondrocytes), together with morphological evidence of altered vascular invasion, were seen in the growth plate of RAPA animals. This study indicates that rapamycin can severely impair body growth in fastgrowing rats and distort growth-plate structure and dynamics. These undesirable effects must be kept in mind when rapamycin is administered to children.

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Immunolocalization of matrix metalloproteinase-13 on bone surface under osteoclasts in rat tibia

Cited by 65 publications

References 51 publications

Histochemical aspects of the vascular invasion at the erosion zone of the epiphyseal cartilage in MMP-9-deficient mice

Histochemical aspects of the vascular invasion at the erosion zone of the epiphyseal cartilage in MMP-9-deficient mice

Delayed repair of tendon to bone injuries leads to decreased biomechanical properties and bone loss

Rapamycin retards growth and causes marked alterations in the growth plate of young rats

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