Clinical and theoretical contrast of common non-septic causes of bone degeneration
More details
Hide details
Scientific Society of Students, Medical University, Lublin, Poland
Department of Internal Medicine, Medical University, Lublin, Poland
Arun Prashar   

Department of Internal Medicine, Medical University, Staszica11, 20-081 Lublin, Poland.
J Pre Clin Clin Res. 2012;6(1):7–9
There is an abundance of diseases that cause dysfunctional bone remodeling. Some of these disorders that are commonly seen are porosis, thyrotoxicosis, Multiple Myeloma, and various cancers/neoplasms. They are all capable of causing the degeneration of bone and adversely affecting its structural integrity and stability. There are numerous etiologies that can be implicated in the degeneration of bone, spanning across many disciplines. Unless one is a specialist in all areas, discerning the correct diagnosis can be an arduous task. Usually, when there are a number of different pathologies causing a similar defect, e.g. bone degeneration, they can exhibit similar semblances. Under such circumstances an incorrect diagnosis is often made which results in practitioners administering a battery of unnecessary tests and medications. Aside from the added expense, it is also detrimental to the patient’s morbidity and mortality, as this is when the majority of unwarranted complications arise; all of which contribute to the rising costs of patient healthcare. It is the objective of the presented paper to provide the most salient information to improve the ability of general practitioners to recognize and manage these scenarios, specifically those involving the degeneration of bone. It is to be hoped that it will minimize mistakes and the financial burdens they levy. Generally, the diseases mentioned above have already been extensively researched within their individual spheres in the medical community. Although, publications specifically scrutinizing their similarities and differences within clinical constructs are sparse. In dealing with issues such as bone degeneration where it can be attributed to a multitude of causes it is often most useful to focus on those that are the most prevalent. Understanding their differences on a theoretical level can compound the benefits yielded in a clinical setting, especially with regard to diagnosis, management, and treatment.
Lewis JL, Daly PA, Landsberg L. The Merck Manual of Medicine. 19th rev. ed. Whitehouse Station (NJ): Merck & Co., Inc. 2011; 837-54: 909-14.
Hadidy EH, Ghonaim M, Gawad SS, Atta MA. Impact of severity, duration, and etiology of hyperthyroidism on bone turnover markers and bone mineral density in men. BMC Endocrine Disorders. 2011; 11: 15.
Chavassieux P, Seeman E, Delmas PD. Insights into Material and Structural Basis of Bone Fragility from Diseases Associated with Fractures: How Determinants of the Biomechanical Properties of Bone Are Compromised by Disease. Endocrine Reviews. 2007; 28(2): 151-64.
Prevention and Management of Osteoporosis. Report of a WHO Scientific Group. World Health Organ Tech Rep Ser. 2003; 921: 1-164.
Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. Report of a WHO Study Group. World Health Organ Tech Rep Ser. 1994; 843: 1-129.
Lee J, Vasikaran S. Current recommendations for laboratory testing and use of bone turnover markers in management of osteoporosis. Ann Lab Med. 2012; 32(2): 105-12.
Harvey CB, O’Shea PJ, Scott AJ, Robson H, Siebler T, Shalet SM. Molecular mechanisms of thyroid hormone effects on bone growth and function. Mol Genet Metab. 2002; 75: 17-30.
Nicholls JJ, Brassill MJ, Williams GR, Bassett JH. The skeletal consequences of thyrotoxicosis. J Endocrinol. 2012 Mar;[Epub ahead of print].
Mosekilde L, Eriksen EF, Charles P. Effects of thyroid hormones on bone and mineral metabolism. Endocrin Metab Clin North Am. 1990;19: 35-63.
Ginsberg J. Diagnosis and management of Graves’ disease. CMAJ. 2003; 168(5): 575-85.
Bringhurst FR, Demay MB, Kronenberg HM, Wysolmerski JJ. Insogna KL. In: Kronenberg HM, Schlomo M, Polansky KS, Larsen PR, eds. Williams Textbook of Endocrinology. 11th ed. St. Louis, Mo: WB Saunders; 2008: chap. 27, 266.
Roodman GD. Review Article: Mechanisms of Bone Metastasis. N Engl J Med. 2004; 350: 1655-64.
Coleman RE. Clinical features of metastatic bone disease and risk of skeletal morbidity. Clin Cancer Res. 2006; 12: 6243s-69s.
Tian E, Zhan F, Walker R, Rasmussen E, Ma Y, Barlogie B, et al. The Role of the Wnt-Signaling Antagonist DKK1 in the Development of Osteolytic Lesions in Multiple Myeloma. N Engl J Med. 2003; 349: 2483-94.
International Myeloma Working Group. Criteria for the classification of monoclonal gammopathies, multiple myeloma and related disorders: a report of the International Myeloma Working Group. Br J Haematol. 2003; 121(5): 749-57.
Jimenez-Andrade JM, Mantyh WG, Bloom AP, Ferng AS, Geffre CP, Mantyh PW. Bone cancer pain. Ann NY Acad Sci. 2010; 1198: 173-81.
Pelosof LC, Gerber DE. Paraneoplastic Syndromes: An approach to diagnosis and Treatment. Mayo Clin Proc. 2010; 85(9): 839-54.
Khan AA, Bilezikian JP, Kung AW, Ahmed M, Dubois SJ, Ho AY, et al. Alendronate in primary hyperparathyroidism: a double-blind, randomized, placebo-controlled trial. J ClinEndocrinolMetab. 2004; 89(7): 3319-25.
Selby PL, Peacock M. Ethinyl estradiol and norethindrone in the treatment of primary hyperparathyroidism in postmenopausal women. N Engl J Med. 1986; 314: 1481-5.
Common cancers and the tumor markers linked to them. http://www. Descriptions/TumorMarkers/tumor-markers-common-ca-and-t-m (accessed: April 6, 2012).