osteolysis/protease

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Protease expression in giant cell tumour of bone: a comparative study on feline and human samples.

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Human giant cell tumour of bone (GCTB) is a rare low grade of malignancy tumour with tendency to recur. During tumourigenesis the bone remodeling balance is subverted by the tumour cellular components that interacting with bone matrix induce release of growth factors and cytokines, promoting cell

Expression of proteases in giant cell lesions of the jaws, tendon sheath and salivary glands.

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BACKGROUND Peripheral giant cell granuloma (GC) of the jaw is a tumour-like lesion, situated on the gingiva. The aim of this study was to: (a) better define the cellular compartments of the lesion and (b) compare the protease expression-profile in GC lesions of the jaws to GC lesions of other

Effects of hydroxyapatite particulate debris on the production of cytokines and proteases in human fibroblasts.

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Cytokines and proteases are secreted by fibroblasts in response to particulate wear debris, and these proteins are felt to play an important role in the development of osteolysis and implant loosening. Although metallic and polyethlyene debris have been studied extensively, little is known about the

Simultaneous labeling of mast cell proteases and protease mRNAs at the bone-implant interface of aseptically loosened hip implants.

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Human mast cells (MC) exhibit two distinct phenotypes based on the protease content of their secretory granules. MC(TC) cells express tryptase, chymase, cathepsin G, and mast cell carboxypeptidase, while MC(T) cells express only tryptase. Both mast cell phenotypes were assessed near regions of

Maspin expression inhibits osteolysis, tumor growth, and angiogenesis in a model of prostate cancer bone metastasis.

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Emerging evidence indicates that tumor-associated proteolytic remodeling of bone matrix may underlie the capacity of tumor cells to colonize and survive in the bone microenvironment. Of particular importance, urokinase-type plasminogen activator (uPA) has been shown to correlate with human prostate

Cathepsin G recruits osteoclast precursors via proteolytic activation of protease-activated receptor-1.

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Metastatic breast cancer shows extreme tropism for the bone microenvironment, leading to the establishment of osteolytic metastases. Perpetuation of tumor-induced osteolysis requires a continuous supply of osteoclast precursors migrating into the bone microenvironment that can subsequently

Cathepsin K is the principal protease in giant cell tumor of bone.

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Giant cell tumor (GCT) of bone is a neoplasm of bone characterized by a localized osteolytic lesion. The nature of GCT is an enigma and the cell type(s) and protease(s) responsible for the extensive localized clinicoradiological osteolysis remain unresolved. We evaluated protease expression and

Cathepsin G enhances mammary tumor-induced osteolysis by generating soluble receptor activator of nuclear factor-kappaB ligand.

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Breast cancer commonly causes osteolytic metastases in bone, a process that is dependent on tumor-stromal interaction. Proteases play an important role in modulating tumor-stromal interactions in a manner that favors tumor establishment and progression. Whereas several studies have examined the role

The USP14-NLRC5 pathway inhibits titanium particle-induced osteolysis in mice by suppressing NF-κB and PI3K/AKT activities.

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Total hip arthroplasty (THA) is a widely used surgical intervention for treating patients with end-stage degenerative and inflammatory osteoarthropathy. However, wear particles from the artificial titanium joint can induce osteolysis, limiting the long-term survivorship of THA. Monocyte/macrophage

Familial pycnodysostosis: identification of a novel mutation in the CTSK gene (cathepsin K).

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BACKGROUND Pycnodysostosis, an autosomal recessive skeletal dysplasia, is characterized by short stature, osteosclerosis, delayed cranial suture closure, hypoplastic mandible, acro-osteolysis, hypoplastic clavicle, and dental anomalies. The disorder is caused by CTSK gene defects, a gene localized

Pycnodysostosis with Multi-Segmental Spinal Canal Stenosis due to Ossification of the Yellow Ligament.

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Pycnodysostosis is an autosomal recessive disorder characterized by osteosclerosis, small stature, acro-osteolysis of the distal phalanges, loss of the mandibular angle, separated cranial sutures with open fontanels, and frequent fractures. One identified cause of the disease is reduced activity of

Sequential Bilateral Rapid Destructive Inflammatory Coxarthrosis in a Patient with Human Immunodeficiency Virus.

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The diagnostic criteria for sequential rapidly destructive coxarthrosis remain unclear and this condition is rarely reported in patients with human immunodeficiency virus (HIV). Here, we report a case of an HIV-infected 73-year old female who experienced hip joint destruction. The patient was

A patient with pycnodysostosis presenting with seizures and porencephalic cysts.

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Pycnodysostosis is a rare autosomal recessive disorder caused by mutations in the cysteine protease Cathepsin K gene located on chromosome 1q21. It has a well characterized skeletal phenotype which include short stature, generalized increased bone density with propensity of fractures, open calvarial

Bone microenvironment modulates expression and activity of cathepsin B in prostate cancer.

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Prostate cancers metastasize to bone leading to osteolysis. Here we assessed proteolysis of DQ-collagen I (a bone matrix protein) and, for comparison, DQ-collagen IV, by living human prostate carcinoma cells in vitro. Both collagens were degraded, and this degradation was reduced by inhibitors of

[Bone hyperresorption in bone metastases].

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MECHANISMS OF BONE LOSS: In patients with bone metastases, bone loss is the consequence of a dissociated process combining excessive bone resorption and inhibited bone formation. This destructive process occurs in response to soluble factors secreted by metastatic cells (PTH-rP, cytokines) which

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