Human intervertebral disc anulus tissue was obtained in a prospective study of cell senescence.
Localization of the senescence biomarker beta-galactosidase (senescence associated beta-galactosidase, SA-beta-gal) was used for quantitative determination of the senescent cells percentage.
Discs were obtained from surgical specimens or control donors.
Discs were also studied from the lumbar spine of the sand rat.
Scientists aimed to determine the incidence of cell senescence in human discs with Thompson Grades I through V using immunocytochemistry to quantify the percentage of cells positive for the senescence biomarker SA-beta-gal. presuming that ell senescence has been recognized as a potential factor playing a role in age-related disc degeneration.
Senescent cells are viable but have lost the ability to divide.
Senescence cells, however, are metabolically active.
By analyzing 57 discs specimens from 54 subjects for senescent cells using immunocytochemistry for anti-SA-beta-gal immunocytochemical localization.
The fraction of positive cells was determined with quantitative histomorphometry.
Results of quantitative histomorphometry of human discs show an overall incidence of SA-beta-gal-positive cells of 29.9% (± 24.8, SD), with a range from 0 to 92.01%.
Analysis by ANOVA of the senescent cellspercentage grouped by Thompson grade showed significant increases in senescence with increasing disc degeneration (P < 0.0001).
Further analysis with Tukey's test showed significant differences between the senescent cells percetage in Grades I/II versus IV, and versus V.
SA-beta-gal-positive cells were also present in discs of the aging sand rat spine.
So concluding it can be stated that quantitative analysis of immunohistochemical localization of SA-beta-gal identified a sizeable population of senescent cells in the aging/degenerating disc.
It is important to discover more about the senescent disc cell population because these cells persist and accumulate over time within the disc.
Since senescent cells cannot divide, senescence may reduce the disc's ability to generate new cells to replace existing ones lost to necrosis or apoptosis.