Aetiology

The aetiology of DISH remains largely unknown.[1][2]​​​ Several possible contributory factors to the development of the condition have been implicated, including genetic, metabolic, hormonal, inflammatory, and signal transduction system aberrations, as well as vascular and mechanical effects.[1][2]​ Vitamin A toxicity as well as use of vitamin A derivatives such as retinoids may also have a role in the disease process.[11][12][13]​​​​ Exposure to fluoride has been suggested as a potential contributor to the development of DISH; however, no clear evidence of this has been found to date.

Growth hormone, which has been identified as being elevated in the serum and synovial fluid of patients with DISH, may stimulate osteoblast proliferation, which subsequently might result in excessive ossification.[9]

The key risk factors for developing DISH are age >50 years, male sex, and obesity.[2][6][7][8][14][15]​​​​ Diabetes mellitus, metabolic syndrome, and hypertension are associated conditions,and may have a role in the disease process; these conditions may often precede the diagnosis of DISH.[2][16][17]​​​

A weaker risk factor is possible genetic predisposition.[2] Single-nucleotide polymorphisms in the COL6A1 and FGF2 genes may be linked to the development of DISH, according to preliminary data.[2][4]​​ HLA-B8 has also been noted to be present in some patients with DISH.[14]

Pathophysiology

Although the pathophysiology of DISH is currently unknown, several mechanisms have been proposed as having a role in the development of the condition.[2][9]​​

The pathognomonic feature of DISH is the development of new bone, and this is an area of ongoing research.[9] The new bone in the spine creates an osteophyte (a small bony bridge or spur) connecting one vertebral body to the adjacent one. This new bone, which contains largely cortical and a small amount of cancellous bone, is contiguous with the upper and lower vertebral bodies. The woven bone (which forms the osteophyte) indicates that the formation of new bone is undergoing continual remodelling. Local fibroblasts, chondrocytes, collagen fibres, and calcified matrix are probably influenced by genetic, vascular, metabolic, and mechanical factors because new bone originates predominantly at entheseal sites.[9] Signal transduction pathways are ultimately impacted by metabolic derangements, and those specially associated with osteoblast differentiation have been linked to the development of DISH.

There have been clusters of disease within families, occurring within the third decade, which could indicate a genetic role in the pathophysiology.[9] Single-nucleotide polymorphisms in the COL6A1 and FGF2 genes may be linked to the development of DISH, according to preliminary data.[2][4]

On imaging, the osteophytes of DISH are most likely to be seen on the right anterior thoracic spine, directly across from the pulsating aorta.[1] The descending aorta may act protectively as a mechanical barrier, preventing the development of the bony manifestations of DISH on the left side of the thoracic vertebral bodies. Similarly, in the cervical spine, pulsations from the carotid artery may prevent the development of hyperostosis on the lateral sides of cervical vertebral bodies.[1]

Historically, ossification of the anterior longitudinal ligament was thought to be the primary location of DISH. Now there is evidence that ossifications in DISH may occur in additional locations in the spine.[1]

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