Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/27484
Title: Chondroid metaplasia of paraspinal connective tissue in the degenerative spine: a case report
Authors: STEVENS, Sjoerd 
AGTEN, Anouk 
Wisanto, E.
VERBRUGGHE, Jonas 
TIMMERMANS, Annick 
VANDENABEELE, Frank 
Issue Date: 2018
Source: 9th Biennial Congress of the Belgian Back Society, Brussel, 01/12/2018
Abstract: Introduction: The extracellular matrix (ECM) and its progenitor cells most likely play a role in degeneration of paraspinal muscles and their surrounding connective tissues. Fibro-adipogenic cells are suggested to contribute to the formation of extraskeletal cartilage and bone. When cartilage tissue is formed in a foreign place outside the skeleton, it is diagnosed as chondroid metaplasia. Chondroid metaplasia is a benign condition, found in connective tissues in response to chronic mechanical stress, but can also be found in in more malignant pathologies. Case report: We report a case of chondroid metaplasia within the paraspinal tissue of a 51 year old male, during a routine paraspinal muscle biopsy procedure (1). The patient presented completely asymptomatic, reported no history of low back pain or trauma related to his back. The biopsy specimen was histologically analysed, and the patient was referred to the department of radiology for medical imaging of the spinal column. Based on these findings, the specimen was diagnosed as chondroid metaplasia. Discussion: To date there have been no reports on chondroid changes within paraspinal connective tissues. The fibro-adipogenic cell might play an important role in chondroid metaplasia of connective tissue, as it does in degeneration (fatty degeneration and fibrosis) of muscle tissue. Normally, this cell gives rise to fibroblasts that produce the ECM. It’s possible that osteogenic cytokines or dysregulation of bone morphometric protein signalling within an inflammatory context plays a role in the process of transforming fibro-adipogenic cells. We suggest an interaction between fibro-adipogenic cells and local inflammation seen in degenerative spinal conditions, to induce connective tissue degeneration. Conclusion: We presented a case of chondroid metaplasia within paraspinal connective tissue, combined with severe spinal degeneration. Further research is needed to investigate the presence of chondroid metaplasia (and its underlying mechanism) in the process of paraspinal degeneration.
Document URI: http://hdl.handle.net/1942/27484
Category: C2
Type: Conference Material
Appears in Collections:Research publications

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