DOCSLIB.ORG

Osteomalacia Andchronic Renal Failure

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Osteomalacia Andchronic Renal Failure J Clin Pathol: first published as 10.1136/jcp.34.11.1295 on 1 November 1981. Downloaded from J Clin Pathol 1981 ;34:1295-1 307 Osteomalacia and chronic renal failure JOHN A KANIS From the Department of Human Metabolism and Clinical Biochemistry, University of Sheffield Medical School, Beech Hill Road, Sheffield S1O 2RX Dialysis and transplantation have revolutionised the Table 1 Features of renal bone disease and some clinical management of chronic renal failure. Many patients manifestations of disturbed calcium and phosphate with end-stage chronic renal failure are surviving for metabolism in chronic renalfailure a long time, but there are some penalties attached to Feature Clinical consequence this survival, namely the complications associated with prolonged renal failure as well as the side I Hyperparathyroidism and osteitis Skeletal deformity, bone fibrosa pain, pruritis? anaemia, effects of the treatments (drugs, dialysis and trans- impotence, neuropathy etc plantation). Major factors which influence the 2 Osteomalacia and decreased Skeletal deformity, bone morbidity and mortality of this population include availability of vitamin D, pain and tenderness, anaemia, accelerated cardiovascular disease, dis- calcium, and phosphate pathological fracture, proximal myopathy, turbances in gonadal function, hypertension and haemolytic anaemia abnormalities in lipid and skeletal metabolism. Significant progress has been made in the past few 3 Osteoporosis Pathological fracture, years concerning the pathophysiology and treatment skeletal deformity renal bone disease. This has been due to advances 4 Osteonecrosis Joint pain of copyright. in our understanding of hormone metabolism, 5 Osteosclerosis and periosteal None known particularly that of vitamin D, and of skeletal new bone formation physiology. Tn addition, large populations of 6 Extraskeletal calcification Depends on site-skin dialysis-or transplant-treated patients have now been ulcers, vascular disease, studied for more than a decade with the result that cardiac failure etc the natural history of this bone disease is more clearly understood. Renal bone disease is a constellation of skeletal abnormalities (Table 1), none of which is specific for Paget's disease, hyperparathyroidism, fracture repair http://jcp.bmj.com/ chronic renal failure. These disorders are frequently, and hyperthyroidism, indicating that an increase in though not invariably, found in combination, and osteoid volume alone (hyperosteoidosis) is an consideration of one of these in isolation has obvious inadequate criterion for osteomalacia.6 7 limitations. Nevertheless, the emphasis of this The amount of osteoid present in bone depends review is on the aetiology and management of upon several factors including the rate of apposition osteomalacia, but several more thorough and of osteoid by osteoblasts, upon the rate of its integrated approaches have appeared recently as calcification, and upon the area of the bone surface on September 30, 2021 by guest. Protected reviews or proceedings of symposia.'-5 involved. When considering osteomalacia it is therefore important to distinguish hyperosteoidosis HISTOLOGICAL DEFINITIONS OF OSTEOMALACIA due to an increase in the proportion of bone surfaces Osteomalacia can have a variety of meanings. The on which osteoid is being deposited, as seen in clinician may apply the term to the syndrome hyperparathyroidism, from that due to a delay or associated with vitamin D deficiency, whereas to the absence of mineralisation-particularly in chronic bone histologist it implies defective mineralisation of renal failure where osteomalacia and hyperpara- bone. There is, however, a need for precision, even in thyroidism often coexist. Much confusion and histological definitions since, for example, a histo- apparently conflicting reports exist in the published logical characteristic of vitamin D deficiency in man is reports concerning the pathophysiology of osteo- an increase in the amount of unmineralised bone malacia and its response to various treatments. A matrix; but increased amounts of osteoid are also notable factor contributing to this confusion has associated with many other disorders with normal or been the lack of precision in defining osteomalacia, augmented rates of mineralisation. These include particularly in appreciating the significance of 1295 J Clin Pathol: first published as 10.1136/jcp.34.11.1295 on 1 November 1981. Downloaded from 1296 Kanis hyperosteoidosis in hyperparathyroid bone disease The double labelling of bone with tetracyclines (Table 2). provides a direct method for measuring mineralis- ation in man,7 9 although the technique is time Table 2 Some of the quantitative measurements made consuming to perform. Nevertheless, care must be on bone biopsies which have been used (often erroneously) taken in the interpretation of findings when hyper- in the assessment ofosteomalacia parathyroidism is present. Thus, woven osteoid,* which may take up tetracycline more easily than I Surface osteoid proportion of trabecular surfaces covered by osteoid (depends on lamellar bone,10 is laid down in hyperparathyroidism resolving power of microscope) so that normal mineralisation measured in woven 2 Osteoid volume proportion of bone matrix (or bone may coexist with metabolic abnormalities sectional area) occupied by which might impair mineralisation in more normal non-mineralised bone matrix bone. 3 Osteoid index mean osteoid seam width: may be An alternative and simpler method of assessing derived indirectly from osteoid mineralisation is to measure the maximum number volume and surface osteoid of osteoid lamellae visible under polarised light." 4 Maximum number of semiquantitative In hyperparathyroidism the "hyperosteoidosis" is osteoid lamellae mainly due to an increase in osteoid surfaces (and 5 Calcification front the proportion of the trabecular sometimes an increase in lamellar thickness), rather surface (or osteoid surface) than toan increase in the number of osteoid lamellae.6 undergoing calcification as judged by stains in vitro-for Another simple method is to measure the thickness example, toluidine blue or in vivo of the osteoid seams themselves or to derive this -for example, tetracycline indirectly from the measurement of osteoid area and 6 Appositional rate mean thickness between two the bone surface covered by osteoid-the osteoid tetracycline markers laid down surface osteoid x per unit time index (osteoid area divided by 100).6 7 Bone formation rate derived from 5 and 6 The prevalence of "osteomalacia" according tocopyright. some of these histological criteria is shown in Fig. 1. The definition of osteomalacia as impairment of It is important to recognise that all these indices of mineralisation indicates that evidence for osteo- osteomalacia have their limitations, particularly in malacia should be obtained by indices of mineralis- the presence of hyperparathyroidism. However, ation rather than by the amount of osteoid present. without a clear understanding of what is meant by The extent of the bone surface undergoing calcifica- osteomalacia and the problems of its definition, tion can be measured by suitable staining techniques judgements about its pathophysiology and treatment such as toluidine blue in vitro or tetracycline can be misleading. labelling in vivo. A decrease in the calcification http://jcp.bmj.com/ front is commonly thought to reflect a decreased rate CLINICAL, BIOCHEMICAL AND RADIOGRAPHIC of mineralisation and hence osteomalacia. There are FEATURES OF OSTEOMALACIA several objections to this view. Thus, the calcification The diagnosis of osteomalacia in chronic renal front does not measure the rate of mineralisation failure depends mainly on the histological examin- but only its extent. Also the calcification front ation of bone, since most patients have no character- correlates well with the proportion of bone surface istic clinical, biochemical, or radiographic features. covered by active-looking osteoblasts in patients The frequency with which osteomalacia causes on September 30, 2021 by guest. Protected with chronic renal failure, and is therefore a better symptoms is very variable and in the Oxford Renal index of the number of functional osteoblasts than Unit, symptoms are confined to 10-20% of affected of the adequacy of bone mineralisation.8 Moreover, patients whereas in the Newcastle Renal Unit, where calcification fronts are commonly expressed as a the incidence of osteomalacia is greater12 (see Fig. 2), proportion of the non-mineralised (osteoid) bone symptoms appear also to be more frequent. surface, clearly an inadequate baseline in renal Symptoms of osteomalacia include bone pain and osteodystrophy, where surface osteoid may be tenderness, and proximal muscle weakness. Pains in increased because of augmented bone turnover due the lower limbs, pelvis and back are particularly to hyperparathyroidism. Indeed, reports that common and may be worse on exercise. It is our osteomalacia has improved in response to treatment experience'3 that bone pain occurs with equal such as vitamin D may be misleading where the frequency in osteomalacia and osteitis fibrosa and is "improvement"-that is, reduction in the calcifica- therefore not a diagnostic feature. Fractures, tion front, is due to a decrease in the amount of the *Osteoid is normally laid down in tight lamellar bundles and bone trabecular surface occupied by osteoid. woven osteoid requires a degree of structural disorganisation. J Clin Pathol: first published as 10.1136/jcp.34.11.1295
Load more

Recommended publications
  • 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.
    [Show full text]
  • Diagnosis and Treatment of Intramedullary Osteosclerosis
    Abe et al. BMC Musculoskeletal Disorders (2020) 21:762 https://doi.org/10.1186/s12891-020-03758-5 CASE REPORT Open Access Diagnosis and treatment of intramedullary osteosclerosis: a report of three cases and literature review Kensaku Abe, Norio Yamamoto, Katsuhiro Hayashi, Akihiko Takeuchi* , Shinji Miwa, Kentaro Igarashi, Takashi Higuchi, Yuta Taniguchi, Hirotaka Yonezawa, Yoshihiro Araki, Sei Morinaga, Yohei Asano and Hiroyuki Tsuchiya Abstract Background: Intramedullary osteosclerosis (IMOS) is a rare condition without specific radiological findings except for the osteosclerotic lesion and is not associated with family history and infection, trauma, or systemic illness. Although the diagnosis of IMOS is confirmed after excluding other osteosclerotic lesions, IMOS is not well known because of its rarity and no specific feature. Therefore, these situations might result in delayed diagnosis. Hence, this case report aimed to investigate three cases of IMOS and discuss imaging findings and clinical outcomes. Case presentation: All three cases were examined between 2015 and 2019. The location of osteosclerotic lesions were femoral diaphyses in the 60-year-old man (Case 1) and 41-year-old woman (Case 2) and tibial diaphysis in the 44-year-old woman (Case 3). All cases complained of severe pain and showed massive diaphyseal osteosclerotic lesions in plain radiograms and computed tomography (CT) scans. Cases 2 and 3 were examined using the triphasic bone scan, and a fusiform-shaped intense area of the tracer uptake on delayed bone image was detected in both cases without (Case 2) or slightly increased vascularity (Case 3) on the blood pool image, which was reported as a specific finding of IMOS.
    [Show full text]
  • Hypophosphatasia: Current Literature for Pathophysiology, Clinical Manifestations, Diagnosis, and Treatment
    Open Access Review Article DOI: 10.7759/cureus.8594 Hypophosphatasia: Current Literature for Pathophysiology, Clinical Manifestations, Diagnosis, and Treatment Abdulai Bangura 1 , Lisa Wright 2 , Thomas Shuler 2 1. Department of Research, Trinity School of Medicine, Ratho Mill, VCT 2. Department of Orthopaedics, Carilion Clinic, Roanoke, USA Corresponding author: Abdulai Bangura, [email protected] Abstract Hypophosphatasia (HPP) is a rare inherited bone disorder identified by impaired bone mineralization. There are seven subtypes of HPP mainly characterized by their age of onset. These subtypes consist of perinatal (prenatal) benign, perinatal lethal, infantile, childhood, adult, odontohypophosphatasia, and pseudohypophosphatasia. Due to limited awareness of the condition, either misdiagnosis or delayed diagnosis is common. Furthermore, the condition is frequently treated with contraindicated drugs. This literature illustrates the most recent findings on the etiology, pathophysiology, clinical manifestations, diagnosing, and treatment for HPP and its subtypes. The etiology of the disease consists of loss-of-function mutations of the ALPL gene on chromosome one, which encodes for tissue nonspecific isoenzyme of alkaline phosphatase (TNAP). A decrease of TNAP reduces inorganic phosphate (Pi) for bone mineralization and allows for an increase in inorganic pyrophosphate (PPi) and phosphorylated osteopontin (p-OPN), which further reduces bone mineralization. The combination of these processes softens bone and mediates a clinical presentation similar to rickets/osteomalacia. HPP has an additional wide range of clinical features depending on its subtype. Although a concrete diagnostic guideline has not yet been established, many studies have supported a similar method of identifying HPP. Clinical features, radiological findings, and/or biomarker levels of the disorder should raise suspicion and encourage the inclusion of HPP as a differential diagnosis.
    [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]
  • Secondary Hyperparathyroidism Mimicking Osteomyelitis
    Henry Ford Health System Henry Ford Health System Scholarly Commons Case Reports Medical Education Research Forum 2019 5-2019 Secondary Hyperparathyroidism Mimicking Osteomyelitis Mohamad Hadied Henry Ford Health System Tammy Hsia Henry Ford Health System Anne Chen Henry Ford Health System Follow this and additional works at: https://scholarlycommons.henryford.com/merf2019caserpt Recommended Citation Hadied, Mohamad; Hsia, Tammy; and Chen, Anne, "Secondary Hyperparathyroidism Mimicking Osteomyelitis" (2019). Case Reports. 84. https://scholarlycommons.henryford.com/merf2019caserpt/84 This Poster is brought to you for free and open access by the Medical Education Research Forum 2019 at Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Case Reports by an authorized administrator of Henry Ford Health System Scholarly Commons. Secondary Hyperparathyroidism Mimicking Osteomyelitis Tammy Hsia, Mohamad Hadied MD, Anne Chen MD Henry Ford Hospital, Detroit, Michigan Background Case Report Discussion • The advent of dialysis​ technology has improved outcomes for patients • This case highlights renal osteodystrophy from secondary with end stage renal disease. hyperparathyroidism, a common sequelae of chronic kidney disease. • End stage renal disease leads to endocrine disturbances such as • Secondary hyperparathyroidism can manifest with numerous clinical secondary hyperparathyroidism. signs and symptoms including widespread osseous resorptive • Literature is sparse on exact incidence and burden of secondary changes that can mimic osteomyelitis. hyperparathyroidism among populations with end stage renal disease. • In this case, severe knee pain, elevated inflammatory markers and • This case reports examines a case of secondary hyperparathyroidism radiography findings misled the outside hospital to an incorrect secondary to renal osteodystrophy that was mistaken for acute diagnosis of osteomyelitis, resulting in unnecessary and incorrect osteomyelitis.
    [Show full text]
  • A Case of Osteitis Fibrosa Cystica (Osteomalacia?) with Evidence of Hyperactivity of the Para-Thyroid Bodies
    A CASE OF OSTEITIS FIBROSA CYSTICA (OSTEOMALACIA?) WITH EVIDENCE OF HYPERACTIVITY OF THE PARA-THYROID BODIES. METABOLIC STUDY II Walter Bauer, … , Fuller Albright, Joseph C. Aub J Clin Invest. 1930;8(2):229-248. https://doi.org/10.1172/JCI100262. Research Article Find the latest version: https://jci.me/100262/pdf A CASE OF OSTEITIS FIBROSA CYSTICA (OSTEOMALACIA?) WITH EVIDENCE OF HYPERACTIVITY OF THE PARA- THYROID BODIES. METABOLIC STUDY IIF By WALTER BAUER,2 FULLER ALBRIGHT3 AND JOSEPH C. AUB (From the Medical Clinic of the Massachutsetts General Hospital, Boston) (Received for publication February 5, 1929) INTRODUCTION In a previous paper (1) we have pointed out certain characteristic responses in the calcium and phosphorus metabolisms resulting from parathormone4 administration to essentially normal individuals. In the present paper, similar studies will be reported on a patient who presented a condition suggestive of idiopathic hyperparathyroidism. CASE HISTORY The patient, Mr. C. M., sea captain, aged 30, was transferred from the Bellevue Hospital Service to the Special Study Ward of the Massachusetts General Hospital through the courtesy of Dr. Eugene F. DuBois, for further investigation of his calcium metabolism and for consideration of parathyroidectomy. His complete case history has been reported by Hannon, Shorr, McClellan and DuBois (2). It describes a man invalided for over three years with symptoms resulting from a generalized skeletal decalcification. (See x-rays, figs. 1 to 4.) 1 This is No. VII of the series entitled "Studies of Calcium and Phosphorus Metabolism" from the Medical Clinic of the Massachusetts General Hospital. 2 Resident Physician, Massachusetts General Hospital. ' Research Fellow, Massachusetts General Hospital and Harvard Medical School.
    [Show full text]
  • CKD: Bone Mineral Metabolism Peter Birks, Nephrology Fellow
    CKD: Bone Mineral Metabolism Peter Birks, Nephrology Fellow CKD - KDIGO Definition and Classification of CKD ◦ CKD: abnormalities of kidney structure/function for > 3 months with health implications ≥1 marker of kidney damage: ACR ≥30 mg/g Urine sediment abnormalities Electrolyte and other abnormalities due to tubular disorders Abnormalities detected by histology Structural abnormalities (imaging) History of kidney transplant OR GFR < 60 Parathyroid glands 4 glands behind thyroid in front of neck Parathyroid physiology Parathyroid hormone Normal circumstances PTH: ◦ Increases calcium ◦ Lowers PO4 (the renal excretion outweighs the bone release and gut absorption) ◦ Increases Vitamin D Controlled by feedback ◦ Low Ca and high PO4 increase PTH ◦ High Ca and low PO4 decrease PTH In renal disease: Gets all messed up! Decreased phosphate clearance: High Po4 Low 1,25 OH vitamin D = Low Ca Phosphate binds calcium = Low Ca Low calcium, high phosphate, and low VitD all feedback to cause more PTH release This is referred to as secondary hyperparathyroidism Usually not seen until GFR < 45 Who cares Chronically high PTH ◦ High bone turnover = renal osteodystrophy Osteoporosis/fractures Osteomalacia Osteitis fibrosa cystica High phosphate ◦ Associated with faster progression CKD ◦ Associated with higher mortality Calcium-phosphate precipitation ◦ Soft tissue, blood vessels (eg: coronary arteries) Low 1,25 OH-VitD ◦ Immune status, cardiac health? KDIGO KDIGO: Kidney Disease Improving Global Outcomes Most recent update regarding
    [Show full text]
  • Pathogenesis and Diagnostic Criteria for Rickets and Osteomalacia
    Endocrine Journal 2015, 62 (8), 665-671 OPINION Pathogenesis and diagnostic criteria for rickets and osteomalacia —Proposal by an expert panel supported by Ministry of Health, Labour and Welfare, Japan, The Japanese Society for Bone and Mineral Research and The Japan Endocrine Society Seiji Fukumoto1), Keiichi Ozono2), Toshimi Michigami3), Masanori Minagawa4), Ryo Okazaki5), Toshitsugu Sugimoto6), Yasuhiro Takeuchi7) and Toshio Matsumoto1) 1)Fujii Memorial Institute of Medical Sciences, Tokushima University, Tokushima 770-8503, Japan 2)Department of Pediatrics, Osaka University Graduate School of Medicine, Suita 565-0871, Japan 3)Department of Bone and Mineral Research, Research Institute, Osaka Medical Center for Maternal and Child Health, Izumi 594-1101, Japan 4)Department of Endocrinology, Chiba Children’s Hospital, Chiba 266-0007, Japan 5)Third Department of Medicine, Teikyo University Chiba Medical Center, Ichihara 299-0111, Japan 6)Internal Medicine 1, Shimane University Faculty of Medicine, Izumo 693-8501, Japan 7)Division of Endocrinology, Toranomon Hospital Endocrine Center, Tokyo 105-8470, Japan Abstract. Rickets and osteomalacia are diseases characterized by impaired mineralization of bone matrix. Recent investigations revealed that the causes for rickets and osteomalacia are quite variable. While these diseases can severely impair the quality of life of the affected patients, rickets and osteomalacia can be completely cured or at least respond to treatment when properly diagnosed and treated according to the specific causes. On the other hand, there are no standard criteria to diagnose rickets or osteomalacia nationally and internationally. Therefore, we summarize the definition and pathogenesis of rickets and osteomalacia, and propose the diagnostic criteria and a flowchart for the differential diagnosis of various causes for these diseases.
    [Show full text]
  • Adult Osteomalacia a Treatable Cause of “Fear of Falling” Gait
    VIDEO NEUROIMAGES Adult osteomalacia A treatable cause of “fear of falling” gait Figure Severe osteopenia The left hand x-ray suggested the diagnosis of osteomalacia because of the diffuse demineralization. A 65-year-old man was hospitalized with a gait disorder, obliging him to shuffle laterally1 (video on the Neurology® Web site at www.neurology.org) because of pain and proximal limb weakness. He had a gastrectomy for cancer 7 years previously, with severe vitamin D deficiency; parathormone and alkaline phosphatase were increased, with reduced serum and urine calcium and phosphate. There was reduced bone density (figure). He was mildly hypothyroid and pancytopenic. B12 and folate levels were normal. Investigation for an endocrine neoplasm (CT scan, Octreoscan) was negative. EMG of proximal muscles was typical for chronic myopathy; nerve conduction studies had normal results. After 80 days’ supplementation with calcium, vitamin D, and levothyroxine, the patient walked properly without assistance (video); pancytopenia and alkaline phosphatase improved. Supplemental data at This unusual but reversible gait disorder may have resulted from bone pain and muscular weakness related to www.neurology.org osteomalacia2 and secondary hyperparathyroidism, with a psychogenic overlay. Paolo Ripellino, MD, Emanuela Terazzi, MD, Enrica Bersano, MD, Roberto Cantello, MD, PhD From the Department of Neurology, University of Turin (P.R.), and Department of Neurology, University of Eastern Piedmont (E.T., E.B., R.C.), AOU Maggiore della Carità, Novara, Italy. Author contributions: Dr. Ripellino: acquisition of data, video included; analysis and interpretation of data; writing and editing of the manuscript and of the video. Dr. Terazzi: analysis and interpretation of data.
    [Show full text]
  • Periapical Radiopacities
    2016 self-study course two course The Ohio State University College of Dentistry is a recognized provider for ADA CERP credit. ADA CERP is a service of the American Dental Association to assist dental professionals in identifying quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses or instructors, nor does it imply acceptance of credit hours by boards of dentistry. Concerns or complaints about a CE provider may be directed to the provider or to the Commission for Continuing Education Provider Recognition at www.ada.org/cerp. The Ohio State University College of Dentistry is approved by the Ohio State Dental Board as a permanent sponsor of continuing dental education. This continuing education activity has been planned and implemented in accordance with the standards of the ADA Continuing Education Recognition Program (ADA CERP) through joint efforts between The Ohio State University College of Dentistry Office of Continuing Dental Education and the Sterilization Monitoring Service (SMS). ABOUT this COURSE… FREQUENTLY asked QUESTIONS… . READ the MATERIALS. Read and Q: Who can earn FREE CE credits? review the course materials. COMPLETE the TEST. Answer the A: EVERYONE - All dental professionals eight question test. A total of 6/8 in your office may earn free CE questions must be answered correctly credits. Each person must read the contact for credit. course materials and submit an online answer form independently. SUBMIT the ANSWER FORM ONLINE. You MUST submit your answers ONLINE at: Q: What if I did not receive a confirmation ID? us http://dentistry.osu.edu/sms-continuing-education A: Once you have fully completed your .
    [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]
  • Molecular Characterization of Three Canine Models of Human Rare Bone Diseases: Caffey, Van Den Ende-Gupta, and Raine Syndromes
    RESEARCH ARTICLE Molecular Characterization of Three Canine Models of Human Rare Bone Diseases: Caffey, van den Ende-Gupta, and Raine Syndromes Marjo K. Hytönen1,2,3, Meharji Arumilli1,2,3, Anu K. Lappalainen4, Marta Owczarek-Lipska5, Vidhya Jagannathan5, Sruthi Hundi1,2,3, Elina Salmela1,2,3, Patrick Venta6, Eva Sarkiala4, Tarja Jokinen1,4, Daniela Gorgas7, Juha Kere2,3,8, Pekka Nieminen9, Cord Drögemüller5☯, a11111 Hannes Lohi1,2,3☯* 1 Department of Veterinary Biosciences, University of Helsinki, Helsinki, Finland, 2 Research Programs Unit, Molecular Neurology, University of Helsinki, Helsinki, Finland, 3 The Folkhälsan Institute of Genetics, Helsinki, Finland, 4 Department of Equine and Small Animal Medicine, University of Helsinki, Helsinki, Finland, 5 Institute of Genetics, Vetsuisse Faculty, University of Bern, Bern, Switzerland, 6 Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, United States of America, 7 Division of Clinical Radiology, Department of Clinical Veterinary Medicine, Vetsuisse Faculty, OPEN ACCESS University of Bern, Bern, Switzerland, 8 Department of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden, 9 Department of Oral and Maxillofacial Diseases, University of Helsinki, Helsinki, Citation: Hytönen MK, Arumilli M, Lappalainen AK, Finland Owczarek-Lipska M, Jagannathan V, Hundi S, et al. ☯ (2016) Molecular Characterization of Three Canine These authors contributed equally to this work. * [email protected] Models of Human Rare Bone Diseases: Caffey, van den Ende-Gupta, and Raine Syndromes. PLoS Genet 12(5): e1006037. doi:10.1371/journal. pgen.1006037 Abstract Editor: Leigh Anne Clark, Clemson University, UNITED STATES One to two percent of all children are born with a developmental disorder requiring pediatric hospital admissions.
    [Show full text]