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.
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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.
Mode of Spread
- Pott's disease is a result of hematogenous spread of the infection, to the cancellous bone of the vertebral bodies. The spread can be via the arterial or the venous route.
- 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 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 adjecent vertebra.
- 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.
- The spread of infection via the intraosseous venous system causes central vertebral body lesions. Therefore, in patients with noncontiguous spinal involvement or involvement of multiple vertebra, it signifies the infection spread is via the venous route.
- The spread of infection below the anterior or posterior longitudinal ligaments affects multiple contiguous vertebrae.
Pathogenesis
- The infection initially affects the anterior aspect of the vertebral body adjacent to the subchondral plate. Then the infection spreads to the adjacent intervertebral disks.
- 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.
- 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.
- The infection results in the destruction of the intervertebral disk 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 vertebrae.
- The destruction of the disk 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.
- 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 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.
Genetics
- A study of 109 patients in the china with spinal TB, showed higher frequencies of FokI polymorphism in the vitamin-D receptor gene of patients with tuberculosis.[1]
Microscopic Pathology
- Histologic examination of the biopsy specimen demonstrate epithelioid cell granulomas, lymphocytic infiltration and multinucleated and Langhans giant cells.
References
- ↑ 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.