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Biochemical and morphological changes in herniated human intervertebral disc.

R Ahsan¹, N Tajima, E Chosa

¹Department of Orthopaedic Surgery, Miyazaki Medical College, 5200 Kihara, Kiyotake-cho, Miyazaki 889-1692, Japan.

Journal of Orthopaedic Science : Official Journal of the Japanese Orthopaedic Association

|January 17, 2002

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Intervertebral disc herniation involves programmed cell death, indicated by DNA fragmentation and increased caspase-3 activity. Oxidative stress, evidenced by lipid peroxidation and collagenase activity, contributes to cell death in herniated discs.

Area of Science:

Biochemistry
Molecular Biology
Pathology

Background:

Intervertebral disc herniation pathogenesis requires clarification.
Understanding molecular and morphologic features is crucial.

Purpose of the Study:

Analyze biochemical and morphological features of herniated disc tissues.
Identify factors contributing to intervertebral disc herniation.

Main Methods:

Analyzed 32 herniated and 4 control disc specimens.
Performed collagen analysis, enzyme activity assays (collagenase, caspase-3), lipid peroxidation, metal level analysis, morphologic studies, and genetic analysis.
Utilized in situ nick translation and immunohistochemistry.

Main Results:

Related Experiment Videos

Detected apoptotic DNA fragments and increased caspase-3 activity in herniated discs.
Confirmed absence of Type II collagen in herniated discs, present in controls.
Observed increased lipid peroxidation and collagenase activity, with low metal levels, suggesting oxidative stress.
Electron microscopy indicated enhanced programmed cell death.

Conclusions:

Programmed cell death and oxidative stress are implicated in herniated disc pathogenesis.
Absence of Type II collagen may be a feature of herniated discs.
Potential ethnic variations in herniated disc disease warrant further investigation.