Differentiating Osteoporosis from other diseases: Difference between revisions
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* On physical examination, demonstrates [[visual impairment]] | * On physical examination, demonstrates [[visual impairment]] | ||
* On laboratory studies, demonstrates high amounts of [[ | * On laboratory studies, demonstrates high amounts of [[homocysteine]] in [[urine]] | ||
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=== '''Idiopathic transient osteoporosis of hip''' === | === '''Idiopathic transient osteoporosis of hip''' === | ||
Primarily, it is thought to be seen most often in women during the [[third trimester]] of [[pregnancy]]; but it described also in middle aged men. Acute [[hip]] pain is the main characteristic of the [[disease]]; totally, self-limited after 6-8 months. Sometimes it may be explained as early or benign [[avascular necrosis | Primarily, it is thought to be seen most often in women during the [[third trimester]] of [[pregnancy]]; but it described also in middle aged men. Acute [[hip]] pain is the main characteristic of the [[disease]]; totally, [[Self-limiting|self-limited]] after 6-8 months. Sometimes it may be explained as early or benign [[Avascular necrosis|avascular necrosis (AVN)]]. Subchondral [[Cortical bone|cortical]] loss and diffuse [[osteopenia]] of the [[femoral]] head and neck are the [[pathognomonic]] features. Treatment includes joint protection, limited weight bearing, and [[NSAID]]s.<ref name="pmid12812240">{{cite journal| author=Balakrishnan A, Schemitsch EH, Pearce D, McKee MD| title=Distinguishing transient osteoporosis of the hip from avascular necrosis. | journal=Can J Surg | year= 2003 | volume= 46 | issue= 3 | pages= 187-92 | pmid=12812240 | doi= | pmc=3211740 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12812240 }} </ref> | ||
=== '''Osteomalacia''' === | === '''Osteomalacia''' === | ||
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=== '''Scurvy''' === | === '''Scurvy''' === | ||
Regarding the major role of [[vitamin C]] in the biosynthesis of [[collagen]], its | Regarding the major role of [[vitamin C]] in the biosynthesis of [[collagen]], its deficiency may lead to dysfunction of every [[collagen]] containing [[Organ (anatomy)|organs]]; such as [[bones]]. New [[bone]] formation is disturbed and the old [[bone]] becomes brittle due to lack and poor quality of [[collagen]]. Treatment is [[vitamin C]] replacement.<ref name="pmid6309911">{{cite journal| author=Chojkier M, Spanheimer R, Peterkofsky B| title=Specifically decreased collagen biosynthesis in scurvy dissociated from an effect on proline hydroxylation and correlated with body weight loss. In vitro studies in guinea pig calvarial bones. | journal=J Clin Invest | year= 1983 | volume= 72 | issue= 3 | pages= 826-35 | pmid=6309911 | doi=10.1172/JCI111053 | pmc=1129247 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6309911 }} </ref> | ||
=== '''Osteogenesis imperfecta''' === | === '''Osteogenesis imperfecta''' === | ||
[[Osteogenesis imperfecta]] defect mostly in [[collagen]] | [[Osteogenesis imperfecta]] defect mostly in [[Type-I collagen|collagen type I]] synthesis and also improper functioning of [[Osteoblast|osteoblasts]]. [[Short stature]], [[scoliosis]], tooth defects, hearing defects, blue [[sclera]], and propensity for [[Bone fracture|fractures]] are the main clinical features.<ref name="pmid19878741">{{cite journal |vauthors=Van Dijk FS, Pals G, Van Rijn RR, Nikkels PG, Cobben JM |title=Classification of Osteogenesis Imperfecta revisited |journal=Eur J Med Genet |volume=53 |issue=1 |pages=1–5 |year=2010 |pmid=19878741 |doi=10.1016/j.ejmg.2009.10.007 |url=}}</ref> | ||
=== '''Multiple myeloma''' === | === '''Multiple myeloma''' === | ||
[[Multiple myeloma]] is a [[malignant]] proliferation of the [[Plasma cell|plasma cells]], mostly in [[bone marrow]]. It accounts for 40% of all [[bone tumors]]. Diffuse [[bone]] pain and [[tenderness]] are common. When study the disease radiologically, osteolytic lesions could be found on the [[bones]]. The prognosis is poor. [[Chemotherapy]] is the mainstay of treatment.<ref name="pmid12780789">{{cite journal |vauthors= |title=Criteria for the classification of monoclonal gammopathies, multiple myeloma and related disorders: a report of the International Myeloma Working Group |journal=Br. J. Haematol. |volume=121 |issue=5 |pages=749–57 |year=2003 |pmid=12780789 |doi= |url=}}</ref> | [[Multiple myeloma]] is a [[malignant]] proliferation of the [[Plasma cell|plasma cells]], mostly in [[bone marrow]]. It accounts for 40% of all [[bone tumors]]. Diffuse [[bone]] pain and [[tenderness]] are common. When study the disease radiologically, osteolytic lesions could be found on the [[bones]]. The [[prognosis]] is poor. [[Chemotherapy]] is the mainstay of treatment.<ref name="pmid12780789">{{cite journal |vauthors= |title=Criteria for the classification of monoclonal gammopathies, multiple myeloma and related disorders: a report of the International Myeloma Working Group |journal=Br. J. Haematol. |volume=121 |issue=5 |pages=749–57 |year=2003 |pmid=12780789 |doi= |url=}}</ref> | ||
=== '''Homocystinuria''' === | === '''Homocystinuria''' === | ||
[[Homocystinuria]] is an [[autosomal recessive]] inherited disorder that affects the metabolism of the [[amino acid]] [[methionine]]. [[Failure to thrive]], visual problems and musculoskeletal problems are the major presentations.<ref name="pmid324277">{{cite journal |vauthors=Grieco AJ |title=Homocystinuria: pathogenetic mechanisms |journal=Am. J. Med. Sci. |volume=273 |issue=2 |pages=120–32 |year=1977 |pmid=324277 |doi= |url=}}</ref> | |||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2], Cafer Zorkun, M.D., Ph.D. [3], Raviteja Guddeti, M.B.B.S.[4]
Overview
Osteoporosis must be differentiated from other diseases that cause decreasing in bone mineral density (BMD), such as idiopathic transient osteoporosis of hip, osteomalacia, scurvy, osteogenesis imperfecta, multiple myeloma, homocystinuria, and hypermetabolic resorptive osteoporosis.
Differentiating osteoporosis from other diseases
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Idiopathic transient osteoporosis of hip
Primarily, it is thought to be seen most often in women during the third trimester of pregnancy; but it described also in middle aged men. Acute hip pain is the main characteristic of the disease; totally, self-limited after 6-8 months. Sometimes it may be explained as early or benign avascular necrosis (AVN). Subchondral cortical loss and diffuse osteopenia of the femoral head and neck are the pathognomonic features. Treatment includes joint protection, limited weight bearing, and NSAIDs.[1]
Osteomalacia
Inability to mineralize the new formed bone matrix, which is caused by deficiency of vitamin D in adults. It is kind of low-turnover bone disease, in which osteoblasts are always scant. Diffuse bone pain, fatigue, and fractures are the common symptoms. It also can progress to osteoporosis.[2]
Scurvy
Regarding the major role of vitamin C in the biosynthesis of collagen, its deficiency may lead to dysfunction of every collagen containing organs; such as bones. New bone formation is disturbed and the old bone becomes brittle due to lack and poor quality of collagen. Treatment is vitamin C replacement.[3]
Osteogenesis imperfecta
Osteogenesis imperfecta defect mostly in collagen type I synthesis and also improper functioning of osteoblasts. Short stature, scoliosis, tooth defects, hearing defects, blue sclera, and propensity for fractures are the main clinical features.[4]
Multiple myeloma
Multiple myeloma is a malignant proliferation of the plasma cells, mostly in bone marrow. It accounts for 40% of all bone tumors. Diffuse bone pain and tenderness are common. When study the disease radiologically, osteolytic lesions could be found on the bones. The prognosis is poor. Chemotherapy is the mainstay of treatment.[5]
Homocystinuria
Homocystinuria is an autosomal recessive inherited disorder that affects the metabolism of the amino acid methionine. Failure to thrive, visual problems and musculoskeletal problems are the major presentations.[6]
References
- ↑ Balakrishnan A, Schemitsch EH, Pearce D, McKee MD (2003). "Distinguishing transient osteoporosis of the hip from avascular necrosis". Can J Surg. 46 (3): 187–92. PMC 3211740. PMID 12812240.
- ↑ Hiramatsu R, Ubara Y, Sawa N, Hasegawa E, Kawada M, Imafuku A; et al. (2016). "Bone Histology of Two Cases with Osteomalacia Related to Low-dose Adefovir". Intern Med. 55 (20): 3013–3019. doi:10.2169/internalmedicine.55.6806. PMC 5109571. PMID 27746441.
- ↑ Chojkier M, Spanheimer R, Peterkofsky B (1983). "Specifically decreased collagen biosynthesis in scurvy dissociated from an effect on proline hydroxylation and correlated with body weight loss. In vitro studies in guinea pig calvarial bones". J Clin Invest. 72 (3): 826–35. doi:10.1172/JCI111053. PMC 1129247. PMID 6309911.
- ↑ Van Dijk FS, Pals G, Van Rijn RR, Nikkels PG, Cobben JM (2010). "Classification of Osteogenesis Imperfecta revisited". Eur J Med Genet. 53 (1): 1–5. doi:10.1016/j.ejmg.2009.10.007. PMID 19878741.
- ↑ "Criteria for the classification of monoclonal gammopathies, multiple myeloma and related disorders: a report of the International Myeloma Working Group". Br. J. Haematol. 121 (5): 749–57. 2003. PMID 12780789.
- ↑ Grieco AJ (1977). "Homocystinuria: pathogenetic mechanisms". Am. J. Med. Sci. 273 (2): 120–32. PMID 324277.