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Henry Ford Hospital Medical Journal Osteomalacia Henry Ford Hospital Medical Journal Volume 31 Number 4 Article 11 12-1983 Osteomalacia Boy Frame Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Frame, Boy (1983) "Osteomalacia," Henry Ford Hospital Medical Journal : Vol. 31 : No. 4 , 213-216. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol31/iss4/11 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Henry Ford Hosp Med J Vol 31, No 4,1983 Osteomalacia Boy Frame, MD" fd. Note - This overview was originally presented at the Recent advances in laboratory methods and techniques International Symposium on Clinical Disorders of Bone related to bone and mineral metabolism have provided a and Mineral Metabolism, May 9-13, 1983. The following detailed study of factors important in bone formation. list indicates the presentations given in this session at the Osteomalacia results from a disturbance in mineraliza­ Symposium and the contents ofthe corresponding chap­ tion of bone matrix. Theoretically, bone matrix may fail ter in the Proceedings of the Symposium published by to mineralize because of abnormalities in collagen and Excerpta Medica. The numbers in parentheses refer to matrix proteins, or because of an alteration in mineral pages in this volume. Complete information about the metabolism at the mineralization front. The result is an contents ofthe Proceedings can be found at the back of accumulation of increased quantities of unmineralized this issue. bone matrix (osteoid) over bone surfaces. Spatial distributions of aluminum, phosphorus and cal­ Rickets is more apparent in children who have otherwise cium in mineralizingepiphy seal growth plates of aluminum- normal growth patterns, including that of the cartilage treated rats by electron spectroscopic imaging. A.L. present in the growth plates of long bones. Likewise, Arsenault, F.P. Ottensmeyer, and A.B. Hodsman (220) osteomalacia is less apt to occur when normal bone matrix formation is deficient. In order for a defect in tfistologic evolution of vitamin-D depletion in patients bone mineralization to be fully expressed, adequate with intestinal malabsorption of dietary deficiency. D.S. bone matrix must first be deposited. Rao, A. Villanueva, M. Matthews, B. Pumo, B. Frame, M. Kleerekoper, and A.M. Parfitt (224) The Table lists some of the factors currently considered to be possibly significant in the formation of bone matrix Primary biliary cirrhosis and alcoholic cirrhosis as exam­ and mineralization. ples of chronic liver disease associated with bone dis­ ease. R.R. Recker, W. Maddrey, H. Herlong, M. Sorrell, Recent studies suggest that bone resorption itself may be and R. Russell (227) important as an initiating event for osteoblast formation and function in the bone remodeling unit (BMU). A high Chronic hypophosphatemia without osteomalacia. M.C. molecular weight polypeptide which has been isolated de Vernejoul, P.J. Marie, L. Miravet, and A. Ryckewaert from tissue cultures and demineralized human bone (232) matrix, stimulates osteoblast proliferation and matrix Bone disease in patients receiving total parenteral nutri­ formation. Impaired release or other defect in this cou­ tion. S.M. Ott, N.A. Maloney, G.L. Klein, A.C. Alfrey, pling or skeletal growth factor could theoretically influ­ M.E. Ament, J.W. Coburn, and D.J. Sherrard (237) ence subsequent osteoblast vigor and function. The pathogenesis of tumor-induced osteomalacia: A Collagen synthesis is the initial, major component of new perspective. P.C. Brazy, B. Lobuagh, K.W. Lyles, and bone matrix formation. Maturation of collagen, which M.K. Drezner (242) appears to be important for mineralization, is character­ ized by increasing intra- and extrafibrillar cross-linking of collagen fibers. Some defects in mineralization may result from an abnormality in collagen structure. For instance, in the rare skeletal disorder known as fibro- •Department of Internal Medicine, Bone and Mineral Metabolism Division, Henry Ford Hospital Address reprint requests to Dr. Frame, Bone and Mineral Metabolism Division, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, Ml 48202. 213 Frame genesis imperfecta ossium, marked distortion of the zation. Osteoblast influence is less important in this lat­ normally polarized collagen fibers appears to result in ter phase of mineral deposition. impaired mineralization and increased numbers of widened osteoid seams. A number of precisely timed chemical and physiological factors must interact for mineralization to proceed nor­ The chronologic age of the person as well as the age of mally. Ambient concentrations of calcium and particu­ the osteoblasts may influence the rate and extent of larly of phosphate are important. Since osteomalacia matrix formation. Decreases in the matrix appositional occurs in many patients with chronic hypophosphate­ rate correlates with age and distance from the cement mia, other modulating factors are also important. In this line in individual BMUs. Only insulin and growth hor­ section, M.C. de Vernejoul and associates (pp. 232 ff.) mone, the latter via somatomedin, directly stimulate report on 19 male patients with chronic hypophos­ bone collagen synthesis. Other hormones primarily play phatemia due to a renal phosphate leak independent of a modulating role in collagen formation. parathyroid hormone. Whilethere was noosteoid accum­ ulation, decreased osteoblast appositional rate was never­ Recently, noncollagenous bone matrix proteins have theless present. As in rickets, normal growth of bone been evaluated as possible causes of defective minerali­ matrix may be necessary before a mineralization defect zation. Osteocalcin (gla protein) has been extensively can be fully expressed. studied, but its ultimate role in bone metabolism is still to be determined. Osteocalcin has an affinity for binding to Relatives of patients with X-linked hypophosphatemic hydroxyapatite but only after the latter's maturation rickets and osteomalacia may exhibit hypophosphate­ from an initial amorphous mineral phase. Another bone mia without apparent bone involvement. However, matrix protein, osteonectin appears to facilitate the many of these patients have not had careful bone biopsy nucleation of calcium phosphate mineral onto the sur­ studies with current histomorphometric techniques to face of type I collagen. exclude a defect in mineralization. Chronic hypocalce­ mia appears to result in rickets and osteomalacia only Proteoglycans and glycoproteins are other important extracollagenous proteins in bone matrix. While their role in mineralization needs further clarification, they do TABLE have a high binding affinity for calcium, which appar­ Factors Influencing Bone Matrix ently depends on the presence of a large number of free Formation and Mineralization acidic groups. Theoretically, excessive calcium binding Bone resorption in bone remodeling units (BRUs) to proteoglycans might interfere with normal mineral • Release of a coupling factor that stimulates osteoblasts deposition at the mineralization front. In fact, certain Osteoblast function rare forms of osteomalacia may be related to a defect in • Collagen formation and maturation concentration or function of one or more of the matrix 1. Chronologic age of person proteins. One form of osteomalacia that could result 2. Insulin 3. Growth hormone (via somatomedin) from such a defect is axial osteomalacia. In this skeletal • Bone matrix proteins affliction, osteomalacia of the axial skeleton (exhibiting a 1. Osteocalcin (Gla protein) coarsened trabecular pattern on skeletal x-rays) is not 2. Osteonectin associated with any obvious disturbance in mineral or 3. Proteoglycans vitamin D metabolism. An abnormality in one of the Mineralization at the mineralization front extracollagenous matrix proteins could account for this • Ambient Ca, PO^ concentrations mineralization defect. • pH at mineralization front • Amorphous Ca, PO.,(ACP) preceding Because methods of study are available, most identified hydroxyapatite formation (?) • Vitamin D metabolites forms of osteomalacia have been related to disturbances 1. Maintain adequate ambient Ca, PO,, levels in mineral and vitamin D metabolism. After appropriate 2. (?) Direct effect on osteoblasts and/or mineralization front maturation of bone matrix overa period of 10 to 15 days, • Parathyroid hormone primary mineralization occurs, and about 80% of the • Piezoelectric fields (exercise and stress) mineral is deposited in the first few days. This primary • Inhibitors of mineralization 1. Pyrophosphates ) destroyed by mineralization is largely controlled by the osteoblasts 2. ATP (adenosine triphosphate) V phosphatases and nearby osteoid osteocytes. The remainder of the 3. Foreign ions, such as aluminum \ and ATPases mineral is deposited at a slower rate over a six-month • Matrix vesicles period or more, a process known as secondary minerali­ 1. Facilitates mineral and enzyme concentration at the mineralization front 214 Osteomalacia rarely. Examples are seen primarily in rapidly growing minerals and enzymes, appearing at the initial site of children who have subsisted on a calcium deficient diet. mineral deposition. Hydrogen ion concentration appears to bean important Bone matrix
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