Scoliosis pathophysiology: Difference between revisions

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{{Scoliosis}}
{{Scoliosis}}


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==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
The exact pathogenesis of scoliosis is not fully understood.


OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.


OR
It is thought that scoliosis is the result of nutritional, endocrine, or genetic factors.


Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.


OR
OR
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==Pathophysiology==
==Pathophysiology==
*Idiopathic scoliosis(IS) is the most common form of spinal deformity seen in healthy children and adoloscent during growth.
*The pathophysiology of scoliosis in not clearly understood.
*Animal studies have shown that pinealectomies lead to development of scoliosis due to lack of melatonin.<ref name="pmid13629950">{{cite journal| author=THILLARD MJ| title=[Vertebral column deformities following epiphysectomy in the chick]. | journal=C R Hebd Seances Acad Sci | year= 1959 | volume= 248 | issue= 8 | pages= 1238-40 | pmid=13629950 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13629950  }} </ref><ref name="pmid10528372">{{cite journal| author=Machida M, Murai I, Miyashita Y, Dubousset J, Yamada T, Kimura J| title=Pathogenesis of idiopathic scoliosis. Experimental study in rats. | journal=Spine (Phila Pa 1976) | year= 1999 | volume= 24 | issue= 19 | pages= 1985-9 | pmid=10528372 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10528372  }} </ref><ref name="pmid7822371">{{cite journal| author=Machida M, Dubousset J, Imamura Y, Iwaya T, Yamada T, Kimura J| title=Role of melatonin deficiency in the development of scoliosis in pinealectomised chickens. | journal=J Bone Joint Surg Br | year= 1995 | volume= 77 | issue= 1 | pages= 134-8 | pmid=7822371 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7822371  }} </ref>


===Genetics===
===Genetics===

Revision as of 17:02, 28 November 2018

Scoliosis Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2]


Overview

The exact pathogenesis of scoliosis is not fully understood.


It is thought that scoliosis is the result of nutritional, endocrine, or genetic factors.


OR


[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].

OR

The progression to [disease name] usually involves the [molecular pathway].

OR

The pathophysiology of [disease/malignancy] depends on the histological subtype.

Overview

Pathophysiology

  • Idiopathic scoliosis(IS) is the most common form of spinal deformity seen in healthy children and adoloscent during growth.
  • The pathophysiology of scoliosis in not clearly understood.
  • Animal studies have shown that pinealectomies lead to development of scoliosis due to lack of melatonin.[1][2][3]








Genetics

In the case of the most common form of scoliosis, Adolescent Idiopathic Scoliosis, there is a clear Mendelian inheritance but with incomplete penetrance.

In April 2007, researchers at Texas Scottish Rite Hospital for Children identified the first gene associated with idiopathic scoliosis, CHD7. The medical breakthrough was the result of a 10-year study and is outlined in the May 2007 issue of the American Journal of Human Genetics.[4]

Associated conditions

Scoliosis is sometimes associated with other conditions such as

However, the majority of people with adolescent scoliosis have no pain or other abnormalities.


Pathophysiology

Pathogenesis

  • The exact pathogenesis of [disease name] is not fully understood.

OR

  • It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
  • [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
  • Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
  • [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
  • The progression to [disease name] usually involves the [molecular pathway].
  • The pathophysiology of [disease/malignancy] depends on the histological subtype.

Genetics

  • [Disease name] is transmitted in [mode of genetic transmission] pattern.
  • Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
  • The development of [disease name] is the result of multiple genetic mutations.

Associated Conditions

Gross Pathology

  • On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Microscopic Pathology

  • On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

References

  1. THILLARD MJ (1959). "[Vertebral column deformities following epiphysectomy in the chick]". C R Hebd Seances Acad Sci. 248 (8): 1238–40. PMID 13629950.
  2. Machida M, Murai I, Miyashita Y, Dubousset J, Yamada T, Kimura J (1999). "Pathogenesis of idiopathic scoliosis. Experimental study in rats". Spine (Phila Pa 1976). 24 (19): 1985–9. PMID 10528372.
  3. Machida M, Dubousset J, Imamura Y, Iwaya T, Yamada T, Kimura J (1995). "Role of melatonin deficiency in the development of scoliosis in pinealectomised chickens". J Bone Joint Surg Br. 77 (1): 134–8. PMID 7822371.
  4. Texas Scottish Rite Hospital for Children Research: Scoliosis Research

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References

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