The human skeleton has the unique function of calcium storage and liberation in addition to locomotion and hematopoiesis, and acting as the body framework. Under the complex homeostatic regulation of calcitonin and parathormone as well as the influence of auxiliary hormones and vitamin D, living bones are ceaselessly engaged with deposition and removal of calcium salts in the form of bone production and resorption, which are mediated by the activities of osteoblasts and osteoclasts, respectively. Basically, skeletal diseases are reflected first as quantitative changes in osseous calcium salts and serum calcium levels. The mobilization of calcium salts from and excessive deposition on bone in bone disorders, both nongenetic and genetic, may result in demineralization or decalcification and osteosclerosis, respectively. Then, with the advance of disease, pathological and anatomical skeletal changes may follow manifesting in the form of osteopenia, osteoporosis, osteolysis, sclerosis, eburnation, bone defect, growth disturbance, and deformity, either singly or in combination. Thus, in order to ideally detect bone disorders at an early stage, the calcium metabolic profile of bone must be obtained by an appropriate means before anatomical change takes place.
Slip Capital Femoral Epiphysis Reactive Arthritis Calcium Salt Diffuse Idiopathic Skeletal Hyperostosis Skeletal Disorder
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Amor B, Cherot A, Delbarre, et al (1977) Hydroxyapatite rheumatism and HLA markers. J Rheumatol Suppl 3:101–104 PubMedGoogle Scholar
Bahk YW, Chung SK, Park YH, et al (1998) Pinhole SPECT imaging in normal and morbid ankles. J Nucl Med 39:130–139 PubMedGoogle Scholar
Benli IT, Akalin S, Boysan E, et al (1992) Epidemiological, clinical and radiological aspects of osteopoikilosis. J Bone Joint Surg Br 74:504–506 PubMedGoogle Scholar
Black B, Dooley J, Pyper A, Reed M (1993) Multiple hereditary exostoses. An epidemiologic study of an isolated community in Manitoba. Clin Orthop Rel Res 287:212–217 Google Scholar
Bonde CT, Vielfreund L (2001) Buschke-Ollendorff syndrome. Connective tissue nevi in osteopoikilosis. Ugeskr Laeger 8:170–171 Google Scholar
Dahlin DC, Unni KK (1986) Chondroma. In: (eds) Bone tumors, 4th edn. Thomas, Springfield Google Scholar
Fong KY (2000) The genetics of spondyloarthropathies. Ann Acad Med Singapore 29:370–375 PubMedGoogle Scholar
Goldman AB (1995) Heritable diseases of connective tissue, epiphyseal dysplasia, and related conditions. In: Resnick D, Niwayama K (eds) Diagnosis of bone and joint disorders, 3rd edn. Saunders, Philadelphia Google Scholar
Groshar D, Rosenbaum M, Rosner I (1997) Enthesopathies, inflammatory spondyloenthesopathies and bone scintigraphy. J Nucl Med 38:2003–2005 PubMedGoogle Scholar
Kahn MA (1988) Ankylosing spondylitis and heterogeneity of HLA-B27. Semin Arthritis Rheum 18:134–141 CrossRefGoogle Scholar
Kim SH, Chung SK, Bahk YW, et al (1999) Whole-body and pinhole bone scintigraphic manifestations of Reiter’s syndrome: distribution patterns and early and characteristic signs. Eur J Nucl Med 26:163–170 PubMedCrossRefGoogle Scholar
Leirisalo M, Skylv G, Kousa M, et al (1982) Follow-up study on patients with Reiter’s disease and reactive arthritis, with special reference to HLA-B27. Arthritis Rheum 25:249–259 PubMedCrossRefGoogle Scholar
McAlister WH, Herman TE (1995) Osteochondrodysplasias, dysostoses, chromosomal aberrations, mucopolysaccharidoses, and mucolipidoses. In: Resnick D, Niwayama G (eds) Diagnosis of bone and joint disorders, 3rd edn. Philadelphia, Saunders Google Scholar
McCarty DJ, Gatter RA (1966) Recurrent acute inflammation associated with focal apatite crystal deposition. Arthritis Rheum 9:804–819 PubMedCrossRefGoogle Scholar
Medina M, Viglietti AL, Gozzeli L, et al (2000) Indium111 labelled white blood cell scintigraphy in cranial and spinal septic lesions. Eur J Nucl Med 27:1473–1480 PubMedCrossRefGoogle Scholar
Morris R, Metzger AL, Bluestone R, et al (1974) HL-A W27 – A clue to the diagnosis and pathogenesis of Reiter’s syndrome. New Engl J Med 290:554–556 PubMedCrossRefGoogle Scholar
Mullaji AB, Emery RJH, Joysey VC, et al (1993) HLA and slipped capital femoral epiphysis. J Orthop Rheumatol 6:167–169 Google Scholar
Ochsner PE (1978) Multiple cartilaginous exostoses and neoplastic degeneration: review of the literature. Z Orthop Ihre Grenzgeb 116:369–378 PubMedGoogle Scholar