Differentiating Osteoporosis from other diseases: Difference between revisions
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==='''Idiopathic transient osteoporosis of hip'''=== | ==='''Idiopathic transient osteoporosis of hip'''=== | ||
* It was initially thought to be seen in women during the [[third trimester]] of [[pregnancy]] but it is seen also in middle-aged men. | |||
* Acute [[hip]] pain is the main feature of the [[disease]], usually [[Self-limiting|self-limited]] and resolves 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''' === | ||
Osteomalacia is the inability to mineralize the newly formed [[bone]] matrix, caused by the deficiency of [[vitamin D]] in adults. It is | * Osteomalacia is the inability to mineralize the newly formed [[bone]] matrix, caused by the deficiency of [[vitamin D]] in adults. | ||
* It is due to low turn-over of [[bone]] in which [[osteoblasts]] are deficient. | |||
* Diffuse [[bone]] pain, fatigue, and [[fractures]] are the most common symptoms. | |||
* It can also 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''' === | === '''Scurvy''' === | ||
[[Vitamin C]] deficiency causes defective [[collagen]] synthesis, leading to dysfunction of every [[collagen]] containing [[Organ (anatomy)|organ]] | * [[Vitamin C]] deficiency causes defective [[collagen]] synthesis, leading to dysfunction of every [[collagen]] containing [[Organ (anatomy)|organ]] 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]] is mainly induced by defect in the synthesis of [[Type-I collagen|collagen type I]] along with improper [[Osteoblast|osteoblasts]] functioning. [[Short stature]], [[scoliosis]], tooth defects, hearing defects, blue [[sclera]], and propensity for [[Bone fracture|fractures]] are the main clinical features of the [[disease]].<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> | * [[Osteogenesis imperfecta]] is mainly induced by defect in the synthesis of [[Type-I collagen|collagen type I]] along with improper [[Osteoblast|osteoblasts]] functioning. | ||
* [[Short stature]], [[scoliosis]], tooth defects, hearing defects, blue [[sclera]], and propensity for [[Bone fracture|fractures]] are the main clinical features of the [[disease]].<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. Radiologically, osteolytic lesions could be found in 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. | |||
* Radiologically, osteolytic lesions could be found in 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]] disorder that affects the metabolism of the [[amino acid]] [[methionine]] | * [[Homocystinuria]] is an [[autosomal recessive]] disorder that affects the metabolism of the [[amino acid]] [[methionine]]. | ||
* Clinical features include [[failure to thrive]], visual and musculoskeletal problems.<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> | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Medicine]] | | ||
[[Category:Medicine]] | |||
[[Category:Primary care]] | [[Category:Primary care]] | ||
[[Category:Endocrinology]] | [[Category:Endocrinology]] | ||
[[Category:Up-To-Date]] | [[Category:Up-To-Date]] | ||
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Revision as of 17:51, 7 November 2017
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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 a decrease in the 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
Osteoporosis must be differentiated from other diseases that cause a decrease in the bone mineral density (BMD), such as idiopathic transient osteoporosis of hip, osteomalacia, scurvy, osteogenesis imperfecta, multiple myeloma, homocystinuria, and hypermetabolic resorptive osteoporosis. The major similarities and differences among the diseases are discussed in the following table:
Diseases | History and Physical Examination | Imaging findings | Laboratory Findings | Other Findings | |||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Bone pain | Fatigue | Short stature | Scoliosis | Bone tenderness | BMD | Sub-chondral cortical loss | Bone fracture | Vitamin C | Ca | Vitamin D | ALKph | ||
Osteoporosis | + | - | + | - | + | ↓↓↓ | - | + | ↓ | - | - | - | |
Idiopathic transient osteoporosis of hip | + | - | - | - | - | ↓↓ | + | - | - | - | - | ↑ |
|
Osteomalacia | - | - | - | - | - | ↓ | - | + | - | ↓ | ↓ | - | |
Scurvy | + | + | - | - | - | - | - | + | - | - | - | - | |
Osteogenesis imperfecta | - | - | + | + | - | ↓ | - | + | - | - | - | - |
|
Multiple myeloma | + | + | - | - | + | ↓ | - | + | - | - | - | ↑ |
|
Homocystinuria | + | - | - | - | - | ↓ | - | + | - | - | - | - |
Idiopathic transient osteoporosis of hip
- It was initially thought to be seen in women during the third trimester of pregnancy but it is seen also in middle-aged men.
- Acute hip pain is the main feature of the disease, usually self-limited and resolves 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
- Osteomalacia is the inability to mineralize the newly formed bone matrix, caused by the deficiency of vitamin D in adults.
- It is due to low turn-over of bone in which osteoblasts are deficient.
- Diffuse bone pain, fatigue, and fractures are the most common symptoms.
- It can also progress to osteoporosis.[2]
Scurvy
- Vitamin C deficiency causes defective collagen synthesis, leading to dysfunction of every collagen containing organ 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 is mainly induced by defect in the synthesis of collagen type I along with improper osteoblasts functioning.
- Short stature, scoliosis, tooth defects, hearing defects, blue sclera, and propensity for fractures are the main clinical features of the disease.[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.
- Radiologically, osteolytic lesions could be found in the bones.
- The prognosis is poor.
- Chemotherapy is the mainstay of treatment.[5]
Homocystinuria
- Homocystinuria is an autosomal recessive disorder that affects the metabolism of the amino acid methionine.
- Clinical features include failure to thrive, visual and musculoskeletal problems.[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.