International Journal of Spine Surgery

June 30, 2020; Vol. 14; No. 3; pp. 341–346

Sudhir G, Balasubramaniam S, Jayabalan V, Sundaram S, Kumar V, Kailash K.

This study cites 23 references.


Diabetes mellitus (DM) stands as a pervasive health concern, affecting millions globally and leading to multi-organ dysfunction. A recent study published in the International Journal of Spine Surgery explores the impact of type 2 diabetes on human intervertebral discs, shedding light on the accelerated senescence and degeneration observed in these crucial spinal structures.

Understanding the Intervertebral Disc:

The human intervertebral disc comprises a gelatinous nucleus pulposus (NP) and an outer annulus fibrosus. Notochordal cells, remnants from early development, gradually transform into chondrocyte-like cells by the second decade of life.

Key Points from the Study:

  • Diabetes Mellitus as a Health Challenge:
  • DM is a major contributor to morbidity, with an estimated incidence of 300 million cases in 2015.
  • Accounting for 90% of diabetic cases, DM can impact various organ systems, leading to complications such as cardiovascular disease, chronic renal failure, retinopathy, and neuropathy.
  • Senescence and Hyperglycemia:
  • Senescence, a mechanism preventing damaged DNA cells from proliferating, is accelerated by hyperglycemia.
  • Hyperglycemia-induced senescence is implicated in premature disc degeneration, affecting intervertebral discs similarly to other organs.
  • Study Results:
  • The research demonstrates that type 2 diabetes accelerates stress-induced senescence in human intervertebral discs, resulting in early degeneration.
  • Samples from diabetic patients exhibited severe degenerative changes compared to the control group.
  • Intense changes in the nucleus pulposus included increased cellularity, clustering of chondrocytes, and disorganization of the nuclear matrix.
  • Hyperglycemia and Disc Degeneration:
  • Hyperglycemia is identified as a key factor in early disc degeneration, affecting surgery outcomes for degenerative disc disease in diabetic patients.
  • Excessive production of reactive oxygen species mediates cellular apoptosis, senescence, and autophagy, contributing to cellular and organ damage.
  • Mechanisms for Accelerated Degeneration:
  • Increased production of advanced glycation end products (AGEs) and the generation of reactive oxygen species contribute to mitochondrial damage and cellular autophagy.
  • High glucose levels accelerate senescence in nucleus pulposus cells in a dose and time-dependent manner.
  • Preventing Degeneration Through Blood Glucose Control:
  • Adequate control of blood glucose is emphasized as a crucial factor in preventing early disc degeneration and halting the progression of the degeneration cascade.


This groundbreaking study provides valuable insights into the intricate relationship between type 2 diabetes and intervertebral disc health. Understanding the mechanisms of accelerated senescence and degeneration opens avenues for preventive strategies, highlighting the importance of managing blood glucose levels in preserving the integrity of intervertebral discs and averting early disc degeneration.