CLINICAL SCIENCES

Clinical Investigations

Ruptured Achilles tendons are

significantly more degenerated than
tendinopathic tendons

CHERYL TALLON, NICOLA MAFFULLI, and STANLEY W. B. EWEN

Department of Orthopaedic Surgery, University of Aberdeen Medical School, Aberdeen, SCOTLAND; Department of
Trauma and Orthopaedic Surgery, Keele University School of Medicine, Stoke on Trent, Staffordshire, ENGLAND; and
Department of Pathology, University of Aberdeen Medical School, Aberdeen, SCOTLAND

ABSTRACT
TALLON, C., N. MAFFULLI, and S. W. B. EWEN. Ruptured Achilles tendons are significantly more degenerated than tendinopathic
tendons. Med. Sci. Sports Exerc., Vol. 33, No. 12, 2001, pp. 1983–1990. Objective: To ascertain whether there is an association
between tendinopathic 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 performed using hematoxylin and eosin and alcian blue/periodic acid–Schiff stained
slides. The slides were interpreted using a semiquantitative grading scale assessing fiber structure, fiber arrangement, rounding of the
nuclei, regional variations in cellularity, increased vascularity, decreased collagen stainability, hyalinization, and glycosaminoglycan.
We calculated a pathology 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 ranging from 0.170
to 0.750 (kappa statistics). Results: We studied biopsy samples from the Achilles tendon of patients undergoing open repair for a
subcutaneous 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 from individuals with no known tendon pathology (N ⫽ 16; average age, 65 ⫾ 19.1 yr; range,
46 – 82). The highest mean score of ruptured tendons was significantly 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 greater that that of control tendons (10.5 ⫾ 6.1 vs 5.9 ⫾ 7.3)
(P ⬍ 0.001). Conclusion: Ruptured and tendinopathic tendons are histologically significantly more degenerated than control tendons.
The general pattern of degeneration 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 unidentified, pathological
mechanism that has acted on both of these tendon populations. Key Words: TENDINOSIS, ETIOLOGY, SURGERY, HISTOPA-
THOLOGY

P
revious studies on the histology of Achilles tendon
ruptures have shown that a degenerative process had
taken place before the rupture occurred (2,11,12). The
histological picture was studied by Kannus and Jozsa (12),
when they evaluated specimens obtained from the biopsy of
891 spontaneously ruptured tendons, including 397 Achilles
tendons. Using 445 age- and sex-matched controls, they
described a variety of degenerative changes within the ten-
don. Degenerative tendinopathy was found to be the most
0195-9131/01/3312-1983/$3.00/0
MEDICINE & SCIENCE IN SPORTS & EXERCISE®
Copyright © 2001 by the American College of Sports Medicine
Submitted for publication January 2001.
Accepted for publication March 2001.
1983
common disorder in tendons that have ruptured spontane-
ously, but calcification and mucoid changes have also been
described (3,4,10,12). All the ruptured tendons have preex-
isting histopathological alterations, but such changes were
much less frequent in the control tendons (12).
Other studies have shown morphological and metabolism
changes with increasing age (9,23). One of these metabolic
changes seen is an increase in the production of type III
collagen from damaged tenocytes (17) and chondroid meta-
plasia (22), which results in the tendon becoming cartilage-
like, and therefore less able to withstand tensile forces.
Cumulative microtrauma weakens collagen cross-linking,
noncollagenous matrix, and vascular elements of the tendon
(11). When a tendon has been strained repeatedly to more than
4% of its original length, it is unable to endure any further
TABLE 1. Median values for each semiquantitative histopathological criterion in each group.
FS FA N RVC
Control 1 1 0 0
Ruptured 2 2 2 3
Tendinopathic 1 1 3 2
FS, fiber structure; FA, fiber arrangement; N, cell nuclei; RVC, regional variations in cellularity; V, vascularity; DCS, decreased collagen stainability; H, hyalinization; GAG,
glycosaminoglycan.
Median values for each criterion in each group.
tension, and injury will occur (7) with a break in collagen
structure. Tissue hypoxia and consequent free radical–induced
tendon changes resulting from ischemia-reperfusion injury
could also be major factors in the pathogenesis of a tendino-
pathic tendon (1,5,6). Another factor in the development of
tendon degeneration could be exercise-induced hyperthermia.
Histopathologically, these tendons reveal disordered arrange-
ment of collagen fibrils and an increase in vascularity (15) with
an increase in the amount of mucoid ground substance, where
tenocytes, if present, are chondroid in appearance (22).
Although preexisting tendinosis has been observed in
ruptured tendons (3,8,12), it is still unknown why some
patients are symptomatic, and develop tendinopathy, and
others are asymptomatic despite the presence of advanced
histological changes (13,14). It could be possible that two
separate pathological processes occur in patients who rup-
ture their Achilles tendon without any previous pain, and
those who suffer from chronic tendinopathy pain.
We therefore sought to ascertain whether there is an
association between tendinopathic and ruptured tendons,
hypothesizing that the histopathological aspects of tendino-
sis in tendinopathic tendons are less advanced than those
found in a rupture (15). Therefore, we compared nonrup-
tured tendon samples to ruptured and tendinopathic tendon
samples.
METHODS
Tendon Samples
All procedures were approved by the Ethical Committee
of the Grampian University Hospitals Trust. All patients
and, when applicable, their families gave written informed
consent that the procedures described in this article could be
carried out, as required by British law.
Control (nonruptured) tendons (N ⴝ 16; average
age 65 ⴞ 19.1; range, 46 – 82). Samples were obtained
from two sources: 1) patients undergoing amputation for
peripheral vascular disease admitted to the department of
vascular surgery of Aberdeen Royal Infirmary between
April 1996 and December 1998, and 2) patients who died of
cardiovascular accidents while inpatients at Aberdeen Royal
Infirmary between April 1996 and December 1998. The
Achilles tendon was harvested in the post mortem room
under sterile conditions through a medial approach. The
tendon was freed from surrounding tissue, and as much
muscle and fat as possible were removed. The tendon was
cut horizontally at the superior and inferior ends. Previous
1984 Official Journal of the American College of Sports Medicine
All Criteria All Criteria
V DCS H GAG (1st Score) (2nd Score)
0 0 0 0 2 2.5
2 2 1 2 17 16
2 2 0 2 11 13
studies (15) showed that there were no statistically signifi-
cant differences in the histopathological appearance of
Achilles tendons from amputated legs and from patients
deceased for cardiovascular causes. Therefore, the results
from these two groups of patients were grouped together,
and such tendons will be referred to as “control tendons.”
Tendinopathic Achilles tendons (N ⴝ 13; average
age, 35.7 ⴞ 12.9 yr; range, 18 – 67). Samples of tendi-
nopathic tendons were obtained from patients undergoing
exploration of their Achilles tendons at Woodend Hospital,
Aberdeen, during the period June 1999 until November
1999. During the operation, a sample 3 ⫻ 3 ⫻ 3 mm was
removed within the area of degeneration.
Ruptured Achilles tendons (N ⴝ 35; average age,
48.4 ⴞ 16.9 yr; range, 26 – 80). Samples of ruptured
tendons were obtained from patients who sustained a uni-
lateral subcutaneous tear of the Achilles tendon repaired in
the trauma theater at Aberdeen Royal Infirmary in the period
January 1997 to December 1998. During surgical repair of
the ruptured tendon, performed within 48 h of the injury and
without using a tourniquet, two samples measuring approx-
imately 3 ⫻ 3 ⫻ 3 mm were removed from both the
proximal and distal stumps of the tendon.
Preparation of Slides
The specimens obtained were placed in 20 mL of sterile
10% formalin and fixed in 10% neutral buffered formalin
(10% NBF) for 24 – 48 h and processed to paraffin wax;
5-␮m sections were then mounted onto 3-aminopropyltri-
ethoxysilane (APES) coated slides and dried at 37°C
overnight.
Sections were dewaxed in two 10-min changes of xylene,
followed by one change in absolute alcohol, 95% alcohol,
for 10 min each to rehydrate the sections. The sections were
then rinsed under running tap water. Sections were stained
using hematoxylin and eosin, and using the alcian blue (pH
2.5)/periodic acid–Schiff (AB/PAS) method for the detec-
tion of glycosaminoglycan (GAG) rich areas.
Assessment of Tendon Degeneration
Per each tendon sample and per each staining technique,
three slides were randomly selected and examined using a
light microscope (⫻600, SM-LUX, Leitz, Wetzlar, Germa-
ny). The identification number on each slide was covered
with a removable sticker, and each slide was numbered
using randomly generated numbers. After one of the authors
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TABLE 2. Results of semiquantitative histopathological assessment.
Controls (N ⴝ 16) Tendinopathic (N ⴝ 23) Ruptured (N ⴝ 35)
0 1 2 3 0 1 2 3 0 1 2 3
Scores following first FS 7 5 1 2 3 12 7 1 1 8 13 13
semiquantitative FA 7 5 1 2 3 12 7 1 1 8 13 13
assessment N 9 2 2 2 2 4 5 12 2 5 13 15
RVC 10 2 0 3 6 2 12 3 5 6 5 19
V 11 0 3 1 8 3 8 4 9 5 9 12
DCS 8 1 4 2 3 5 11 4 4 7 7 17
H 11 1 1 2 16 1 6 0 17 8 2 8
GAG 10 4 1 0 5 5 8 5 5 3 15 12
Scores following FS 8 3 1 2 3 10 9 1 0 12 10 13
second FA 8 3 1 2 3 10 9 1 0 12 10 13
semiquantitative N 11 1 1 2 5 4 3 11 2 5 8 20
assessment
RVC 10 3 1 1 8 1 6 8 4 3 9 19
V 11 1 1 1 8 2 10 3 5 5 6 19
DCS 8 2 3 2 7 3 6 7 5 1 8 21
H 11 2 0 2 16 5 2 0 15 6 8 6
GAG 6 8 1 0 5 3 8 7 7 4 13 11
FS, fiber structure; FA, fiber arrangement; N, cell nuclei; RVC, regional variations in cellularity; V, vascularity; DCS, decreased collagen stainability; H, hyalinization; GAG,
glycosaminoglycan.

(C.T.) interpreted all the slides once, the stickers were
removed, a new sticker was applied, and the slides were
renumbered using a new series of randomly generated num-
bers. The degree of staining was reassessed by the same
author, and the two results were compared. If an inconsis-
tency (more than one grade on the scoring system described
in Table 1) existed between the two results, the slides were
reassessed with the help of a consultant pathologist
(S.W.B.E.) with a special interest in musculoskeletal pa-
thology. The area of each specimen showing the most ad-
vanced pathological changes was selected, and the worst
possible results for each slide were used in this study.
The criteria used to score the slides were adapted from a
semiquantitative grading scale described by Movin (20).
Using this method, we assessed 1) fiber structure, 2) fiber
arrangement, 3) rounding of the nuclei, 4) regional varia-
tions in cellularity, 5) increased vascularity, 6) decreased
collagen stainability, 7) hyalinization, and 8) GAG content.
The hematoxylin and eosin stained slides were used to
assess the first seven variables, using a four-point scoring
system, where 0 indicates a normal appearance, 1 is slightly
abnormal, 2 is moderately abnormal, and 3 is markedly
abnormal.
The sections stained with AB/PAS were examined ste-
reologically to assess the GAG-rich areas. The areas were
examined using a square lattice of 36 points placed on the
projection screen. The intersection points on the GAG-rich
areas (stained blue) were recorded 10 times for each slide,
making a total maximum score of 360 points for each
specimen. By taking quartiles after all the slides had been
scored, these scores were then converted to the previous
four-point scoring system using the following groups:
0 ⫽ 0 to 10, 1 ⫽ 11 to 51, 2 ⫽ 51 to 206, and 3 ⫽ 207 to
360. Overall, the total score for a given slide could vary
between 0 (normal tendon) and 24 (most severe degenera-
tion detectable).
DEGENERATION IN RUPTURED AND TENDINOPATHIC TENDONS
Statistical Analysis
Nonparametric statistical methods were used for ordinal
data and for continuous variables. Kappa statistics was used
to analyze the intraobserver reproducibility of the classifi-
cation of the tendon appearance. Differences in the patho-
logical variables, comparing all groups, were analyzed using
the chi-square test. As the total scores were not normally
distributed, the Mann-Whitney U test was used to determine
whether the difference between the two independent tendon
groups was statistically significant, and the Kruskal-Wallis
test was used to test the three sample groups together. The
SPSS (release 9.0.1. standard version, SPSS, Inc., Chicago,
IL) statistical package was used to analyze the results. A
probability level of P ⬍ 0.05 was considered significant.
RESULTS
The distribution of the duplicate scores is shown in Table
2, and the median values for each criterion in each group are
shown in Table 1. The mean values for the control tendons
was 5.9 ⫾ 7.4 and 5.1 ⫾ 6.8 for the first and second reading,
respectively. The mean values for the tendinopathic tendons
was 10.5 ⫾ 6.1 and 11.2 ⫾ 5.8 for the first and second
reading, respectively. The mean values for the ruptured
tendons was 17.4 ⫾ 4.9 and 15.9 ⫾ 5.9 for the first and
second reading, respectively.
Within each specific category of tendon pathology, the
chi-square test showed no association between control, ten-
dinopathic, and ruptured tendons. All variables were signif-
icantly different (Mann-Whitney U test, 0.05 ⬍ P ⬍ 0.001).
The distribution of the scores for each category marked is
shown in Table 1.
Kappa statistics. The intraobserver reproducibility of
the scores was evaluated using kappa statistics. The results
are shown in Table 3, ranging from 0.170 (poor agreement
when assessing hyalinization) to 0.750 (good to excellent
agreement when assessing GAG content).
Medicine & Science in Sports & Exercise姞 1985
TABLE 3. Results of kappa statistics assessing intraobserver reproducibility of the semiquantitative histopathological scores.
FS FA N RVC V DCS H GAG
Control/ruptured 0.434 0.434 0.474 0.401 0.468 0.461 0.217 0.759
Control/tendinopathic 0.501 0.501 0.539 0.392 0.546 0.444 0.274 0.677
Ruptured/tendinopathic 0.382 0.382 0.432 0.355 0.455 0.399 0.170 0.750
All groups 0.494 0.494 0.518 0.370 0.524 0.455 0.289 0.668
FS, fiber structure; FA, fiber arrangement; N, cell nuclei; RVC, regional variations in cellularity; V, vascularity; DCS, decreased collagen stainability; H, hyalinization; GAG,
glycosaminoglycan.

Chi-square test. The chi-square test was performed to
ascertain whether there was any difference within the cri-
teria scored, comparing sample groups. The results of each
set of blinded scores are shown in Table 4.
There was a significant difference in all criteria except
hyalinization, which was rarely seen in either control, ten-
dinopathic, or ruptured specimens. When comparing the
control group with the tendinopathic group, five of the
criteria were seen to be significantly different. Fiber struc-
ture, fiber arrangement, and vascularity were significantly
different when comparing the ruptured and tendinopathic
groups.
Mann-Whitney U test. This test compared the differ-
ences in the total scores in two independent, nonnormally
distributed sample groups.
All of these groups were significantly different, showing
that all of the samples are from separate populations. The
higher rank means, in both scores, showed that the ruptured
tendons were significantly more degenerate than the tendi-
nopathic tendon specimens, and these were, in turn, more
degenerate than the controls (Table 5).
Kruskal-Wallis test. This tested the total scores, com-
paring all groups at once. Comparing all of the groups in the
same analysis, it was again seen that the mean rank of the
ruptured group was higher than that of the tendinopathic
group, which was greater than that of the control group
(Table 6).
Histopathological Appearance
The mean pathology sum score of ruptured tendons
was significantly greater than the mean pathology score
of the tendinopathic tendons, and this, in turn, was sig-
nificantly greater than the mean pathology score of the
control tendons (20.5 ⫾ 3.6 vs 6.5 ⫾ 2.1).
Fiber structure. In the control specimens, the fibers
were arranged close and parallel to each other (Fig. 1). In the
ruptured specimens, the fibers showed increased waviness,
separation and, in some cases, a complete loss of structure
and hyalinization. The tendinopathic specimens tended to
show generally less waviness than the ruptured specimens.
Fiber arrangement. In the control tendons, the fibers
were arranged parallel to each other. In ruptured and tendi-
nopathic samples, this parallel arrangement was lost and
haphazard (Fig. 2).
Cell nuclei. Normally, the tenocyte nuclei were flat-
tened and spindle shaped, sometimes arranged in rows. In
the ruptured and tendinopathic samples, the tenocytes first
decreased in number; then, as the pathologic changes pro-
gressed, the nuclei became progressively rounded. In some
instances, these tenocytes resembled chondrocytes (Fig. 3).
Regional variations in cellularity. The whole area of
the slide was assessed for these variations in cellularity. The
control specimens showed little variation in cellularity, un-
like the ruptured and tendinopathic specimens. In those
specimens with the highest evidence of degeneration, there
were areas of densely packed cells compared with the sur-
rounding area. In both the tendinopathic and ruptured spec-
imens, there was mostly a generalized increase in cellularity
as a whole, but also focal areas of cellular proliferation were
seen.
Vascularity. In some cases, the rupture samples showed
random blood vessel formation throughout the section, in-

TABLE 4. Results of chi-square test to ascertain whether there was any difference within the criteria scored, comparing sample groups (P values are shown).
P Value of Groups
Criteria Control/Ruptured Control/Tendinopathy Tendinopathic/Ruptured
Chi-square test scores following first FS 0.001 0.000 0.046
semiquantitative assessment FA 0.001 0.000 0.046
N 0.001 0.000 0.006
RVC 0.002 0.000 0.008
V 0.01 0.041 0.105
DCS 0.014 0.003 0.057
H 0.366 0.013 0.169
GAG 0.000 0.001 0.01
Chi-square test scores following FS 0.000 0.01 0.009
second semiquantitative assessment FA 0.000 0.01 0.009
N 0.000 0.029 0.265
RVC 0.000 0.039 0.161
V 0.000 0.06 0.005
DCS 0.008 0.593 0.093
H 0.179 0.190 0.056
GAG 0.001 0.004 0.995
FS, fiber structure; FA, fiber arrangement; N, cell nuclei; RVC, regional variations in cellularity; V, vascularity; DCS, decreased collagen stainability; H, hyalinization; GAG,
glycosaminoglycan.

1986 Official Journal of the American College of Sports Medicine http://www.acsm-msse.org

TABLE 5. Results of Mann-Whitney U test to compare the differences in the total scores in two independent, nonnormally distributed sample groups.
Mann-Whitney U test following first
semiquantitative assessment
Mann-Whitney U test following second
semiquantitative assessment
creasing with the degeneration of the tendon (Fig. 4). These
blood vessels were less common in the tendinopathic sam-
ples. Normally, these vascular bundles run parallel to the
collagen fibers.
Collagen stainability. Collagen fibers stain a deep
color, as seen mostly in the control specimens. The ruptures
and tendinopathic samples appeared paler pink in color,
showing decreased collagen stainability.
Hyalinization. Very few specimens showed any evi-
dence of hyalinization, and analytical statistics showed that
this histopathological criterion was poorly reproducible (Ta-
ble 3).
Glycosaminoglycans. The GAG-rich areas stain blue
with AB/PAS. Areas of blue staining occurred in the patho-
logic tendons (Fig. 5), whereas a pink staining was observed
in the control specimens (Fig. 6).
DISCUSSION
This study has shown that samples of ruptured and ten-
dinopathic tendons both show profound histopathological
changes, that these changes are more pronounced in rup-
tured than tendinopathic tendons, and that nonruptured,
aged tendon samples have little evidence of histopathology.
Histopathological findings. The histopathological
findings described in the present study are consistent with
those described by other authors in Achilles tendon ruptures
(12) and chronic Achilles tendinopathy (18,19).
The most prominent features seen in the samples from
ruptured Achilles tendons were marked collagen degenera-
tion and disorganization, increased cellularity and rounding
of nuclei and, in some specimens, hypervascularity. There
were similar areas of degeneration within the tendinopathic
tendons. However, these changes were not as pronounced,
as confirmed by the lower median scores obtained (11
compared with 17). There was an increased content of GAG
seen in both the ruptured and the tendinopathic tendons
(median scores of 2). The increase in extracellular matrix,
coupled with the decrease in collagen fibers, shows an
imbalance between the two structural components of the
tendon tissue. It is not certain which process precedes the
other. It has been suggested that the increase in GAG con-
tent may be a result of mechanical overloading, and this, in
its turn, may affect the fiber structure and arrangement,
leading to a reparative response with neovascularization.
This imbalance between injury and repair leads to tissue
damage (18). Although a similar histopathological picture is
seen in the ruptured and tendinopathic tendons, it remains
unclear why these processes present so differently in a
DEGENERATION IN RUPTURED AND TENDINOPATHIC TENDONS
P Value Higher Mean Rank
Control/ruptured 0.000 Ruptured
Control/tendinopathic 0.008 Tendinopathic
Ruptured/tendinopathic 0.005 Ruptured
Control/ruptured 0.001 Ruptured
Control/tendinopathic 0.007 Tendinopathic
Ruptured/tendinopathic 0.0019 Ruptured
clinical situation (13,14). The chi-square test confirmed that
the fiber structure, fiber arrangement, and vascularity were
all significantly different (P ⬍ 0.05), and the Mann-Whit-
ney U test showed that the total scores for the criteria
assessed were significantly different when comparing the
ruptured and tendinopathic groups (P ⬍ 0.01). The present
study therefore shows that the tendinopathic tendons are
significantly less degenerated than the ruptured tendons.
The control specimens had a parallel and organized ar-
rangement of collagen fibers and elongated tenocytes, de-
spite coming from patients up to 30 yr older than those in the
other two groups. The control specimens exhibited signifi-
cantly less degeneration in all criteria except hyalinization
(which we were able to identify in only a very few speci-
mens) when compared with the ruptured group, and signif-
icantly less degeneration in all criteria when compared with
the tendinopathic group. Therefore, these aged tendons ex-
hibited little evidence of degeneration. Merkel et al. (18)
proposed that normal aging of connective tissue is morpho-
logically different from degeneration, and our data would
confirm their statement. Aging tissue has a low rate of
metabolism and exhibits a progressive decrease in elasticity
and tensile strength.
Reliability of histopathological investigations. In
this study, each slide was scored twice by the same inves-
tigator with the help of a consultant pathologist with a
special interest in the musculoskeletal system. The kappa
statistics assessed the measure of agreement between the
two scores. When comparing all groups, the scores varied
from fair (0.289) to good (0.668), showing how difficult it
is to recognize specific patterns in histology and the impor-
tance of having well-trained individuals to interpret the
slides. To improve on these kappa statistics, the assessment
could be repeated several more times. Also, using another
observer would decrease observer bias.
It is possible that these changes seen in the ruptured
tendons could be secondary abnormalities occurring after
the rupture. However, all patients were operated on within
48 h from the time of the rupture, and it is unlikely that such
profound histopathological change could occur in such a
time frame.
TABLE 6. Kruskal-Wallis test, testing the total histopathological scores, comparing
all groups at the same time.
Mean Rank
1st Scores 2nd Scores
Control 19.60 17.64
Ruptured 46.11 46.61
Tendinopathic 34.48 32.59
P value 0.001 0.001
Medicine & Science in Sports & Exercise姞 1987
FIGURE 1—Hematoxylin and eosin stain of a control Achilles tendon
in a 59-yr-old man who underwent amputation for peripheral vascular
disease. There are closely packed, lightly stained parallel bundles of
collagen fibers that contain the flattened nuclei of tenocytes. Original
magnification, ⴛ150.
Limitations of the present study. There are several
limitations to this study. For example, our study population
of ruptured, tendinopathic, and control tendons is relatively
small, and our control tendons came from patients with
various degrees of vascular disease. However, the Achilles
tendon is normally a relatively avascular structure (17). It is
therefore likely that our tendon samples were representative
of normality, given the age of the patients. A possible
solution could have been to use ultrasonography-guided
percutaneous biopsy to obtain samples of tendons in live
healthy individuals (18), or to use tendons from younger
patients undergoing traumatic amputations. However, for
ethical and practical reasons, neither of these alternatives
was possible, and the differences between the control and
ruptured tendons are strong enough to justify our conclu-
sions. Also, as aging causes at least some morphological
changes in the tendons, and given that our control tendons
were harvested from donors at least 20 yr older than patients
with a ruptured Achilles tendon, the use of an age-matched
FIGURE 2—Hematoxylin and eosin stain of Achilles tendon adjacent
to the rupture in a 51-yr-old male squash player. Note the disorgani-
zation within the tissue, with loss of the normal collagen fiber distri-
bution, hypercellularity, increased waviness, separation, with nearly
complete loss of the tendon structure. The whole area is hypercellular.
Original magnification, ⴛ150.
1988 Official Journal of the American College of Sports Medicine
FIGURE 3—Hematoxylin and eosin stain of the tendinopathic area of
Achilles tendon in a 32-yr-old female triathlete. Slight hypercellularity,
with rounding of the tenocyte nuclei. Original magnification, ⴛ150.
control population would have further highlighted the his-
topathological differences that we have described.
When interpreting the results of the present study, it
should be considered that we only used two staining meth-
ods. Obviously, extra lipids, calcium deposits, collagen de-
naturation, pathological tenocyte metabolism, collagen
types, and foreign materials in the control group could have
been detected using more advanced histochemical and im-
munohistochemical techniques. However, the staining tech-
niques used in the present study have many advantages: they
are widely available, cost-effective, and require little tech-
nical abilities, and most pathologists are familiar with them
and are accustomed to interpreting a variety of specimens
stained in this fashion.
Finally, we have no reference data on the level of tendon
degeneration in the general Scottish adult population. Al-
though we have reported the epidemiological characteristics
of a cohort of 4201 patients with Achilles tendon rupture in
the last 15 years (17), we are not aware of any study
detailing the histopathological appearance of Achilles ten-
don degeneration in this populace.
FIGURE 4 —Hematoxylin and eosin stain of the tendinopathic area of
Achilles tendon in a 29-yr-old male middle-distance runner. Marked
random blood vessel formation. The collagen fibers have a disorga-
nized appearance, and the whole section is hypercellular. Original
magnification, ⴛ150.
http://www.acsm-msse.org
FIGURE 5—AB/PAS stain of a control Achilles tendon in a 76-yr-old
farmer, who ruptured his Achilles tendon while plowing a field. There
is increased GAG-containing matrix, and collagen fiber disruption.
Original magnification, ⴛ150.
CONCLUSION
Ruptured and tendinopathic tendons are histologically
significantly more degenerated than control tendons. The
general pattern of degeneration was common to the ruptured
and tendinopathic tendons, but there was a statistically more
advanced degree of degeneration in the ruptured tendons. It
is therefore possible that there is a common, as yet uniden-
tified, pathological mechanism that has acted on both of
these tendon populations. We have recently shown that
tenocytes from ruptured Achilles tendons produce greater
quantities of type III collagen than tenocytes from normal
Achilles tendons (16,21). This altered production of colla-
gen may be one reason for the histopathological alterations
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FIGURE 6 —AB/PAS stain of a control Achilles tendon in a 62-yr-old
man, who died of a cardiovascular accident. GAG-containing matrix is
minimal and hardly appreciable as foci between the collagen fibers.
Original magnification, ⴛ150.
described in this study, and may result in the tendon being
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Many thanks are given to Miss Linda Lothian for her help with the
manuscript.
Address for correspondence: Nicola Maffulli, Department of
Trauma and Orthopaedic Surgery, Keele University School of Med-
icine, North Staffordshire Hospital, Thornburrow Drive, Hartshill,
Stoke on Trent, Staffordshire, ST4 7QB, ENGLAND; E-mail:
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