Scoliosis pathophysiology
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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.The observation that curve development and progression correlate with the period of rapid adolescent growth appears to support a biomechanical contribution. However, multiple theories exist that attempt to explain the process by which the development takes place, and while each makes sense from a biomechanical standpoint, it has been difficult to directly correlate these theories to the in vivo scoliotic spine.
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.
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]
- Dysfunctional melatonin signal pathway involving MT2 receptors affecting osteoblast have been recommended.[4][5]
- Calmodulin, a calcium-binding receptor protein, controls contraction in platelets and muscles, and interacts with melatonin. Increased levels of calmodulin in platelets and a disproportionate distribution of calmodulin in paraspinal muscles have been suggested in IS patients.[6][7][8]
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.[9]
Associated conditions
Scoliosis is sometimes associated with other conditions such as
- Cerebral palsy
- Spinal muscular atrophy
- Familial dysautonomia
- CHARGE syndrome
- Friedreich's ataxia
- Spina bifida
- Marfan's syndrome
- Neurofibromatosis
- Connective tissue disorder
- Craniospinal axis disorders (e.g., syringomyelia, Arnold-Chiari malformation).
- Roussy-levy disease
- Charcot-marie-tooth disease
- Duchenne muscular dystrophy
- Limb girdle dystrophy
- Arthrogyposis
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
- ↑ THILLARD MJ (1959). "[Vertebral column deformities following epiphysectomy in the chick]". C R Hebd Seances Acad Sci. 248 (8): 1238–40. PMID 13629950.
- ↑ 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.
- ↑ 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.
- ↑ Moreau A, Wang DS, Forget S, Azeddine B, Angeloni D, Fraschini F; et al. (2004). "Melatonin signaling dysfunction in adolescent idiopathic scoliosis". Spine (Phila Pa 1976). 29 (16): 1772–81. PMID 15303021.
- ↑ Wang WW, Man GC, Wong JH, Ng TB, Lee KM, Ng BK; et al. (2014). "Abnormal response of the proliferation and differentiation of growth plate chondrocytes to melatonin in adolescent idiopathic scoliosis". Int J Mol Sci. 15 (9): 17100–14. doi:10.3390/ijms150917100. PMC 4200781. PMID 25257530.
- ↑ Wu JZ, Wu WH, He LJ, Ke QF, Huang L, Dai ZS; et al. (2016). "Effect of Melatonin and Calmodulin in an Idiopathic Scoliosis Model". Biomed Res Int. 2016: 8460291. doi:10.1155/2016/8460291. PMC 5155075. PMID 28042574.
- ↑ Lowe T, Lawellin D, Smith D, Price C, Haher T, Merola A; et al. (2002). "Platelet calmodulin levels in adolescent idiopathic scoliosis: do the levels correlate with curve progression and severity?". Spine (Phila Pa 1976). 27 (7): 768–75. PMID 11923672.
- ↑ Acaroglu E, Akel I, Alanay A, Yazici M, Marcucio R (2009). "Comparison of the melatonin and calmodulin in paravertebral muscle and platelets of patients with or without adolescent idiopathic scoliosis". Spine (Phila Pa 1976). 34 (18): E659–63. doi:10.1097/BRS.0b013e3181a3c7a2. PMID 19680092.
- ↑ Texas Scottish Rite Hospital for Children Research: Scoliosis Research