Pott's disease pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hardik Patel, M.D.
Overview
Pott's disease occurs usually due to hematogenous spread of tuberculous infection from an extraspinal source. Pott's disease usually involves more than one vertebra and manifests as a combination of osteomyelitis and arthritis.
Pathophysiology
Source of infection
- The primary source of infection is either from a pulmonary site or a genitourinary site.[1]
Mode of Spread
- Pott's disease is a result of hematogenous spread of infection, to the cancellous bone of the vertebral body. The spread can be via the arterial or the venous route.[2]
- Normally, a rich vascular plexus is present in the sub-chondral region of each vertebrae. The blood supply is derived from anterior and posterior spinal arteries. The presence of rich vascular plexus facilitates the hematogenous spread of infection to the spine. The characteristic involvement is multiple contiguous vertebra is due to the blood supply, the segmental arteries from the anterior and posterior spinal arteries divide to form segmental arteries which supply two adjacent vertebra.[3]
- The Batson's venous plexus is a valve-less venous system and the blood flow through the plexus is bi-directional which is depends on the pressure in the intra-abdominal and intra-thoracic compartments during exertion or activities which such as coughing.[4]
- The spread of infection via the intraosseous venous system causes central vertebral body lesions. Therefore, in patients with non contiguous spinal involvement or involvement of multiple vertebra, it signifies the infection spread is via the venous route.[5]
- The spread of infection below the anterior or posterior longitudinal ligaments affects multiple contiguous vertebrae.
Pathogenesis
- The infection in classic spinal tuberculosis initially affects the anterior aspect of the vertebral body adjacent to the subchondral plate. Then the infection spreads to the adjacent intervertebral discs.[6]
- The common site affected in spinal tuberculosis in children is the intervertebral discs due to the high vascularity. In adults or in old age the vertebral bodies are commonly affected due to age related avascularity.[7][8]
- The common lesions of vertebra in spinal tuberculosis include paradiskal, anterior, and central lesions.
- The most commonly involved sites are the upper lumbar and the lower thoracic vertebrae, the body of the vertebra is typically affected than the arch.[6]
- The infection results in the destruction of the intervertebral disc space and the adjacent vertebral bodies, collapse of the spinal elements, and anterior wedging resulting in a characteristic angulation and gibbus formation. Gibbus is a palpable deformity due to the involvement of multiple vertebra.[6]
- The destruction of the disc space and the wedging results in spinal deformity. Kyphosis is more prominent if the disc and bone destruction occurs in the thoracic spine due to the collapse in the anterior spine. The granuloma or the abscess can cause narrowing of the spinal canal leading to paraplegia secondary to cord compression.[7]
- In patients with anterior spinal tuberculosis, motor fibers are compressed first affecting the motor function. This is because the motor fibres are anteriorly placed in relation to the sensory fibers in spinal cord.
- In patients with posterior spinal tuberculosis, the motor fibers are compressed first again, and this is because the motor fibers are more susceptible to pressure and sensory fibers are susceptible to ischemia.[9]
Genetics
- A study of 109 patients in the china with spinal tuberculosis, showed higher frequencies of FokI polymorphism in the vitamin-D receptor gene of patients with tuberculosis when compared to controls.[10][11]
Microscopic Pathology
- Histologic examination of the biopsy specimen demonstrate epithelioid cell granulomas, lymphocytic infiltration and multinucleated Langhans giant cells.
References
- ↑ Rajasekaran S, Kanna RM, Shetty AP (2014). "Pathophysiology and Treatment of Spinal Tuberculosis". JBJS Rev. 2 (9). doi:10.2106/JBJS.RVW.M.00130. PMID 27490153.
- ↑ Cooper C, Fellner R, Heubi O, Maixner F, Zink A, Lösch S (2016). "Tuberculosis in early medieval Switzerland--osteological and molecular evidence". Swiss Med Wkly. 146: w14269. doi:10.4414/smw.2016.14269. PMID 26826871.
- ↑ Batirel A, Erdem H, Sengoz G, Pehlivanoglu F, Ramosaco E, Gülsün S; et al. (2015). "The course of spinal tuberculosis (Pott disease): results of the multinational, multicentre Backbone-2 study". Clin Microbiol Infect. 21 (11): 1008.e9–1008.e18. doi:10.1016/j.cmi.2015.07.013. PMID 26232534.
- ↑ Formica M, Cavagnaro L, Formica C (2015). "Pott disease". Spine J. 15 (3): 556–7. doi:10.1016/j.spinee.2014.11.006. PMID 25459741.
- ↑ Kim JH, Kim SH, Choi JI, Lim DJ (2014). "Atypical noncontiguous multiple spinal tuberculosis: a case report". Korean J Spine. 11 (2): 77–80. doi:10.14245/kjs.2014.11.2.77. PMC 4124923. PMID 25110488.
- ↑ 6.0 6.1 6.2 Ekinci S, Tatar O, Akpancar S, Bilgic S, Ersen O (2015). "Spinal Tuberculosis". J Exp Neurosci. 9: 89–90. doi:10.4137/JEN.S32842. PMC 4644140. PMID 26609247.
- ↑ 7.0 7.1 Kilborn T, Janse van Rensburg P, Candy S (2015). "Pediatric and adult spinal tuberculosis: imaging and pathophysiology". Neuroimaging Clin N Am. 25 (2): 209–31. doi:10.1016/j.nic.2015.01.002. PMID 25952174.
- ↑ Tin SS, Wiwanitkit V (2014). "Noncontiguous multiple spinal tuberculosis". Korean J Spine. 11 (4): 259. doi:10.14245/kjs.2014.11.4.259. PMC 4303286. PMID 25620992.
- ↑ Shim HK, Cho HL, Lee SH (2014). "Spinal tuberculosis at the posterior element of spinal column: case report". Clin Neurol Neurosurg. 124: 146–50. doi:10.1016/j.clineuro.2014.05.021. PMID 25051165.
- ↑ Zhang HQ, Deng A, Guo CF, Wang YX, Chen LQ, Wang YF; et al. (2010). "Association between FokI polymorphism in vitamin D receptor gene and susceptibility to spinal tuberculosis in Chinese Han population". Arch Med Res. 41 (1): 46–9. doi:10.1016/j.arcmed.2009.12.004. PMID 20430254.
- ↑ Panwar A, Garg RK, Malhotra HS, Jain A, Singh AK, Prakash S; et al. (2016). "25-Hydroxy Vitamin D, Vitamin D Receptor and Toll-like Receptor 2 Polymorphisms in Spinal Tuberculosis: A Case-Control Study". Medicine (Baltimore). 95 (17): e3418. doi:10.1097/MD.0000000000003418. PMC 4998689. PMID 27124026.