Differentiating Osteoporosis from other diseases: Difference between revisions
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==Differentiating osteoporosis from other diseases== | ==Differentiating osteoporosis from other diseases== | ||
* '''[[Idiopathic]] transient osteoporosis of [[Hip (anatomy)|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). Sub-chondoral 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> | * '''[[Idiopathic]] transient osteoporosis of [[Hip (anatomy)|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). Sub-chondoral 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> | ||
[[Image:Transient-hip-osteoporosis.jpg|300px|center|thumb|Idiopathic transient osteoporosis of hip; note to the decreased bone density in left femur.]] | [[Image:Transient-hip-osteoporosis.jpg|300px|center|thumb|Idiopathic transient osteoporosis of hip; note to the decreased bone density in left femur.]]<ref name="urlIdiopathic transient osteoporosis of the hip | Radiology Reference Article | Radiopaedia.org">{{cite web |url=++++https://radiopaedia.org/articles/idiopathic-transient-osteoporosis-of-the-hip |title=Idiopathic transient osteoporosis of the hip | Radiology Reference Article | Radiopaedia.org |format= |work= |accessdate=}}</ref> | ||
* '''[[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]].<ref name="pmid27746441">{{cite journal| author=Hiramatsu R, Ubara Y, Sawa N, Hasegawa E, Kawada M, Imafuku A et al.| title=Bone Histology of Two Cases with Osteomalacia Related to Low-dose Adefovir. | journal=Intern Med | year= 2016 | volume= 55 | issue= 20 | pages= 3013-3019 | pmid=27746441 | doi=10.2169/internalmedicine.55.6806 | pmc=5109571 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27746441 }} </ref> | * '''[[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]].<ref name="pmid27746441">{{cite journal| author=Hiramatsu R, Ubara Y, Sawa N, Hasegawa E, Kawada M, Imafuku A et al.| title=Bone Histology of Two Cases with Osteomalacia Related to Low-dose Adefovir. | journal=Intern Med | year= 2016 | volume= 55 | issue= 20 | pages= 3013-3019 | pmid=27746441 | doi=10.2169/internalmedicine.55.6806 | pmc=5109571 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27746441 }} </ref> | ||
* '''[[Scurvy]]''': 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> | * '''[[Scurvy]]''': 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> | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2],Raviteja Guddeti, M.B.B.S.[3]
Overview
Osteoporosis must be differentiated from other diseases include: idiopathic transient osteoporosis of hip, osteomalacia, scurvy, osteogenesis imperfecta, multiple myeloma, homocystinuria, and hypermetabolic resorptive osteoporosis; which can all present with some similar features, too.
Differentiating osteoporosis from other diseases
- 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). Sub-chondoral 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.[3]
- 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.[4]
- 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. [5]
- 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.[6]
- 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.[7]
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.
- ↑ [++++https://radiopaedia.org/articles/idiopathic-transient-osteoporosis-of-the-hip "Idiopathic transient osteoporosis of the hip | Radiology Reference Article | Radiopaedia.org"] Check
|url=value (help). - ↑ 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.