Histological difference in ligament flavum between degenerative lumbar canal stenosis and non-stenotic group: A prospective, comparative study.

BACKGROUND: 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.

AIM: To compare the histopathological changes in LF between the degenerative LCS and non-stenotic (non-LCS) group.

METHODS: 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.

RESULTS: Out of 82 cases, 74 were analysed, 34 in LCS and 40 in non-LCS group. The mean ± SD age of presentation in LCS and non- LCS group was 49.2 ± 8.9 and 43.1 ± 14.3 respectively. The LCS group ( n = 34) exhibited significant differences in fibrosis ( P = 0.002), elastic fiber degeneration ( P = 0.01), % elastic fragmentation (66.5 ± 16.3 vs 29.5 ± 16.9), % elastic, content (26.9 ± 6.7 vs 34.7 ± 8.4), % collagen content (63.6 ± 10.4 vs 54.9 ± 6.4), reduction of elastic/collagen (0.4 ± 0.1 vs 0.6 ± 0.1), and ligamentocyte number (39.1 ± 19.1 vs 53.5 ± 26.9) as compared to non-LCS group ( n = 40). The calcification ( P = 0.08) and Pearson's correlation between duration and loss of elastin was not significant. The difference in LF morphology is consistent in patient's ≥ 40 years of age among the groups as found in subgroup analysis. Similarly in the patents < 40 and > 40 in the non-LCS group.

CONCLUSION: LF is vital in the pathogenesis of LCS. The purely elastic LF undergoes a morphological adaptation that includes a reduction in the elastic fibers with a consequent increase in the collagen content, fibrosis, cicatrization, and calcification. The present study provides a detailed morphometric analysis to semiquantitatively delineate the LF changes in patients with LCS from those in patients without LCS.