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Results for “Bone Demineralization, Pathologic”

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294 records · Page 17Linked to original sources

PubMed1997

Recurrence of mandibular molar furcation defects following citric acid root treatment and coronally advanced flap procedures.

This report concerns long-term (4 to 5 years) clinical evaluation of 22 resolved (complete bone closure) mandibular Class 2 furcation defects following coronally advanced flap procedures and citric acid root treatment with or without adjunctive implantation of freeze-dried, demineralized allogeneic bone. Sixteen buccal furcation sites in 12 patients were available for the follow-up evaluation. The furcation involvement was independently evaluated by a panel of three examiners, each using three furcation index systems. Oral hygiene standards, gingival health, probing depth, clinical attachment level, gingival recession, tooth vitality, and detectable caries or root resorption were also recorded. Mean attachment level at the furcation sites was 5.8 +/- 2.9 mm, compared to 4.5 +/- 2.2 mm and 3.5 +/- 1.3 mm over the prominence of the mesial and distal roots, respectively. The clinical examination further revealed that 12 out of 16 sites exhibited recurrent Class 2 furcation involvement. Of the 16 teeth examined, one had received endodontic treatment, while the remaining 15 responded within the normal range to pulp testing. One tooth had developed caries in the furcation region. No teeth demonstrated periradicular pathology. The results of this study question the long-term stability of furcation bone regeneration following coronally advanced flap procedures.

Bone Transplantation↗

PubMed1994

Bone tissue composition: biochemical anatomy of bone.

Bone is chemically built up as a mineralized matrix which comprises collagen and a small amount of noncollagenous proteins. This paper points out some useful methods to evaluate the bone composition. Demineralizing extraction of bone powder with EDTA allows the determination of matrix size and degree of extractability. These parameters vary with bone type, anatomical site of the bone, disease, species, and drug treatment. The study of bone particles in situ can be done by separation of bone powder according to their density. A shift of the bone particles to higher density fractions reflects an increased amount of older, more mineralized osteons in the bone with its consequences on the mechanical competence of the bone. Quantity and quality of bone matrix mineralization are related to bone cell activity which can be studied indirectly by further exploration of the composition of the bone matrix. Many noncollagenous proteins are buried in the extracellular bone matrix from where they can be released when bone is resorbed. These proteins can then act on bone cells in an autocrine or paracrine manner. Altered concentrations of noncollagenous proteins in bone matrix are described in three pathological conditions associated with changes in other bone properties: osteoarthritis, osteopenia, and osteogenesis imperfecta. The functional significance and origin of these changes will have to be subjected to further study.

Animals↗

PubMed1995

A missense mutation (I278T) in the cystathionine beta-synthase gene prevalent in pyridoxine-responsive homocystinuria and associated with mild clinical phenotype.

Cystathionine beta-synthase (CBS) deficiency is an autosomal recessive disorder characterized by homocystinuria and multisystem clinical disease. Patients responsive to pyridoxine usually have a milder clinical phenotype than do nonresponsive patients, and we studied the molecular pathology of this disorder in an attempt to understand the molecular basis of the clinical variation. We previously reported a T833C transition in exon 8 causing a substitution of threonine for isoleucine at codon 278 (I278T). By PCR amplification and sequencing of exon 8 from genomic DNA we have now detected the I278T mutation in 7 of 11 patients with in vivo pyridoxine responsiveness and in 0 of 27 pyridoxine-nonresponsive patients. Two pyridoxine-responsive patients are homozygous and five are heterozygous for I278T. We have now observed the I278T mutation in 41% (9 of 22) of the independent alleles in pyridoxine-responsive patients of varied ethnic backgrounds. In two of the compound heterozygotes we identified a novel mutation (G139R and E144K) in the other allele. The finding that the two patients who are homozygous for I278T have only ectopia lentis and mild bone demineralization suggests that this mutation is associated with both in vivo pyridoxine responsiveness and mild clinical disease. Compound heterozygous patients who have one copy of this missense mutation are likely to retain some degree of pyridoxine responsiveness.

Adult↗

PubMed1992

The healing of segmental bone defects, induced by recombinant human bone morphogenetic protein (rhBMP-2). A radiographic, histological, and biomechanical study in rats.

Subcutaneous implants of a recombinant human form of the bone-inducing protein rhBMP-2 (recombinant human bone morphogenetic protein-2) in rats have resulted in the local induction of endochondral bone formation. To test the osteoinductive activity of rhBMP-2 in an osseous location, we created five-millimeter segmental defects in the femora of forty-five adult male Sprague-Dawley rats. Two doses of lyophilized rhBMP-2 (1.4 or 11.0 micrograms) were implanted in each defect, together with guanidine-hydrochloride extracted demineralized rat-bone matrix as a carrier, and the results were compared with those in rats that had implantation of guanidine-hydrochloride extracted demineralized rat-bone matrix only. The formation and healing of bone were determined by radiographic, histological, and mechanical analysis. Both doses of rhBMP-2 induced formation of endochondral bone in the osseous defects in a dose-related manner. Implantation of 11.0 micrograms of rhBMP-2 yielded significant (p less than 0.05) bone formation, resulting in radiographic, histological, and mechanical evidence of union. Despite new-bone formation in the defects that had received 1.4 micrograms of rhBMP-2, no instances of union were observed.

Animals↗

PubMed2003

Quantification of tartrate resistant acid phosphatase distribution in mouse tibiae using image analysis.

Tartrate resistant acid phosphatase (TRAP) activity of bone is a suitable biochemical marker for osteoclastic bone resorption. Qualitatively, the histochemical distribution of TRAP has been used to identify osteoclasts responsible for bone resorption; however, there have been few attempts to quantify TRAP localization. We describe a method for evaluating bone resorption by quantifying area percentages of positive TRAP localization using image analysis. Mouse tibiae were paraffin embedded following demineralization in disodium ethylenediamine tetraacetic acid. Longitudinal sections of tibia were cut from 15 levels in the left and the right limbs of six mice (180 sections total) and stained for TRAP distribution. Positive TRAP localization was quantified by pixel area count and reported as a percentage of the total tissue area specified. The 1.85 mm2 region of interest was placed at the midpoint of the epiphyseal growth plate containing the provisional calcification layer and the primary spongiosa, while excluding cortical bone of each mouse tibia. The percentage of TRAP localization ranged from 0.95 to 1.31% and was not significantly different from level to level or limb to limb in each mouse (p > 0.100). Within the same region of interest, an osteoclast count along the bone perimeter also was performed. We demonstrated a strong correlation (r2 = 0.903) between the conventional histomorphometric osteoclast index and positive TRAP localization, validating the latter as an alternative method to assess bone resorption. Quantitative analysis of TRAP is significant because it allows statistical comparisons between treatment groups, promotes precise pathological diagnoses and facilitates a reference data base that may aid the study of bone related diseases involving increased bone resorption.

Acid Phosphatase↗

PubMed1992

[Fracture of the upper extremity of the femur in elderly women: respective role of fall and bone demineralization].

Fractures of the proximal femur in elderly individuals are becoming increasingly common in the industrialized world and represent a heavy burden in both socioeconomic and human terms. Two factors are key to the pathophysiology of these fractures: falls and decreased bone strength due to osteoporosis. Femoral and vertebral bone density was measured in 40 elderly women (83 +/- 5 years) who experienced a fall; in those who developed a femoral fracture as a result of the fall, femoral bone density was lower by 12 to 21% (z score: -0.7 to -1.04) than in those with no fracture, after adjustment for age, height and weight. Femoral neck and trochanteric area measurements had the best predictive value (area under the RoC curve: 75% +/- 8%). These was no difference by anatomic fracture type (neck or trochanter). Patients with pertrochanteric fractures had lower vertebral bone densities than controls. These findings, together with recent prospective data, demonstrate that in addition to falls, bone loss (osteoporosis) promotes the occurrence of fractures of the proximal femur in elderly patients. This has important practical implications for the detection and prevention of these fractures.

Accidental Falls↗