Objective. To ascertain whether there is an association between tendinopath
ic and ruptured Achilles tendons, hypothesizing that the histopathological
aspects of tendinosis in tendinopathic tendons are less advanced than those
found in ruptured Achilles tendons. Methods: This was a comparative cohort
study at a university teaching hospital. Histological examination was perf
ormed using hematoxylin and eosin and alcian blue/periodic acid-Schiff stai
ned slides. The slides were interpreted using a semiquantitative grading sc
ale assessing fiber structure, fiber arrangement, rounding of the nuclei, r
egional variations in cellularity, increased vascularity, decreased collage
n stainability, hyalinization, and glycosaminoglycan. We calculated a patho
logy score giving up to three marks for each of the above variables, with 0
being normal and 3 being maximally abnormal. All the histology slides were
assessed twice in a blinded manner, the agreement between two readings ran
ging from 0.170 to 0.750 (kappa statistics). Results: We studied biopsy sam
ples from the Achilles tendon of patients undergoing open repair for a subc
utaneous rupture of their Achilles tendon (N = 35; average age (+/- SD), 48
.4 +/- 16.9 yr; range, 26-80), biopsy specimens from the Achilles tendon of
patients undergoing exploration for Achilles tendinopathy (N = 13; average
age, 35.7 +/- 12.9 yr; range, 18-67) and specimens of Achilles tendons fro
m individuals with no known tendon pathology (N = 16; average age, 65 +/- 1
9.1 yr; range, 46-82). The highest mean score of ruptured tendons was signi
ficantly greater than that of tendinopathic tendons (17.4 +/- 4.9 vs 10.5 /- 6.1, P < 0.001), and highest mean score of tendinopathic tendons was gre
ater that that of control tendons (10.5 +/- 6.1 vs 5.9 +/- 7.3) (P < 0.001)
. Conclusion: Ruptured and tendinopathic tendons are histologically signifi
cantly more degenerated than control tendons. The general pattern of degene
ration was common to the ruptured and tendinopathic tendons, but there was
a statistically significant greater degree of degeneration in the ruptured
tendons. It is therefore possible that there is a common, as yet unidentifi
ed, pathological mechanism that has acted on both of these tendon populatio
ns.