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S D Boden

Publications and source records attributed to S D Boden.

101 records · Page 6Linked to original sources
PubMed1990

Calcium homeostasis.

Precise maintenance of the physiologic levels of both extracellular and intracellular ionized calcium is essential to life. Calcium and phosphate homeostasis is complex, yet three important hormones are responsible for modulating most of the extracellular control of these minerals. Parathyroid hormone acts directly on bone and kidney and indirectly on the intestine to maintain or restore the serum calcium level. The signal for increased PTH synthesis and secretion is a decrease in the serum ionized calcium concentration and a decrease in serum levels of 1,25(OH)2-D. Calcitonin is produced in parafollicular cells of the thyroid and inhibits bone resorption in pharmacologic doses. These cells recognize the calcium signal in a different way. A diminution in serum calcium decreases calcitonin production and release. The role of calcitonin in normal human physiology, however, remains in dispute. Finally, the biologically potent metabolite of vitamin D, 1,25(OH)2-D, stimulates intestinal absorption of calcium and phosphate. It also probably plays a role in the orderly mineralization and resorption of bone and has some influence on renal resorption of filtered calcium and phosphorus. A major stimulus to its production by proximal renal tubule cells is elevated PTH and decreased serum levels of calcium and phosphate. The absence of PTH as well as high serum calcium and phosphate levels can reduce its synthesis and secretion. These three hormones along with other mediators and messengers work in concert to maintain the normal calcium homeostasis. A disturbance at any level in this intricate regulatory network will result in a host of compensatory changes that may lead to clinical disease. A complete understanding of these normal mechanisms is a prerequisite to investigating the etiology and treatment of the various pathologic responses seen with many of the metabolic bone disorders.

Calcitonin↗
PubMed1989

Retinyl acetate-induced arthritis in C3H-A(vy) mice.

Severely impaired musculoskeletal mobility in C3H-A(vy) mice was noted during a pharmacologic trial evaluating the antitumorigenic properties of retinyl acetate (RAc). To determine the etiology of this impairment, we studied 103 female C3H-A(vy) mice that were fed RAc in daily doses of 75-300 micrograms or placebo and were killed after 3-16 months. Whole-body radiographs and histologic sections of the hindlimbs were scored for presence and severity of arthritis. C3H-A(vy) mice treated with RAc in any dose had a significantly higher incidence of arthritis than placebo-treated mice. Histologic evidence of enthesopathic disease closely paralleled the radiographic changes and ranged from small enthesophytes at tendinous and capsular insertions to complete periarticular bony bridging. Articular cartilage was not grossly affected. The incidence and severity of arthritis were significantly correlated with the total dose of RAc administered. The bony metaplasia induced by RAc was similar to the pathologic changes caused by other retinoids. This model may be useful for studying the pathogenesis of periarticular bone formation in diffuse idiopathic skeletal hyperostosis and related syndromes.

Animals↗
PubMed1989

Estrogen receptor mRNA expression in callus during fracture healing in the rat.

Estrogen has profound effects on bone metabolism, yet its precise mechanism of action remains unknown. Several recent investigations have located the estrogen receptor (ER) on osteoblast-like cells, suggesting a potential direct action of estrogen via its own receptor on bone cells. The protective role of estrogen on bone in osteoporosis is well known; however, neither the existence nor the mechanism of an estrogenic role in fracture healing has been well studied. In this investigation we used a modification of polymerase chain reaction (PCR) amplification to detect and quantify ER messenger RNA (mRNA) levels in rat fracture callus previously undetectable by northern analysis. Verification of correctly amplified cDNA fragments was provided by restriction digestion. PCR failed to detect ER mRNA in total RNA extracts from tendon and fibrocartilage. The ER message was present in fracture callus at levels up to 70% of that found in rat uterus, and demonstrated a transient 13-fold increase in transcription by day 14 with return to baseline by day 31 of fracture healing. These data demonstrate that the rat estrogen receptor gene is expressed in fracture callus and suggest that estrogen may play an important role in the normal fracture healing process. In addition, this work adds to the growing body of evidence which supports a possible direct action of estrogen via its receptor on osteogenic cells.

Animals↗
PubMed1989

Precise measurement of vertebral bone density using computed tomography without the use of an external reference phantom.

Bone density measurement by quantitative computed tomography (QCT) commonly uses an external reference phantom to decrease scan-to-scan and scanner-to-scanner variability. However, the peripheral location of these phantoms and other phantom variables is also responsible for a measurable degradation in accuracy and precision. Due to non-uniform artifacts such as beam hardening, scatter, and volume averaging, the ideal reference phantom should be as close to the target tissue as possible. This investigation developed and tested a computer program that uses paraspinal muscle and fat tissue as internal reference standards in an effort to eliminate the need for an external phantom. Because of their proximity, these internal reference tissues can be assumed to reflect more accurately the local changes in the x-ray spectra and scatter distribution at the target tissue. A user interactive computerized histogram plotting technique enabled the derivation of reproducible CT numbers for muscle, fat, and trabecular bone. Preliminary results indicate that the use of internal reference tissues with the histogram technique may improve reproducibility of scan-to-scan measurements as well as inter-scanner precision. Reproducibility studies on 165 images with intentional region-of-interest (ROI) mispositioning of 1.5, 2.5, or 3.5 mm yielded a precision of better than 1% for normals and 1% to 2% for osteoporotic patients--a twofold improvement over the precision from similar tests using the standard technique with an external reference phantom. Such improvements in precision are essential for QCT to be clinically useful as a noninvasive modality for measurement of the very small annual changes in bone mineral density.

Bone Density↗
PubMed1989

Mechanical considerations for the syndesmosis screw. A cadaver study.

The purpose of this study was to examine the mechanical necessity of using a syndesmosis screw to supplement rigid internal fixation of the fibula and medial malleolus in the treatment of pronation-external rotation fractures. The legs of thirty embalmed and five fresh cadavera were dissected and mounted through the tibia to a frame so that multiple radiographs could be made with a constant relationship between the specimen and the x-ray apparatus. A standardized pronation-external rotation load was applied to the foot, and widening of the syndesmosis was studied on mortise radiographs that were made after each experimental step. On the basis of previous investigations, we developed a model for pronation-external rotation injuries that included disruption of the syndesmosis and interosseous membrane up to the level of the fibular fracture. Accordingly, multiple repaired fibular fractures could be simulated at several levels in the same specimen by incremental proximal division of the interosseous membrane. Specimens were separated into two groups. Group I consisted of thirteen specimens in which the deltoid ligament, syndesmosis, and interosseous membrane were serially sectioned in 1.5-centimeter increments. Group II (ten sections) was subjected to the same protocol, except that the deltoid ligament was kept intact until the final step. The five fresh specimens were sectioned in the same way as those in Group I. In Group I, since the simulated pronation-external rotation injury included a deltoid tear, rigid medial fixation was not possible; accordingly, there was rigid fibular fixation only.(ABSTRACT TRUNCATED AT 250 WORDS)

Ankle↗
PubMed1989

Proximal femoral focal deficiency. Evidence for a defect in proliferation and maturation of chondrocytes.

Proximal femoral focal deficiency is a rare congenital malformation, characterized by a failure of normal development of the proximal part of the femur. To our knowledge, there have been no reports on the histology of fetal growth plates that are affected by this disorder. To characterize this focal developmental anomaly further, we studied the histopathology of the growth plates and epiphyses from a twenty-one-week fetus with unilateral proximal femoral focal deficiency. Although the shape of the cartilaginous anlage of the fetus appeared normal, the growth plate of the proximal part of the involved femur was markedly abnormal. The major findings were: (1) striking failure of the proximal growth plate to migrate proximally, away from the central part of the diaphysis, and failure of formation of a normal growth plate; (2) failure of organization of proliferative and hypertrophic chondrocytes into longitudinal columns; (3) truncation of an immature hypertrophic zone that had abnormal septal architecture; and (4) disorganized vascular invasion with a honeycomb rather than a columnar pattern of primary trabeculae. In contrast, the histological characteristics of the growth plates from the distal part of the femur and from all other long bones were normal.

Cartilage↗
PubMed1987

Metatropic dwarfism. Uncoupling of endochondral and perichondral growth.

Metatropic dwarfism is a rare heritable skeletal dysplasia that is thought to result from a defect in endochondral ossification. Histological studies have been few and have yielded inconsistent findings. In addition, no investigator has commented on the structure and function of the perichondral portion of the growth plate in patients who have metatropic dysplasia. To further characterize this disturbance, histological studies were carried out on autopsy specimens from the proximal part of the femur and the iliac crest of a patient who had this disorder. The major findings were: the absence of formation of normal primary spongiosa in the metaphysis; the presence of a thin seal of bone at the chondro-osseous junction, with abnormal metaphyseal vascular invasion and arrest of endochondral growth; and normal-appearing perichondral ring structures with persistence of circumferential growth. These findings suggest an uncoupling of endochondral and perichondral growth and offer an explanation for the dumbbell-shaped morphological structure of the osseous metaphysis that is seen in patients who have metatropic dysplasia. Other observations included prominence of the cartilaginous canals and vascular channels in the reserve zone; clumping of chondrocytes with enhanced staining of the pericellular matrix in the proliferative zone; a decreased ratio of cells to matrix in the hypertrophic zone, with intracellular metachromatic granules and incomplete evolution of chondrocytes; complete absence of an alcian-blue-positive zone of provisional calcification; and, finally, islands of dysplastic chondrocytes in the metaphysis. These abnormalities suggest that metatropic dysplasia is not simply a disorder of endochondral ossification. There appear to be associated defects in the longitudinal proliferation and maturation of chondrocytes and in the production of normal matrix.

Achondroplasia↗