DOCSLIB.ORG

Osteoporosis and Osteomalacia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Osteoporosis and Osteomalacia CHAPTER 50 Osteoporosis and Osteomalacia Laura M. Borgelt and Danielle R. Fixen The United States Bone and Joint Initiative, as part attention to screening patients, provide education, of the Global Alliance for Musculoskeletal Health, perform research, and work to help ensure proper is the U.S. National Action Network of the Global management and follow- up of patients diagnosed Bone and Joint Decade.1 It is a group of patient with these and related disorders as a way to help and healthcare professional organizations, medical prevent the devastating consequences of fracture schools, government agencies, health- system pro- and its potential complications of chronic pain, dis- viders, and industry established to improve preven- ability, and death.1 This includes evaluation of med- tion of bone and joint disorders and the quality of life ications that may cause musculoskeletal conditions for those affected by these conditions. The primary such as osteoporosis and osteomalacia. goal of this initiative is to advance care and reduce Deterioration of bone mass not associated with the burden of disease for individuals with various other chronic illness is referred to as primary osteo- musculoskeletal conditions. Other goals include porosis and is related to aging and decreased gonadal increasing awareness and educating the world on function. Secondary osteoporosis can be viewed as the increasing societal impact of musculoskeletal low bone mineral density or increased risk of fragil- injuries and disorders, empowering patients to par- ity fracture caused by any factor other than aging or ticipate in decisions about their care and treatment, postmenopausal status, such as medical disorders or increase global funding for prevention activities medication exposures.2 Differentiating between pri- and treatment research, and continually seeking mary osteoporosis and the various causes of second- and promoting cost- effective prevention and treat- ary osteoporosis can be challenging due to the many ment of musculoskeletal injuries and disorders. disease states and drugs that may be involved. Indi- Although many musculoskeletal conditions are viduals with secondary osteoporosis experience bone incorporated into its aims, osteoporosis is recog- loss greater than that caused by aging and meno- nized as a significant contributor to the healthcare pause in primary osteoporosis, and it is especially burden worldwide. The spirit of this initiative sug- important, therefore, to identify, accurately evaluate, gests that all healthcare providers should increase and appropriately treat these patients.2 1119 1120 DRUG-INDUCED DISEASES: Prevention, Detection, and Management Osteomalacia is a softening of the bones, typi- incidence are not available. More than two thirds cally due to vitamin D deficiency and less commonly of men, more than half of premenopausal women, due to hypophosphatemia or hypocalcemia. In chil- and approximately one third of postmenopausal dren, this condition is called rickets. Osteomalacia women with osteoporosis have a disease state or can cause fatigue, bone pain, muscle weakness, drug therapy contributing to their bone loss.65 The and difficulty walking and result in bone fracture.3 incidence of drug-­­induced bone loss or increased Drugs that may affect vitamin D metabolism should bone fragility is difficult to quantify, as medications be cautiously prescribed in patients at risk for the usually contribute to an increased risk of osteopo- development of osteomalacia. rosis rather than represent its sole cause. Table 50-1 provides information regarding the risks for bone CAUSATIVE AGENTS loss and fractures with drug use. Vitamin D deficiency is one of the most com- Medications commonly associated with osteoporo- mon secondary causes for bone loss and fractures, sis or osteomalacia are listed in Table 50-1.4-59 The especially in the elderly. Prolonged, severe vitamin D impact of each of the medications on bone mineral deficiency can lead to poor bone mineralization density (BMD) or fracture incidence (or both) is and osteomalacia. The overall incidence of vitamin presented where data are available. D–induced osteomalacia is not precisely known, Glucocorticoids are the most common cause of but it appears to be lower in the United States than drug-­­induced osteoporosis, and their effects appear in many other countries because of fortification of to be dose- and duration-­­dependent.2,45 An increased milk with vitamin D. risk of fracture has been reported for patients tak- ing prednisone 2.5 mg or more daily; national rec- MECHANISMS ommendations indicate prednisone >5 mg/day (or equivalent exposure to other glucocorticoids) for The process through which bone undergoes repair >3 months may result in low bone mass or bone and readjustment is called bone remodeling, and loss.60 Approximately 30–50% of patients receiving there are three main cells involved in this process: long-t­­erm glucocorticoid therapy will experience a osteoblasts, osetocytes, and osteoclasts. Osteoblasts fracture.47,48 are derived from a mesenchymal stem cell precursor and are responsible for synthesizing the organic bone matrix (osteoid) and mineralizing the bone. EPIDEMIOLOGY Osteocytes, which are retired osteoblasts trapped in It is estimated that over 200 million people world- bone, are considered the communication cells and wide suffer from osteoporosis.61 Approximately 10 help coordinate the remodeling cycle at a particu- million Americans have osteoporosis and an addi- lar site. Osteoclasts are derived from hematopoietic tional 43 million have low bone mass or osteope- precursors of the monocyte–macrophage lineage nia as defined by the World Health Organization and are responsible for bone resorption. (WHO).60,62 This accounts for approximately 55% of The remodeling process begins when the people age 50 years and older in the United States. receptor activator of nuclear factor kappa-B ligand More than 2 million fractures were attributed to (RANKL), which is secreted from the osteoblast pre- osteoporosis in 2005 and this number is expected cursor cells, binds to its receptor activator of nuclear to exceed 3 million by 2025.63 Fracture rates in other factor kappa-B (RANK) on the surface of the osteo- countries tend to vary. For example, wrist and hip clast precursor cells. This leads to the differentiation fracture in the United Kingdom occurs at a rate and activation of mature osteoclasts, which in turn about 30% lower than that in the United States and resorb bone through the degradation of the protein hip fracture incidence differs among various Asian matrix and demineralization. Once bone resorption countries.64 Although secondary osteoporosis is is complete at that site, cytokines and growth factors known to be common, precise data regarding its that are involved in chemotaxis, proliferation, and .
Load more

Recommended publications
  • Severe Septicaemia in a Patient with Polychondritis and Sweet's
    81 LETTERS Ann Rheum Dis: first published as 10.1136/ard.62.1.88 on 1 January 2003. Downloaded from Severe septicaemia in a patient with polychondritis and Sweet’s syndrome after initiation of treatment with infliximab F G Matzkies, B Manger, M Schmitt-Haendle, T Nagel, H-G Kraetsch, J R Kalden, H Schulze-Koops ............................................................................................................................. Ann Rheum Dis 2003;62:81–82 D Sweet first described an acute febrile neutrophilic dermatosis in 1964 characterised by acute onset, fever, Rleucocytosis, and erythematous plaques.1 Skin biopsy specimens show infiltrates consisting of mononuclear cells and neutrophils with leucocytoclasis, but without signs of vasculi- tis. Sweet’s syndrome is frequently associated with solid malig- nancies or haemoproliferative disorders, but associations with chronic autoimmune connective tissue disorders have also been reported.2 The aetiology of Sweet’s syndrome is unknown, but evidence suggests that an immunological reaction of unknown specificity is the underlying mechanism. CASE REPORT A 51 year old white man with relapsing polychondritis (first diagnosed in 1997) was admitted to our hospital in June 2001 with a five week history of general malaise, fever, recurrent arthritis, and complaints of morning stiffness. Besides Figure 1 autoimmune polychondritis, he had insulin dependent Manifestation of Sweet’s syndrome in a patient with relapsing polychondritis. diabetes mellitus that was diagnosed in 1989. On admission, he presented with multiple small to medium, sharply demarked, raised erythematous plaques on both fore- dose of glucocorticoids (80 mg) and a second application of http://ard.bmj.com/ arms and lower legs, multiple acne-like pustules on the face, infliximab (3 mg/kg body weight) were given.
    [Show full text]
  • Hypophosphatasia Could Explain Some Atypical Femur Fractures
    Hypophosphatasia Could Explain Some Atypical Femur Fractures What we know Hypophosphatasia (HPP) is a rare genetic disease that affects the development of bones and teeth in children (Whyte 1985). HPP is caused by the absence or reduced amount of an enzyme called tissue-nonspecific alkaline phosphatase (TAP), also called bone-specific alkaline phosphatase (BSAP). The absence of TAP raises the level of inorganic pyrophosphate (Pi), which prevents calcium and phosphate from creating strong, mineralized bone. Without TAP, bones can become weak. In its severe form, HPP is fatal and happens in 1/100,000 births. Because HPP is genetic, it can appear in adults as well. A recent study has identified a milder, more common form of HPP that occurs in 4 of 1000 adults (Dahir 2018). This form of HPP is usually seen in early middle aged adults who have low bone density and sometimes have stress fractures in the feet or thigh bone. Sometimes these patients lose their baby teeth early, but not always. HPP is diagnosed by measuring blood levels of TAP and vitamin B6. An elevated vitamin B6 level [serum pyridoxal 5-phosphate (PLP)] (Whyte 1985) in a patient with a TAP level ≤40 or in the low end of normal can be diagnosed with HPP. Almost half of the adult patients with HPP in the large study had TAP >40, but in the lower end of the normal range (Dahir 2018). The connection between hypophosphatasia and osteoporosis Some people who have stress fractures get a bone density test and are treated with an osteoporosis medicine if their bone density results are low.
    [Show full text]
  • Parathyroid Hormone Stimulates Bone Formation and Resorption In
    Proc. Nati. Acad. Sci. USA Vol. 78, No. 5, pp. 3204-3208, May 1981 Medical Sciences Parathyroid hormone stimulates bone formation and resorption in organ culture: Evidence for a coupling mechanism (endocrine/mineralization/bone metabolism/cartilage/regulation) GuY A. HOWARD, BRIAN L. BOTTEMILLER, RUSSELL T. TURNER, JEANNE I. RADER, AND DAVID J. BAYLINK American Lake VA Medical Center, Tacoma, Washington 98493; and Department of Medicine, University of Washington, Seattle, Washington 98195 Communicated by Clement A. Finch, January 26, 1981 ABSTRACT We have developed an in vitro system, using em- growing rats with PTH results in an increase in formation and bryonic chicken tibiae grown in a serum-free medium, which ex- resorption (4) and a net gain in bone volume (10-12). We have hibits simultaneous bone formation and resorption. Tibiae from recently obtained similar results in vitro for the acute and 8-day embryos increased in mean (±SD) length (4.0 ± 0.4 to 11.0 chronic effects of PTH (13). Moreover, as reported earlier for ± 0.3 mm) and dry weight (0.30 ± 0.04 to 0.84 ± 0.04 mg) during resorption in rat bone (14), the in vitro effect of PTH in our 12 days in vitro. There was increased incorporation of [3H]proline system is an inductive one in that the continued presence of into hydroxyproline (120 ± 20 to 340 ± 20 cpm/mg of bone per PTH is unnecessary for bone resorption and bone formation to 24 hr) as a measure of collagen synthesis, as well as a 62 ± 5% increase in total calcium and 45Ca taken up as an indication of ac- be stimulated for several days (13).
    [Show full text]
  • Direct Measurement of Bone Resorption and Calcium
    Proc. Natl. Acad. Sci. USA Vol. 77, No. 4, pp. 1818-1822, April 1980 Biochemistry Direct measurement of bone resorption and calcium conservation during vitamin D deficiency or hypervitaminosis D ([3Hltetracycline/collagen/chicks/growth modeling/kinetics) LEROY KLEIN Departments of Orthopaedics, Biochemistry, and Macromolecular Science, Case Western Reserve University, Cleveland, Ohio 44106 Communicated by Oscar D. Ratnoff, December 20,1979 ABSTRACT When bone is remodeled during the growth of complication, various workers (11, 12) have expressed the need a given size bone to a larger size, some bone is resorbed and for a more direct measurement of bone turnover. In addition, some is deposited. Much of the resorbed bone mineral, calcium, tracer methods for calcium kinetics involve only plasma tracer can be reutilized during bone formation. The net and absolute effects of normal growth, vitamin D deficiency, or vitamin D concentrations and focus on net pool turnover rather than on excess were compared on bone resortion, bone formation, and more absolute measurements of bone turnover (13). calcium reutilization. Growing chic were relabeled exten- Bone resorptiont has been observed directly by using histo- sively with three isotopes: 45Ca, [3Htetracycline, and [3H]pro- logical measurements of the increase in diameter of the bone line. Data were obtained weekly during 3 weeks of control marrow space in rapidly growing rats (14). Resorption has been growth, vitamin D deficiency, or vitamin D overdosage while measured kinetically by either 45Ca under steady-state condi- on a nonradioactive diet. Bone resorption as measured by in- creases in the marrow (inner) diameter of the midshaft of the tions in adult rats (15) or 40Ca dilution of the natural isotope femur and humerus and by the weekly losses of total [3Hjtetra- 48Ca in human subjects (16).
    [Show full text]
  • Osteomalacia and Osteoporosis D
    Postgrad. med.J. (August 1968) 44, 621-625. Postgrad Med J: first published as 10.1136/pgmj.44.514.621 on 1 August 1968. Downloaded from Osteomalacia and osteoporosis D. B. MORGAN Department of Clinical Investigation, University ofLeeds OSTEOMALACIA and osteoporosis are still some- in osteomalacia is an increase in the alkaline times confused because both diseases lead to a phosphatase activity in the blood (SAP); there deficiency of calcium which can be detected on may also be a low serum phosphorus or a low radiographs of the skeleton. serum calcium. This lack of calcium is the only feature Our experience with the biopsy of bone is that common to the two diseases which are in all a large excess of uncalcified bone tissue (osteoid), other ways easily distinguishable. which is the classic histological feature of osteo- malacia, is only found in patients with the other Osteomalacia typical features of the disease, in particular the Osteomalacia will be discussed first, because it clinical ones (Morgan et al., 1967a). Whether or is a clearly defined disease which can be cured. not more subtle histological techniques will detect Osteomalacia is the result of an imbalance be- earlier stages of the disease remains to be seen. tween the supply of and the demand for vitamin Bone pains, muscle weakness, Looser's zones, D. The the following description of disease is raised SAP and low serum phosphate are the Protected by copyright. based on our experience of twenty-two patients most reliable aids to the diagnosis of osteomalacia, with osteomalacia after gastrectomy; there is no and approximately in that order.
    [Show full text]
  • An Unusual Cause of Back Pain in Osteoporosis: Lessons from a Spinal Lesion
    Ann Rheum Dis 1999;58:327–331 327 MASTERCLASS Series editor: John Axford Ann Rheum Dis: first published as 10.1136/ard.58.6.327 on 1 June 1999. Downloaded from An unusual cause of back pain in osteoporosis: lessons from a spinal lesion S Venkatachalam, Elaine Dennison, Madeleine Sampson, Peter Hockey, MIDCawley, Cyrus Cooper Case report A 77 year old woman was admitted with a three month history of worsening back pain, malaise, and anorexia. On direct questioning, she reported that she had suVered from back pain for four years. The thoracolumbar radiograph four years earlier showed T6/7 vertebral collapse, mild scoliosis, and degenerative change of the lumbar spine (fig 1); but other investigations at that time including the eryth- rocyte sedimentation rate (ESR) and protein electophoresis were normal. Bone mineral density then was 0.914 g/cm2 (T score = −2.4) at the lumbar spine, 0.776 g/cm2 (T score = −1.8) at the right femoral neck and 0.738 g/cm2 (T score = −1.7) at the left femoral neck. She was given cyclical etidronate after this vertebral collapse as she had suVered a previous fragility fracture of the left wrist. On admission, she was afebrile, but general examination was remarkable for pallor, dental http://ard.bmj.com/ caries, and cellulitis of the left leg. A pansysto- lic murmur was heard at the cardiac apex on auscultation; there were no other signs of bac- terial endocarditis. She had kyphoscoliosis and there was diVuse tenderness of the thoraco- lumbar spine. Her neurological examination was unremarkable. on September 29, 2021 by guest.
    [Show full text]
  • Distinguishing Transient Osteoporosis of the Hip from Avascular Necrosis
    Original Article Article original Distinguishing transient osteoporosis of the hip from avascular necrosis Anita Balakrishnan, BMedSci;* Emil H. Schemitsch, MD;* Dawn Pearce, MD;† Michael D. McKee, MD* Introduction: To review the circumstances surrounding the misdiagnosis of transient osteoporosis of the hip (TOH) as avascular necrosis (AVN) and to increase physician awareness of the prevalence and diagnosis of this condition in young men, we reviewed a series of cases seen in the orthopedic unit at St. Michael’s Hospital, University of Toronto. Methods: We studied the charts of patients with TOH referred between 1998 and 2001 with a diagnosis of AVN for demographic data, risk factors, imaging results and outcomes. Results: Twelve hips in 10 young men (mean age 41 yr, range from 32–55 yr) were identified. Nine men underwent magnetic resonance imaging (MRI) before referral, which showed characteristic changes of TOH. All 10 patients were referred for surgical intervention for a diagnosis of AVN. The correct diagnosis was made after reviewing patients’ charts and the scans and was confirmed by spontaneous resolution of both symptoms and MRI findings an average of 5.5 months and 7.5 months, respectively, after consultation. Conclusions: Despite recent publications, the prevalence of TOH among young men is still overlooked and the distinctive MRI appearance still misinterpreted. Symptoms may be severe but resolve over time with reduced weight bearing. The absence of focal changes on MRI is highly suggestive of a transient lesion. A greater level of awareness of this condition is needed to differentiate TOH from AVN, avoiding unnecessary surgery and ensuring appropriate treatment.
    [Show full text]
  • Hematological Diseases and Osteoporosis
    International Journal of Molecular Sciences Review Hematological Diseases and Osteoporosis , Agostino Gaudio * y , Anastasia Xourafa, Rosario Rapisarda, Luca Zanoli , Salvatore Santo Signorelli and Pietro Castellino Department of Clinical and Experimental Medicine, University of Catania, 95123 Catania, Italy; [email protected] (A.X.); [email protected] (R.R.); [email protected] (L.Z.); [email protected] (S.S.S.); [email protected] (P.C.) * Correspondence: [email protected]; Tel.: +39-095-3781842; Fax: +39-095-378-2376 Current address: UO di Medicina Interna, Policlinico “G. Rodolico”, Via S. Sofia 78, 95123 Catania, Italy. y Received: 29 April 2020; Accepted: 14 May 2020; Published: 16 May 2020 Abstract: Secondary osteoporosis is a common clinical problem faced by bone specialists, with a higher frequency in men than in women. One of several causes of secondary osteoporosis is hematological disease. There are numerous hematological diseases that can have a deleterious impact on bone health. In the literature, there is an abundance of evidence of bone involvement in patients affected by multiple myeloma, systemic mastocytosis, thalassemia, and hemophilia; some skeletal disorders are also reported in sickle cell disease. Recently, monoclonal gammopathy of undetermined significance appears to increase fracture risk, predominantly in male subjects. The pathogenetic mechanisms responsible for these bone loss effects have not yet been completely clarified. Many soluble factors, in particular cytokines that regulate bone metabolism, appear to play an important role. An integrated approach to these hematological diseases, with the help of a bone specialist, could reduce the bone fracture rate and improve the quality of life of these patients.
    [Show full text]
  • Biology of Bone Repair
    Biology of Bone Repair J. Scott Broderick, MD Original Author: Timothy McHenry, MD; March 2004 New Author: J. Scott Broderick, MD; Revised November 2005 Types of Bone • Lamellar Bone – Collagen fibers arranged in parallel layers – Normal adult bone • Woven Bone (non-lamellar) – Randomly oriented collagen fibers – In adults, seen at sites of fracture healing, tendon or ligament attachment and in pathological conditions Lamellar Bone • Cortical bone – Comprised of osteons (Haversian systems) – Osteons communicate with medullary cavity by Volkmann’s canals Picture courtesy Gwen Childs, PhD. Haversian System osteocyte osteon Picture courtesy Gwen Childs, PhD. Haversian Volkmann’s canal canal Lamellar Bone • Cancellous bone (trabecular or spongy bone) – Bony struts (trabeculae) that are oriented in direction of the greatest stress Woven Bone • Coarse with random orientation • Weaker than lamellar bone • Normally remodeled to lamellar bone Figure from Rockwood and Green’s: Fractures in Adults, 4th ed Bone Composition • Cells – Osteocytes – Osteoblasts – Osteoclasts • Extracellular Matrix – Organic (35%) • Collagen (type I) 90% • Osteocalcin, osteonectin, proteoglycans, glycosaminoglycans, lipids (ground substance) – Inorganic (65%) • Primarily hydroxyapatite Ca5(PO4)3(OH)2 Osteoblasts • Derived from mesenchymal stem cells • Line the surface of the bone and produce osteoid • Immediate precursor is fibroblast-like Picture courtesy Gwen Childs, PhD. preosteoblasts Osteocytes • Osteoblasts surrounded by bone matrix – trapped in lacunae • Function
    [Show full text]
  • Osteomalacia and Hyperparathyroid Bone Disease in Patients with Nephrotic Syndrome
    Osteomalacia and Hyperparathyroid Bone Disease in Patients with Nephrotic Syndrome Hartmut H. Malluche, … , David A. Goldstein, Shaul G. Massry J Clin Invest. 1979;63(3):494-500. https://doi.org/10.1172/JCI109327. Research Article Patients with nephrotic syndrome have low blood levels of 25 hydroxyvitamin D (25-OH-D) most probably because of losses in urine, and a vitamin D-deficient state may ensue. The biological consequences of this phenomenon on target organs of vitamin D are not known. This study evaluates one of these target organs, the bone. Because renal failure is associated with bone disease, we studied six patients with nephrotic syndrome and normal renal function. The glomerular filtration rate was 113±2.1 (SE) ml/min; serum albumin, 2.3±27 g/dl; and proteinuria ranged between 3.5 and 14.7 g/24 h. Blood levels of 25-OH-D, total and ionized calcium and carboxy-terminal fragment of immunoreactive parathyroid hormone were measured, and morphometric analysis of bone histology was made in iliac crest biopsies obtained after double tetracycline labeling. Blood 25-OH-D was low in all patients (3.2-5.1 ng/ml; normal, 21.8±2.3 ng/ml). Blood levels of both total (8.1±0.12 mg/dl) and ionized (3.8±0.21 mg/dl) calcium were lower than normal and three patients had true hypocalcemia. Blood immuno-reactive parathyroid hormone levels were elevated in all. Volumetric density of osteoid was significantly increased in three out of six patients and the fraction of mineralizing osteoid seams was decreased in all.
    [Show full text]
  • The Role of BMP Signaling in Osteoclast Regulation
    Journal of Developmental Biology Review The Role of BMP Signaling in Osteoclast Regulation Brian Heubel * and Anja Nohe * Department of Biological Sciences, University of Delaware, Newark, DE 19716, USA * Correspondence: [email protected] (B.H.); [email protected] (A.N.) Abstract: The osteogenic effects of Bone Morphogenetic Proteins (BMPs) were delineated in 1965 when Urist et al. showed that BMPs could induce ectopic bone formation. In subsequent decades, the effects of BMPs on bone formation and maintenance were established. BMPs induce proliferation in osteoprogenitor cells and increase mineralization activity in osteoblasts. The role of BMPs in bone homeostasis and repair led to the approval of BMP 2 by the Federal Drug Administration (FDA) for anterior lumbar interbody fusion (ALIF) to increase the bone formation in the treated area. However, the use of BMP 2 for treatment of degenerative bone diseases such as osteoporosis is still uncertain as patients treated with BMP 2 results in the stimulation of not only osteoblast mineralization, but also osteoclast absorption, leading to early bone graft subsidence. The increase in absorption activity is the result of direct stimulation of osteoclasts by BMP 2 working synergistically with the RANK signaling pathway. The dual effect of BMPs on bone resorption and mineralization highlights the essential role of BMP-signaling in bone homeostasis, making it a putative therapeutic target for diseases like osteoporosis. Before the BMP pathway can be utilized in the treatment of osteoporosis a better understanding of how BMP-signaling regulates osteoclasts must be established. Keywords: osteoclast; BMP; osteoporosis Citation: Heubel, B.; Nohe, A. The Role of BMP Signaling in Osteoclast Regulation.
    [Show full text]
  • The Products of Bone Resorption and Their Roles in Metabolism: Lessons from the Study of Burns
    Concept Paper The Products of Bone Resorption and Their Roles in Metabolism: Lessons from the Study of Burns Gordon L. Klein Department of Orthopaedic Surgery and Rehabilitation, University of Texas Medical Branch, Galveston, TX 77555-0165, USA; [email protected] Abstract: Surprisingly little is known about the factors released from bone during resorption and the metabolic roles they play. This paper describes what we have learned about factors released from bone, mainly through the study of burn injuries, and what roles they play in post-burn metabolism. From these studies, we know that calcium, phosphorus, and magnesium, along with transforming growth factor (TGF)-β, are released from bone following resorption. Additionally, studies in mice from Karsenty’s laboratory have indicated that undercarboxylated osteocalcin is also released from bone during resorption. Questions arising from these observations are discussed as well as a variety of potential conditions in which release of these factors could play a significant role in the pathophysiology of the conditions. Therapeutic implications of understanding the metabolic roles of these and as yet other unidentified factors are also raised. While much remains unknown, that which has been observed provides a glimpse of the potential importance of this area of study. Keywords: bone resorption; calcium; phosphorus; TGF-β; undercarboxylated osteocalcin Citation: Klein, G.L. The Products of Bone Resorption and Their Roles in 1. Introduction Metabolism: Lessons from the Study of Burns. Osteology 2021, 1, 73–79. In recent years we have learned much about the mechanisms of bone formation and https://doi.org/10.3390/ resorption, the cells involved, and many of the factors that affect and link the two processes.
    [Show full text]