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

Revision as of 20:29, 28 November 2018

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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.
  • Many hypothesis have been postulated.
  • 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]
  • Vertebral bodies are seen wedged in the sagittal plane in IS patients, causing an apical lordosis in thoracic curvatures resulting in rotation of the spine and, secondarily, a lateral spinal curvature.
  • On MRI scans of IS patients, it seen that the length of the spinal cord is shorter in relation to the vertebral column and there is an increased prevalence of cerebellar tonsillar ectopia as well as an uncoordinated growth of the vertebral bodies in relation to the dorsal elements.[9][10][11]
  • This has led to theories proposing a relative anterior spinal overgrowth (RASO) or an uncoupled neuro-osseus growth as a cause of IS.[12]
  • The risk of curve progression in IS is related to skeletal immaturity.
  • It has also been shown that girls with adolescent IS are taller and have a higher growth velocity during puberty in comparison to healthy individuals.[13][14][15]
  • Bone mineral density, growth, and sex hormones have been studied in the pathogenesis of IS.
  • Adolescent girls with IS have lower bone mineral density and a higher bone turnover rate.[16][17]
  • In addition, a decreased level of cartilage oligomeric matrix protein (COMP) in serum is seen in IS patients.[18]
  • A raised levels of growth hormone (GH) and insulin-like growth factor 1 (IGF-1) have been associated with IS.[19][20]
  • A lower circulating levels of leptin, the “satiety” hormone have been suggested in pathogenesis of IS.[21][22][23]
  • Leptin is primarily secreted by adipocytes, and leptin receptor can be detected in chondrocytes and osteoblasts.
  • Leptin regulates the osteogenic differentiation of bone marrow stem cells and the function of chondrocytes by directly binding to leptin receptors.
  • Leptin functions to promotes chondrocyte proliferation and differentiation; regulates chondrocyte function by enhancing the production of collagen, matrix metalloproteinase (MMP), and bone morphogenetic protein (BMP) and remodels the cytoskeleton.

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.[24]

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.


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. ↑ 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.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ 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.
  8. ↑ 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.
  9. ↑ Chu WC, Lam WW, Chan YL, Ng BK, Lam TP, Lee KM; et al. (2006). "Relative shortening and functional tethering of spinal cord in adolescent idiopathic scoliosis?: study with multiplanar reformat magnetic resonance imaging and somatosensory evoked potential". Spine (Phila Pa 1976). 31 (1): E19–25. PMID 16395162.
  10. ↑ Abul-Kasim K, Overgaard A, Karlsson MK, Ohlin A (2009). "Tonsillar ectopia in idiopathic scoliosis: does it play a role in the pathogenesis and prognosis or is it only an incidental finding?". Scoliosis. 4: 25. doi:10.1186/1748-7161-4-25. PMC 2780387. PMID 19909551.
  11. ↑ Guo X, Chau WW, Chan YL, Cheng JC (2003). "Relative anterior spinal overgrowth in adolescent idiopathic scoliosis. Results of disproportionate endochondral-membranous bone growth". J Bone Joint Surg Br. 85 (7): 1026–31. PMID 14516040.
  12. ↑ Chu WC, Lam WM, Ng BK, Tze-Ping L, Lee KM, Guo X; et al. (2008). "Relative shortening and functional tethering of spinal cord in adolescent scoliosis - Result of asynchronous neuro-osseous growth, summary of an electronic focus group debate of the IBSE". Scoliosis. 3: 8. doi:10.1186/1748-7161-3-8. PMC 2474583. PMID 18588673.
  13. ↑ Normelli H, Sevastik J, Ljung G, Aaro S, Jönsson-Söderström AM (1985). "Anthropometric data relating to normal and scoliotic Scandinavian girls". Spine (Phila Pa 1976). 10 (2): 123–6. PMID 4002036.
  14. ↑ Willner S (1974). "A study of growth in girls with adolescent idiopathic structural scoliosis". Clin Orthop Relat Res (101): 129–35. PMID 4837925.
  15. ↑ Chazono M, Soshi S, Kida Y, Hashimoto K, Inoue T, Nakamura Y; et al. (2012). "Height velocity curves in female patients with idiopathic scoliosis". Stud Health Technol Inform. 176: 202–5. PMID 22744490.
  16. ↑ Hung VW, Qin L, Cheung CS, Lam TP, Ng BK, Tse YK; et al. (2005). "Osteopenia: a new prognostic factor of curve progression in adolescent idiopathic scoliosis". J Bone Joint Surg Am. 87 (12): 2709–16. doi:10.2106/JBJS.D.02782. PMID 16322621.
  17. ↑ Cheung CS, Lee WT, Tse YK, Lee KM, Guo X, Qin L; et al. (2006). "Generalized osteopenia in adolescent idiopathic scoliosis--association with abnormal pubertal growth, bone turnover, and calcium intake?". Spine (Phila Pa 1976). 31 (3): 330–8. doi:10.1097/01.brs.0000197410.92525.10. PMID 16449907.
  18. ↑ Gerdhem P, Topalis C, Grauers A, Stubendorff J, Ohlin A, Karlsson KM (2015). "Serum level of cartilage oligomeric matrix protein is lower in children with idiopathic scoliosis than in non-scoliotic controls". Eur Spine J. 24 (2): 256–61. doi:10.1007/s00586-014-3691-2. PMID 25427671.
  19. ↑ Sanders JO, Browne RH, Cooney TE, Finegold DN, McConnell SJ, Margraf SA (2006). "Correlates of the peak height velocity in girls with idiopathic scoliosis". Spine (Phila Pa 1976). 31 (20): 2289–95. doi:10.1097/01.brs.0000236844.41595.26. PMID 16985455.
  20. ↑ Willner S, Johnell O (1981). "Study of biochemical and hormonal data in idiopathic scoliosis in girls". Arch Orthop Trauma Surg. 98 (4): 251–5. PMID 6170273.
  21. ↑ Qiu Y, Sun X, Qiu X, Li W, Zhu Z, Zhu F; et al. (2007). "Decreased circulating leptin level and its association with body and bone mass in girls with adolescent idiopathic scoliosis". Spine (Phila Pa 1976). 32 (24): 2703–10. doi:10.1097/BRS.0b013e31815a59e5. PMID 18007248.
  22. ↑ Wang YJ, Yu HG, Zhou ZH, Guo Q, Wang LJ, Zhang HQ (2016). "Leptin Receptor Metabolism Disorder in Primary Chondrocytes from Adolescent Idiopathic Scoliosis Girls". Int J Mol Sci. 17 (7). doi:10.3390/ijms17071160. PMC 4964532. PMID 27447624.
  23. ↑ Burwell RG, Dangerfield PH, Moulton A, Anderson SI (2008). "Etiologic theories of idiopathic scoliosis: autonomic nervous system and the leptin-sympathetic nervous system concept for the pathogenesis of adolescent idiopathic scoliosis". Stud Health Technol Inform. 140: 197–207. PMID 18810025.
  24. ↑ Texas Scottish Rite Hospital for Children Research: Scoliosis Research

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References

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