Published online Sep 18, 2022. doi: 10.5312/wjo.v13.i9.791
Peer-review started: January 17, 2022
First decision: February 21, 2022
Revised: March 2, 2022
Accepted: August 24, 2022
Article in press: August 24, 2022
Published online: September 18, 2022
Processing time: 241 Days and 17.8 Hours
Ligament flavum (LF) hypertropy is the main etiopathogenesis of lumbar canal stenosis (LCS). The purely elastic LF undergoes a morphological adaptation including a reduction in the elastic fibers and a consequent increase in the collagen content, fibrosis, cicatrization, and calcification. However, the morphometric analysis can delineate the LF in patients with LCS from those without LCS, which would help in better understanding LCS pathogenesis.
The research is motivated due to high footfall of these patient on Orthopedic outpatient department. An interdepartmental meeting was made to analyze these patients and funds were provided by the institute.
To compare the histopathological changes in LF between the degenerative LCS and non-stenotic (non-LCS) group.
The present prospective study was conducted in 82 patients who were divided into two groups, namely LCS and non-LCS. Demographic details of the patients such as duration of symptoms, level of involvement, and number of segments were recorded. The LF obtained from both groups was histopathologically examined for the fibrosis score, elastic fiber degeneration, calcification, and chondroid metaplasia. Morphometrical details included a change in elastin and collagen percentages, elastin/collagen ratio, elastic fiber fragmentation, and ligamentocyte numbers. All parameters were compared between the two groups by using the independent t test, Chi-square test, and Pearson’s correlation test.
Of the total, we selected 74 patients. The number of patients in the LCS and non-LCS groups was 34 and 40, respectively. The mean ± standard deviation of age of presentation in the LCS and non-LCS groups was 49.2 ± 8.9 and 43.1 ± 14.3 years, respectively. The difference in fibrosis (P = 0.002), elastic fiber degeneration (P = 0.01), elastic fragmentation percentage (66.5% ± 16.3% vs 29.5% ± 16.9%), elastic content percentage (26.9% ± 6.7% vs 34.7% ± 8.4%), collagen content percentage (63.6% ± 10.4% vs 54.9% ± 6.4%), reduction of elastic/collagen ratio (0.4 ± 0.1 vs 0.6 ± 0.1), and ligamentocyte number (39.1 ± 19.1 vs 53.5 ± 26.9) between the LCS and non-LCS groups was statistically significant. The difference in calcification (P = 0.08) and Pearson’s correlation between duration and loss of elastin was statistically nonsignificant. Subgroup analysis exhibited a consistent difference in LF morphology in patients aged ≥ 40 years between the two groups. A similar finding was observed in patients aged < 40 and > 40 years in the non-LCS group.
The quality change in elastin fibers and an increase in the collagen content and fibrosis cause loss of elasticity in LF, contributing to LCS pathogenesis. However, calcification did not play a significant role in LCS pathogenesis.
Tne study compare the histopathological changes in LF between the degenerative LCS and non-stenotic (non-LCS) group.