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PubMed2004

Family 2 cystatins inhibit osteoclast-mediated bone resorption in calvarial bone explants.

Osteoclastic bone resorption depends on the activity of various proteolytic enzymes, in particular those belonging to the group of cysteine proteinases. Biochemical studies have shown that cystatins, naturally occurring inhibitors of these enzymes, inhibit bone matrix degradation. Since the mechanism by which cystatins exert this inhibitory effect is not completely resolved yet, we studied the effect of cystatins on bone resorption microscopically and by Ca-release measurements. Calvarial bone explants were cultured in the presence or absence of family 2 cystatins and processed for light and electron microscopic analysis, and the culture media were analyzed for calcium release. Both egg white cystatin and human cystatin C decreased calcium release into the medium significantly. Microscopic analyses of the bone explants demonstrated that in the presence of either inhibitor, a high percentage of osteoclasts was associated with demineralized non-degraded bone matrix. Following a 24-h incubation in the presence of cystatin C, 41% of the cells were adjacent to areas of demineralized non-degraded bone matrix, whereas in controls, this was only 6%. If bone explants were cultured with both PTH and cystatin C, 60% of the osteoclasts were associated with demineralized non-degraded bone matrix, compared to 27% for bones treated with PTH only (P < 0.01). Our study provides evidence that cystatins, the naturally occurring inhibitors of cysteine proteinases, reversibly inhibit bone matrix degradation in the resorption lacunae adjacent to osteoclasts. These findings suggest the involvement of cystatins in the modulation of osteoclastic bone degradation.

Animals↗
PubMed1980

An electron microscopic study of attachments between periodontal fibers and bone during alveolar remodeling.

Three types of periodontal membrane-to-bone attachments are described for remodeling surfaces of the bony alveolar wall. An adhesive type, which is the most widespread means for tooth anchorage on resorptive bone surfaces during active tooth movements, involves the following histogenic steps: A layer of ground substance is first deposited by fibroblast-like cells on the naked surface of recently resorbed bone. As this continues, new precollagen and the dissociated ends of collagenous fibrils become embedded in the accumulating ground substance, and these fibrils in turn become joined to intact collagenous fibrils, blending with the remainder of the periodontal stroma. Such adhesive attachments continuously form and re-form as the resorption front proceeds. A continuous type of attachment also occurs on resorptive bone surfaces in which some (not all) bone matrix fibrils survive the resorptive process. These former bone fibrils become incorporated into the periodontal membrane and are continuous between the bone matrix and the stroma of the contiguous periodontal membrane. An intermediate type of attachment also occurs and is primarily an adhesive attachment that also contains a scattering of fibrils which are continuous from the bone matrix across the resorptive bone surface into the fibrous matrix of the periodontal membrane.

Alveolar Process↗
PubMed1998

Reversing the inhibitory effect of nicotine on spinal fusion using an osteoinductive protein extract.

STUDY DESIGN: The effect on spinal fusion of an osteoinductive bone protein extract in the presence of a known inhibitor of spinal fusion (systemic nicotine) was studied prospectively in an animal model of posterolateral lumbar fusion. OBJECTIVES: To evaluate the ability of a bovine-derived osteoinductive bone protein extract to overcome the inhibitory effect of nicotine in a rabbit spine fusion model. SUMMARY OF BACKGROUND DATA: Multiple studies have demonstrated the ability of a variety of osteoinductive growth factors to serve as a bone graft substitute for lumbar spinal fusion under "normal" healing conditions. METHODS: Forty-eight adult female New Zealand white rabbits underwent spine arthrodesis at L5-L6 while receiving systemic nicotine through a subcutaneous miniosmotic pump. Arthrodesis was performed using one of the following three graft materials: 1) autogenous iliac crest, 2) osteoinductive bone protein delivered in an allogeneic demineralized bone matrix/ collagen carrier, or 3) osteoinductive bone protein delivered with autogenous iliac crest. Fusions were assessed by blinded manual palpation, radiography, and biomechanical testing. RESULTS: Of the 44 rabbits manually tested by blinded observers, all 14 in the osteoinductive bone protein plus autogenous iliac crest bone group had solid fusions (14 of 14), whereas the fusion rate was less in the osteoinductive bone protein plus demineralized bone matrix group (nine of 14, 64%; P = 0.02), and there were no fusions in the autogenous iliac crest only group (0 of 16, 0%; P = 0.000001). The use of osteoinductive bone protein with autogenous bone produced stronger and stiffer fusions compared with those using autogenous bone alone or osteoinductive bone protein with allograft bone. CONCLUSIONS: Cigarette smoking and nicotine are inhibitory factors in the healing of fractures and spine fusions. This study shows that the inhibitory effect of nicotine can be overcome with an osteoinductive bone growth factor in an animal model.

Animals↗
PubMed1981

Isolated skeletal involvement in Cushing's syndrome: response to therapy.

A 38-yr-old male presented with severe symptomatic osteopenia secondary to adrenal hyperfunction without any clinical expression of Cushing's syndrome. The predominantly axial distribution of his osteopenia and the presence of rib fractures healing with abundant callus formation, despite insignificant elevations in serum alkaline phosphatase, were characteristic of glucocorticoid excess syndromes. The histological features of the pretreatment bone biopsy were typical of those associated with excess glucocorticoids, namely decreased quantities of nonmineralized bone matrix, reflecting sites of bone formation, and an increase in the number of osteoclasts, indicating enhanced bone resorption. Six weeks after adrenalectomy, repeat bone biopsy revealed a marked increase in bone matrix synthesis and a significant decrease in bone resorption. These observations suggest that stimulators of skeletal turnover, like sodium fluoride, may be inappropriate in the initial treatment of steroid-induced osteopenia after surgical cure and that vitamin D and calcium therapy offers a more rational approach. Furthermore, the importance of the routine evaluation of adrenal function in any patient presenting with osteopenia is stressed, as well as the fact that relatively isolated skeletal involvement, classically described in micronodular adrenal disease, is not necessarily peculiar to a specific subset of the syndrome but may potentially attend any cause of glucocorticoid excess.

Adrenal Cortex Function Tests↗
PubMed2001

Cellular and molecular basis of fibrous dysplasia.

Recent advances have been made in the cellular and molecular mechanisms involved in monostotic and polyostotic fibrous dysplasia, a rare nonmalignant disease causing bone deformations and fractures. The molecular basis of fibrous dysplasia has been clarified when mutations affecting the stimulatory alpha subunit of G protein (Gs) have been found in dysplastic bone lesions. The histological analysis of dysplastic lesions revealed that the mutations in Gsalpha caused abnormalities in cells of the osteoblastic lineage and therefore in the bone matrix. Further in vitro analyses of bone cells from mutant dysplastic bone lesions revealed that the abnormal deposition of immature bone matrix in fibrous dysplasia results from decreased differentiation and increased proliferation of osteoblastic cells. Finally, the signaling pathway involved in these osteoblastic abnormalities has been identified. It is now apparent that the constitutive elevation in cAMP level induced by the Gsalpha mutations leads to alterations in the expression of several target genes whose promoters contain cAMP-responsive elements, such as c-fos, c-jun, Il-6 and Il-11. This in turn affects the transcription and expression of downstream genes and results in the alterations of osteoblast recruitment and function in dysplastic bone lesions. These mechanisms provide a cellular and molecular basis for the alterations in bone cells and bone matrix in fibrous dysplasia.

Adenylyl Cyclases↗
PubMed1999

The effect of regional gene therapy with bone morphogenetic protein-2-producing bone-marrow cells on the repair of segmental femoral defects in rats.

BACKGROUND: Recombinant human bone morphogenetic proteins (rhBMPs) can induce bone formation, but the inability to identify an ideal delivery system limits their clinical application. We used ex vivo adenoviral gene transfer to create BMP-2-producing bone-marrow cells, which allow delivery of the BMP-2 to a specific anatomical site. The autologous BMP-2-producing bone-marrow cells then were used to heal a critical-sized femoral segmental defect in syngeneic rats. METHODS: Femoral defects in five groups of rats were filled with 5 x 10(6) BMP-2-producing bone-marrow cells, created through adenoviral gene transfer (twenty-four femora, Group I); twenty micrograms of rhBMP-2 (sixteen femora, Group II); 5 x 10(6) beta-galactosidase-producing rat-bone-marrow cells, created through adenoviral gene transfer of the lacZ gene (twelve femora, Group III); 5 x 10(6) uninfected rat-bone-marrow cells (ten femora, Group IV); or guanidine hydrochloride-extracted demineralized bone matrix only (ten femora, Group V). Guanidine hydrochloride-extracted demineralized bone matrix served as a substrate in all experimental groups. Specimens that were removed two months postoperatively underwent histological and histomorphometric analysis as well as biomechanical testing. RESULTS: Twenty-two of the twenty-four defects in Group I (BMP-2-producing bone-marrow cells) and all sixteen defects in Group II (rhBMP-2) had healed radiographically at two months postoperatively compared with only one of the thirty-two defects in the three control groups (beta-galactosidase-producing rat-bone-marrow cells, uninfected rat-bone-marrow cells, and guanidine hydrochloride-extracted demineralized bone matrix alone). Histological analysis of the specimens revealed that defects that had received BMP-2-producing bone-marrow cells (Group I) were filled with coarse trabecular bone at two months postoperatively, whereas in those that had received rhBMP-2 (Group II) the bone was thin and lace-like. Defects that had been treated with bone-marrow cells producing beta-galactosidase (Group III), uninfected bone-marrow cells (Group IV), or guanidine hydrochloride-extracted demineralized bone matrix only (Group V) demonstrated little or no bone formation. Histomorphometric analysis revealed a significantly greater total area of bone formation in the defects treated with the BMP-2-producing bone-marrow cells than in those treated with the rhBMP-2 (p = 0.036). Biomechanical testing demonstrated no significant differences, with the numbers available, between the healed femora that had received BMP-2-producing bone-marrow cells and the untreated (control) femora with respect to ultimate torque to failure or energy to failure. CONCLUSIONS: This study demonstrated that BMP-2-producing bone-marrow cells created by means of adenoviral gene transfer produce sufficient protein to heal a segmental femoral defect. We also established the feasibility of ex vivo gene transfer with the use of biologically acute autologous short-term cultures of bone-marrow cells.

Animals↗
PubMed2004

Appearance of electron-dense segments: indication of possible conformational changes of pre-mineralizing collagen fibrils in the osteoid of rat bones.

To elucidate precise mechanisms of appositional mineralization of bone, structural features of mineralizing collagen fibrils of the osteoid in normal and hypocalcaemic rats were examined in detail by transmission electron microscopy. Ultrathin sections of the osteoid of various types of bones of the rats fed with regular or normal calcium diet often displayed electrondense segments in the specific regions of the collagen fibrils located immediately adjacent to the mineralization front or to the mineralization nodules. Such dense segments appeared only after Ur-Pb staining and were more distinct in undecalcified specimens. Dense segments were undetectable in ultrathin sections picked up on ethylene glycol instead of water in the trough, even after Ur-Pb staining. Collagen fibrils in the widened osteoid of hypocalcaemic rats fed with calcium-free diet failed to show electron-dense segments. A careful comparison between the hydrously or anhydrously processed adjacent sections of a normal rat bone indicated a drastic dissolution of electron-dense material from the bone matrix near the mineralization front in hydrously processed sections and, thus, implicated the presence of labile mineral-matrix complexes in the recently mineralized bone matrix. Such labile sediments were readily dissociated within the ultrathin sections while the sections were floating on water and immediately adsorbed onto the pre-mineralizing collagen fibrils, where some conformational changes might have occurred. These data indicate that highly electron-dense segments appearing in the osteoidal collagen fibrils are a type of process-induced product, which indirectly represent possible structural alterations in the segmental portions of pre-mineralizing collagen fibrils in the osteoid of rat bones.

Animals↗
PubMed2000

Molecular mechanisms of tumor-bone interactions in osteolytic metastases.

In patients with advanced disease, several cancer types frequently metastasize to the skeleton, where they cause bone destruction. Osteolytic metastases are incurable and cause pain, hypercalcemia, fracture, and nerve compression syndromes. It was proposed over a century ago that certain cancers, such as that of the breast, preferentially metastasize to the favorable microenvironment provided by bone. Bone matrix is a rich store of immobilized growth factors that are released during bone resorption. Histological analysis of osteolytic bone metastases indicates that the bone destruction is mediated by the osteoclast rather than directly by the tumor cells. These observations suggest a vicious cycle driving the formation of osteolytic metastases: tumor cells secrete factors stimulating osteoclasts through adjacent bone marrow stromal cells; osteoclastic resorption in turn releases growth factors from the bone matrix; finally, locally released growth factors activate the tumor cells. This vicious cycle model has now been confirmed at the molecular level. In particular, transforming growth factor beta (TGF3beta) is abundant in bone matrix and released as a consequence of osteoclastic bone resorption. Bone-derived TGFbeta plays an integral role in promoting the development and progression of osteolytic bone metastases by inducing tumor production of parathyroid hormone-related protein (PTHrP), a known stimulator of osteoclastic bone resorption. In breast cancer cells TGFbeta appears to stimulate PTHrP secretion by a posttranscriptional mechanism through both Smad and p38 mitogen activated protein (MAP) kinase signaling pathways. Osteolytic metastases can be suppressed in vivo by inhibition of bone resorption, blockade of TGFbeta signaling in tumor cells, and by neutralization of PTHrP. Other factors released from bone matrix may also act on tumor cells in bone, which in turn may produce other factors that stimulate bone resorption, following the vicious cycle paradigm established for TGFbeta and PTHrP. An understanding at the molecular level of the mechanisms of osteolytic metastasis will result in more effective therapies for this devastating complication of cancer.

Bone Neoplasms↗
PubMed1997

Transglutaminase-catalyzed cross-linking of osteopontin is inhibited by osteocalcin.

Osteocalcin, the most abundant noncollagenous protein of bone matrix, has been demonstrated to inhibit bone growth by gene knockout experiments (Ducy, P., Desbois, C., Boyce, B., Pinero, G., Story, B., Dunstan, C., Smith, E., Bonadio, J., Goldstein, S., Gundberg, C., Bradley, A., and Karsenty, G. (1996) Nature 382, 448-452). Its specific functional mechanism in bone metabolism is, however, largely unknown. In this study, we provide evidence that osteocalcin has an inhibitory effect on tissue transglutaminase activity, as measured by cross-linking of osteopontin, another bone matrix protein. Using a set of synthetic peptides, we found that the inhibitory activity resided within the first 13 N-terminal amino acid residues of osteocalcin. An N-terminal peptide also inhibited cross-linking of another tissue transglutaminase substrate, beta-casein. The inhibitory peptide was shown to have affinity for the substrates of transglutaminase rather than for the enzyme. Since the N terminus of osteocalcin exhibits homology to the substrate recognition site sequences of two transglutaminases, we conclude that the inhibitory effect is most likely due to competition with the enzyme for the transglutaminase-binding region of the substrates, osteopontin and beta-casein, which prevents access of the enzyme to them to perform its function. The interference of osteocalcin with osteopontin cross-linking gives osteocalcin a new potential function as the first protein inhibitor of tissue transglutaminase. This suggests a specific role and a plausible mechanism for it as a modulator of maturation, stabilization, and calcification of bone matrix.

Amino Acid Sequence↗
PubMed1994

Abnormalities of phosphoprotein gene expression in three osteopetrotic rat mutations: elevated mRNA transcripts, protein synthesis, and accumulation in bone of mutant animals.

Osteoclast abnormalities that characterize osteopetrosis, a disorder of bone resorption, may derive from aberrant signals from the osteoblast or the bone matrix. In the present studies, both synthesis and the bone matrix content of the major bone phosphoprotein component, osteopontin, were found to be elevated in three osteopetrotic rat mutations (ia, op, and tl). In whole bone, a twofold increase in the content of the characteristic amino acid O-phosphoserine for osteopontin occurred in op and tl mutant long bone, but a smaller (15%) and more variable increase was observed in ia mutant rat long bone. Extraction of the bone matrix components and partial purification by reverse phase chromatography showed a twofold increase in a phosphoprotein fraction relative to other noncollagenous components. Amino acid analysis and staining characteristics of SDS-PAGE fractionated proteins indicated this to be osteopontin. Organ cultures of calvarial bone from 4 day ia osteopetrotic mutant and normal rats in the presence of 3H-proline showed increased synthesis of this 60 kD protein, which was stimulated by vitamin D. Preparation of total cellular RNA from bone of 2- and 6-week-old mutants and normal rats supported increased synthesis of osteopontin as reflected by hybridization with osteopontin cDNA probe, showing significantly higher levels of mRNA transcripts in ia (3-5 fold), tl (1.4-2 fold), and op (6-25 fold) mutant bone compared to normal littermates. The changes in osteopontin mRNA levels in mutant bone were also examined in relation to other growth and phenotype-expressed genes. The findings of increased accumulation of osteopontin in osteopetrotic bone and increased synthesis by osteoblasts are interesting in light of the previously reported decrease in bone osteocalcin content (Endocrinology, 126:966, 1990), confirmed here by decreased osteocalcin mRNA transcripts. Such aberrations in the composition of skeletal extracellular matrix could be a reflection of or a contributing factor to the osteoclast abnormalities of some of these osteopetrotic disorders.

Animals↗
PubMed1981

Heterotopic induction of osteogenesis in mice lethally irradiated and repopulated with syngeneic bone marrow cells.

Decalcified rat bone matrix or sequentially treated rat bone gelatin, as well as dog transitional epithelium when implanted intramuscularly in mice induce cartilage, bone and bone marrow formation. Heterotopic bone induction is markedly reduced or abolished when animals are irradiated prior to implantation of decalcified bone matrix or transitional epithelium. Repopulation of lethally irradiated mice with syngeneic bone marrow cells restores the osteoinductive competence, suggesting that responding cells in bone induction system are derived, or connected with, bone marrow cells.

Animals↗
PubMed1995

Commercially-prepared allograft material has biological activity in vitro.

The well-established finding that implantation of demineralized bone matrix at non-skeletal sites results in formation of cartilage and bone has been attributed to bone morphogenetic proteins/factors. Commercially-available demineralized bone allograft materials are being used currently to reconstruct/regenerate bone. The studies described here focused on establishing biological activity of protein extracts prepared from commercially obtained bone graft material in vitro. Furthermore, the biological activity of these protein extracts in vitro was compared with similar extracts prepared from freshly obtained human bone. Biological activities of bone matrix proteins examined included their ability to promote proliferation, attachment, and migration of gingival fibroblasts using an in vitro system. Guanidine followed by guanidine/EDTA was used to separate bone matrix proteins into proteins associated with soft tissues of bone and proteins retained within the mineral compartment, respectively. Two preparations of each starting material were tested and the biological activity of each preparation was evaluated in triplicate at least three times. Slot blot analysis revealed that commercially-prepared material contained type I collagen; fibronectin; BSP; and BMP-2, 4, and 7. However, the freshly prepared bone extracts appeared to have higher BMP concentrations. The ability of commercial extracts to promote cell proliferation, while significant, was limited and significantly less when compared with similar extracts prepared from freshly obtained bone. All extracts promoted cell attachment significantly, while none of the extracts promoted cell migration. Thus, commercially-prepared material retained proteins having the capacity to influence cell behavior in vivo. However, some biological activity as measured in vitro was lost as a result of tissue processing.

Blotting, Western↗
PubMed2002

[Application of decalcified dental matrix in bone reparation].

OBJECTIVE: To investigate the effect of decalicified dental matrix (DDM) on healing of traumatic fracture and its side-effect. METHODS: From June 1997 to December 1998, 42 patients with closed traumatic long bone fracture (36 males and 6 females, aged from 18 to 57 years with an average of 32 years) were divided into two groups randomly; open reduction and internal fixation were carried out in all patients, but the DDM was used only in experimental group. After operation, the body temperature, ALT, and bone union time were observed and recorded. RESULTS: Following-up 1 to 3 years, the bone union time of experimental group was significantly shorter than that of control group (P < 0.01), there was no significant difference in the temperature and ALT changes between two groups(P > 0.05). No infection occurred. CONCLUSION: DDM can promote the growth of bony callus and enhance the healing of fracture. There is no side-effect.

Adolescent↗
PubMed2005

Surgical treatment of the painful motion segment: matching technology with indications.

STUDY DESIGN: Literature review of current bone graft technology and bone graft substitutes used in spinal fusion applications. OBJECTIVE: We reviewed current bone graft technologies and identified the range of bioactive properties that each possesses, such as osteoconductivity, osteoinductivity, and structural, load-bearing capabilities that can be used to either augment or replace autogenous bone graft in spinal fusions. SUMMARY OF BACKGROUND DATA: Bioactive materials are used in spinal fusion applications to encourage bone formation across an intervertebral motion segment. To be an effective replacement for autogenous bone grafts, a bioactive material must possess the properties of osteoinduction and osteoconduction. METHODS: Literature review. RESULTS: Platelet gel concentrates deliver nonspecific cytokines that influence local cells at the implantation site. Demineralized bone matrix acts as a bone graft enhancer that excludes fibrous tissue of muscle interposition in a fusion mass and is a mildly osteoinductive material. Bone morphogenetic proteins are an integral part of natural bone formation response. They function as differentiation factors that act on mesenchymal stem cells to induce bone formation. CONCLUSIONS: Patient-derived therapies such as platelet gel concentrates contain cytokines that play a role in bone formation; however, none of them is capable of inducing the entire bone formation cascade. Clinical use of these concentrates could possibly interfere with new bone formation. The use of bone marrow aspiration and concentration techniques has not been convincingly studied in spinal fusions in lower order animal or human clinical studies. Demineralized bone matrix contains small and variable amounts of naturally occurring bone morphogenetic proteins. These products can only function as bone graft extenders. Recombinant bone morphogenetic protein products contain much more highly concentrated and focused amounts of bone morphogenetic proteins, and some have been shown to be clinically effective bone graft replacements.

Back Pain↗
PubMed1978

Osteogenesis and chondrogenesis in transplants of Dunn and Ridgway osteosarcoma cell cultures.

Dunn osteosarcomas synthesize 2 times more alkaline phosphatase than do Ridgeway osteosarcomas, 3 times more than do HeLa cells, and 4 to 5 times more than do rat or mouse fibroblast cell cultures. Implants of killed freeze-dried Dunn cell cultures into the thigh muscles are resorbed and replaced by normal cartilage, bone, and bone marrow tissue, while implants of freeze-dried Ridgeway cells are resorbed and replaced by fibrous tissue only. Outgrowths of normal muscle septum connective tissue cells onto the stroma of Ridgeway tumors differentiate into fibrous tissue. Cultures of either tumor on a substratum of bone matrix stroma prepared from normal bone proliferate, assume a spherical shape, and perpetuate the transformed osteoblast-like cell without forming attachments or adapting to the contour of the substratum. Outgrwoths of muscle mesenchymal cells on the Dunn tumor stroma differentiate into cartilage. Dunn osteosarcoma cell cultures proliferate on the inside and produce deposits of normal bone (not tumorous bone) on the outside of diffusion chambers. Killed freeze-dried cell cultures produce transfilter deposits of normal bone and bone marrow, but the quantity is significantly lower. On a substratum of cellulose acetate, outgrowths of muscle connective tissue will differentiate into cartilage when cell-free Dunn stroma is present under the organ culture grid. Tumorigenesis and normal cartilage and bone morphodifferentiation are antithetic, but tumor cells transfer a bone morphogen similar to the bone morphogenetic protein (BMP) of normal bone matrix. BMP recruits mesenchymal cells to proliferate and differentiate into cartilage and bone.

Alkaline Phosphatase↗
PubMed2000

Clinical applications of composite intramembranous bone grafts.

The aim of this article is to introduce the composite intramembranous bone graft mixed with demineralized bone matrix to the clinician and to demonstrate its various clinical applications in the field of clinical orthodontics in the form of case reports. Understanding the mechanism of healing of this composite bone graft provides sound experimental precedent that allows this graft material to become a predictable part of our future orthodontic management. The cases highlighted here took advantage of the several properties of the composite intramembranous demineralized bone matrix graft. An accidental loss of the buccal plate of bone occurred during extraction of a buccally placed premolar for orthodontic purposes. The defect was repaired using chin bone mixed with demineralized bone matrix, and the teeth were successfully moved into the grafted area. A 5-year follow-up showed a stable gingival condition at the grafted area. In this report, ridge augmentation with intramembranous demineralized bone matrix as an adjunct to orthodontic treatment allowed successful placement of endosseous implants. In conclusion, the same graft material was successfully used in the repair of a massive alveolar cleft. Long-term follow-up of these cases showed that this graft is a promising graft material that could be integrated into our orthodontic practice.

Adult↗
PubMed1976

Collagenous bone matrix-induced endochondral ossification hemopoiesis.

Transplantation of collagenous matrix from the rat diaphyseal bone to subcutaneous sites resulted in new bone formation by an endochondral sequence. Functional bone marrow develops within the newly formed ossicle. On day 1, the implanted matrix was a discrete conglomerate with fibrin clot and polymorphonuclear leukocytes. By day 3, the leukocytes disappeared, and this event was followed by migration and close apposition of fibroblast cell surface to the collagenous matrix. This initial matrix-membrane interaction culminated in differentiation of fibroblasts to chondroblasts and osteoblasts. The calcification of the hypertrophied chondrocytes and new bone formation were correlated with increased alkaline phosphatase activity and 45Ca incorporation. The ingrowth of capillaries on day 9 resulted in chondrolysis and osteogenesis. Further remodelling of bony trabeculae by osteoclasts resulted in an ossicle of cancellous bone. This was followed by emergence of extravascular islands of hemocytoblasts and their differentiation into functional bone marrow with erythropoietic and granulopoietic elements and megakaryocytes in the ossicle. The onset and maintenance of erythropoiesis in the induced bone marrow were monitored by 59Fe incorporation into protein-bound heme. These findings imply a role for extracellular collagenous matrix in cell differentiation.

Alkaline Phosphatase↗
PubMed1992

Radiopharmaceuticals for palliation of metastatic osseous lesions: biologic and physical background.

The intimate admixing of bone matrix and bone marrow is a central point in devising therapy of metastatic lesions. Since specific modalities are not yet available for destroying the malignant cells, treatment is usually palliative. The use of stable gallium (Ga-nitrate) and of a diphosphonate (aminohydroxypropylidine diphosphonate disodium) as osteoclast inhibitors is discussed. The marrow, as well as the matrix, can be affected by external radiation. This is also true with bone-seeking radiopharmaceuticals. There is no ideal radiopharmaceutical available for treating metastases in bone, but the characteristics of several presently available (or proposed) are discussed, and possible use of tumor radiation sensitizers or bone marrow protectors is mentioned. Difficulties are also encountered in calculating accurate dosimetry. Clinical experience is needed to determine a reasonable optimal dose with any particular radiopharmaceutical for relief of pain with low bone marrow toxicity.

Bone Neoplasms↗