Index to Chiropractic Literature
Index to Chiropractic Literature
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Monday, October 27, 2025
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Article ID
Title
URL https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6112070/?report=classic
Journal J Chiropr Med. 2018 Jun;17(2):97-105
Author(s)
Subject(s)
Peer Review Yes
Publication Type Review
Abstract/Notes

Objective: The purpose of this paper was to review the literature regarding the mechanisms leading to degeneration in intervertebral disks and to discuss contributing mechanical and biological factors.

Methods: The inclusion criteria for the literature review were research studies conducted in the last 3 decades with free full-text available in English. Review articles and articles pertaining to temporomandibular joints and joints of the body other than the intervertebral disk were excluded. The following databases were searched: PubMed, EBSCOhost, and Google Scholar through September 9, 2016.

Results: A total of 57 articles were used in this review. Intervertebral disk cells require glucose for sustainability and oxygen to synthesize matrix components. Nutrients enter the disk via 2 vascular supply routes: capillary beds of end plates and the peripheral annulus fibrosus. Solute size, shape and charge, compression, and metabolic demand all influence the efficiency of nutrient transport, and alterations of any of these factors may have effects on nutrient transport and, potentially, disk degeneration.

Conclusions: Progressive nutrient transport disruptions may actively contribute in advancing the phases of degenerative disk disease. Such disruptions include dysfunctional loading and spinal position, lack of motion, high frequency loading, disk injury, aging, smoking, an acidic environment, and a lack of nutrient bioavailability.

Author keywords: Intervertebral Disk Disease; Diet, Food, and Nutrition; Intervertebral Disk Degeneration

Author affiliation: Department of Research, Logan University, Chesterfield, Missouri

This abstract is reproduced with the permission of the publisher; click on the above link for free full text. PubMed Record


 

      

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