—REVIEW—

The Japanese Experience with Tendonitis in Racehorses

Masa-aki OIKAWA* and Yoshinori KASASHIMA
Equine Research Institute, Japan Racing Association, 321–4 Tokami-cho, Utsunomiya, Tochigi 320-0856, Japan

Superficial digital flexor tendon (SDFT) injury leading to tendonitis is the most frequent soft J. Equine Sci.
tissue injury in racehorses. As tendonitis has been noted to heal slowly and imperfectly, Vol. 13, No. 2
injured tendons require long periods of rest, and the rate of recurrence of tendonitis upon pp. 41–56, 2002
return to training is high. Between 1, 100 and 1,200 of the 6,400 to 7,000 racehorses
currently registered with the Japan Racing Association (JRA) suffer from tendonitis, and
some 70% of these return to racing without making a comeback in a single race. In view of
this statistic, the JRA has conducted investigational and clinical research from various
perspectives. This paper will review the results of these studies, thus providing insight into
practical methods of treating and preventing tendonitis. The study results are summarized
under the following headings: 1) Introduction; 2) Impacts and loads on the lower limb at the
track; 3) Occurrence of tendonitis at JRA training centers; 4) The hoof and tendonitis; 5)
Ultrasonic diagnostic criteria; 6) Therapeutic regimens; 7) Conclusion. We concluded that
tendon injuries represent irreversible structural alterations that are unlikely to be
significantly altered by therapy, so that the best outcome may be achieved by minimizing the
damage done by the original injury. From this viewpoint, research efforts will be directed
toward prevention and early diagnosis, rather than therapy of established lesions.
Key words: tendonitis, racehorses, tendon injury

Internationally, tendon injury has proved to be a advances in understanding tendonitis.

major problem for the racing industry. The
combination of an unacceptably high incidence of
injury and the long duration of time for recovery and
rehabilitation results in a very high financial cost. The
frequency of injury is also detrimental in terms of
animal welfare. The best way to deal with tendon injury
and the resulting tendonitis is to make every effort to
limit the extent of damage, or if possible to prevent it.
However, thus far it seems that the prognosis for horses
with tendonitis has not improved, nor have any
effective preventive measures been instituted. To
clarify the strategies that can be used to prevent equine
tendonitis, an International Workshop on Equine
Tendonitis was held as part of the Fifth International
Conference on Equine Exercise Physiology from
September 20 to 25, 1998, at Utsunomiya, Tochigi,
Japan [32]. This workshop addressed a number of
objectives in relation to recent and novel scientific
This article was accepted May 20, 2002.
*Corresponding author. e-mail: Masaaki_Oikawa@jra.go.jp
In Japan, as well as in western countries, tendonitis is
a frustrating problem for the racing industry. An
estimated 1,100 to 1,200 of the racehorses registered
with the Japan Racing Association (JRA) suffer from
tendonitis (mainly of the superficial digital flexor
tendon; SDFT), and some 70% of these return to
racing without making a comeback in a single race.
Given that some 1,500 JRA horses are diagnosed as
having bone fractures in any given year, the effects of
tendonitis are quite significant. In view of these
statistics, the JRA has assembled veterinarians,
researchers, facility managers, trainers, and jockeys to
establish a Committee for the Prevention of Accidents
to Racehorses [30, 31]. This committee has conducted
surveys to determine the associated risk factors,
including factors intrinsic to the horses and factors in
the horses’ environment, such as training protocols,
facilities, maintenance protocols, and shoeing/foot
preparations, with the aim of reducing the incidence
and severity of tendonitis. Here, we report some of the
results obtained from these investigations. We focus on
42 M. OIKAWA AND Y. KASASHIMA
Fig. 1. Cross-sectional diagrams of the turf, woodchip and dirt tracks.
the conditions related to the occurrence of tendonitis
during races or training in the JRA, and on the research
currently being adopted to minimize the extent of
tendon damage and to prevent tendonitis.
Impacts and loads on the lower limbs
at the track
Different materials, including woodchips, dirt, and
turf, are used as track surfaces at training centers and
on racetracks belonging to the JRA (Fig. 1) [30, 33]. It
is well known that the conditions of the track surface,
such as hardness and roughness, influence the
incidence of injuries in Thoroughbred racehorses
during training and racing [34]. We developed an
instrument that could be sandwiched between the hoof
and shoe of a horse to reliably measure vertical ground-
reaction forces and three-dimensional acceleration at
the walk, trot and canter on woodchip tracks. Details of
this shoe can be found in the American Journal of
Veterinary Research, volume 61, pp. 979–985 [17].
Each surface material has different features, depending
on its location on the track (straight or corner), the
weather, and the use of the track. Trainers need to
familiarize themselves with all of the characteristics of
these surface materials if they are to prevent tendon
injuries in racehorses and maximize the efficiency of
their training.
Is there any relationship between injuries and the characteris-
tics of the track surface?
Turf and dirt racetracks: In the JRA, the frequency of
injuries (such as broken bones and tendon ruptures)
during races from 1988 to 1997 was compared for turf
tracks and dirt tracks [34, 36]. The results are shown
below. Track surface conditions were determined by
use of a soil-shearing-strength cone penetrometer [27]
and soil-moisture-content tensiometers [4]. Dirt track
conditions were classified as fast, good, muddy, or
sloppy, and turf track conditions were classified as firm,
good, soft, or yielding.
On turf tracks, the occurrence of injuries tended to
be reduced as the condition of the track deteriorated.
On dirt tracks, the occurrence of injuries increased
as the condition of the track deteriorated.
On turf tracks, ‘good (fast)’ tracks were dry and hard
(leading to more impact on the horse’s legs, more high
speed and therefore more injury), and ‘bad (slow)’
tracks were moist and soft (causing less impact). This
may be one of reasons why there were fewer injuries on
slow tracks.
In contrast, dirt tracks in heavy condition showed a
high water content, indicating that the condition
reduces or even eliminates the shock-absorbing effect
of cushioning sand, more impact on the horse’s legs
and therefore more injury [46].
Woodchip and dirt training tracks: The occurrence of
periostitis of the third metacarpal bone was observed in
two groups of horses, one trained on a woodchip track
and the other on a dirt track [29]. The occurrence of
periostitis in dirt-track-trained horses (34.3%) was twice
as high as in horses trained on the woodchip track
(13.4%). The main reason for this result could be the
differing flexibilities of the two types of track. Also, the
fact that the condition of woodchip tracks is affected
little by changes in weather could have contributed to
this result.
 TENDONITIS IN JAPANESE RACEHORSES
Fig. 2. Occurrence of tendonitis at JRA training centers.
How does running on rough track surfaces affect horses?
During running on rough track surfaces with many
foot prints on the surface, the impact on the tip of the
hoof and the outside or inside of the hoof was found to
change at each step [16]. In these cases, the legs were
much more severely stressed than in running on even
tracks, because the joints, bones, tendons, and
ligaments received irregular impacts.
Occurrence of tendonitis at JRA
training centers
The JRA has between 6,400 and 7,000 racehorses, 10
racetracks, and two training centers (the Miho and
Ritto Training Centers) under its management [31].
Of the racehorses, about 4,000 are repeatedly admitted
and discharged from the training centers for training.
The occurrence of tendonitis at JRA training centers
between 1987 and 1997 is shown in Fig. 2 [35].
Between 1,100 and 1,200 racehorses belonging to the
JRA suffer from tendonitis (mainly SDFT), and some
70% of them return to racing but without making a
comeback in a single race on the track [35]. In 1987, a
total of 24 horses at the two training centers suffered
catastrophic tendon and ligament ruptures [35].
However, as shown later, since the construction of
woodchip tracks and uphill tracks with the composition
of the woodchip on the track surface providing better
surface cushioning, the number of the catastrophic
tendon and ligament ruptures has decreased
43
remarkably to about 5 horses a year in recent years
[35]. On the other hand, the number of tendonitis
cases has increased from 937 in 1987 to 1,155 in 1991,
1,372 in 1994, and 1,271 in 1997 [35]. From these data,
we suspected that although the incidence of conditions
that cause catastrophic rupture of tendons and
ligaments by sudden impact on tendons has decreased
after the construction of woodchip tracks and uphill
tracks and one of the causes of the increased incidence
of tendonitis was possibly influenced by the
accumulation of micro-damage to collagen fibrils in the
tendons arising due to repeated stretching and
contraction of the tendon during the daily training on
the woodchip and uphill tracks with deeper cushion
layer of these tracks. To study these matters from the
biomechanical view point, we measured the modulus of
elasticity (a qualitative indicator of the tendon) and the
cross sectional area (an indicator of the thickness), and
analyzed their relationship with exercise history. As a
result of simple regression analysis, the modulus of
elasticity was significantly higher when the career days,
total career distance, number of layups in career, and
total layup time were higher, but was significantly lower
when the frequency of works during the entire career
was high [44]. In addition, given that some 1,500 of the
JRA horses are diagnosed as having bone fractures in
any given year [35], the effects of tendonitis are quite
significant. There were two periods in which the
number of tendonitis cases rose noticeably (Fig. 3)
[35]. These were from 1989 to 1991 (from 1,003 to
1,155 horses) and from 1992 to 1994 (1,145 to 1,372
44 M. OIKAWA AND Y. KASASHIMA
Fig. 3. Relationship between the construction of woodchip tracks and uphill courses and
the rise in the number of horses affected by tendonitis.
horses). We searched for possible changes in the
environment at training centers at those times, and
found that changes of the training protocols in time
trials, the construction of woodchip tracks, the
construction and extension of uphill courses, and the
popularization of diagnostic ultrasound could all be
correlated with the increase in the numbers of
tendonitis cases diagnosed. The mean incidences of
tendonitis and catastrophic ruptures of tendons and
ligaments from 1,992 to 1,971 per total number of
horses registered with the JRA were 11.31 ± 0.65%
(7,321/64,787) and 0.07 ± 0.02% (44/64,747),
respectively (Table 1) [35]. The Occurrence of
tendonitis as a catastrophic injury leading to direct
euthanasia was 8 of 48,000 horses raced at Nakayama
and Tokyo racecourses during the period 1992–1995
(0.017%). All 8 horses had a previous history of injury
in the locomotor apparatus with one of the horses
having a previous history of tendonitis in the same leg
that later experienced a catastrophic injury and
euthanasia. All horses started in races numbered 5 to
10. Seven had 1–5 wins. There was also a tendency that
catastrophic injuries occurred more when the jockey
was of low ranking (Seven of 8 raced on dirt and 6 of 8
in a jockey with a low ranking). The proportion of
deaths attributable to tendon rupture or damage
during training in the period 2000–2001 varied with the
types of tracks: dirt track=0.0006% (3/472,993),
Table 1. The mean incidences of tendonitis and
ca ta s trop hi c r up tur es of ten do ns a n d
ligaments from 1992 to 1997
Tendonitis: 11.31 ± 0.65% (7,321/64,787)*
Catastrophic Cases: 0.07 ± 0.02% (44/64,747)*
*Parentheses indicate the number of affected horses per
horses registered to JRA.
woodchip track=0.0000% (0/226,833 runners), uphill
track=0.0004% (1/284,211 runners) and turf
track=0.0000% (0/5,204 runners) at Miho Training
Center; dirt track=0.0012% (2/170,659 runners),
woodchip track=0.00165 84/249,550 runners), uphill
track=0.0002% (1/401,411 runners) and turf
track=0.0000% (0/4,552 runners) at Ritto Training
Center. The rate of euthanasia because of fractures
from racing at Japan Racing Association (JRA)
racecourses 1985–1994 was 0.06%. Among all JRA
horses, the right forelimb tended to be affected 10% to
20% more frequently than the left, even though in
Japan racehorses train and race both clockwise and
anticlockwise (Fig. 4) [35]. The increasing incidence
of tendonitis with age is probably related to the arduous
nature of the selection process for continued racing, as
well as to age-related weakening of the tendons (Fig. 5)
[35]. Of the horses affected with tendonitis in 1997,
64.5% were male, 32.6% female, and 2.9% geldings
(Fig. 6) [35]. Because many fillies retire earlier than
 TENDONITIS IN JAPANESE RACEHORSES
Fig. 4. Comparison of affected legs with tendonitis at the Ritto Training Center.
Fig. 5. Incidence of tendonitis by age from 1992 to 1997.
colts and geldings, we studied the incidence of
tendonitis in 3-years-olds, which were not of retirement
age. In this group, 66.6% of affected horses were colts
and 34.0% were fillies. In 1997, of the actual number of
starters, the ratio of colts to fillies was 59.7% to 40.2%,
leading to speculation that the incidence of tendonitis
in colts was slightly higher. Why would this be so? The
answer may lie in the fact that colts have more speed,
that more time is required for conditioning and
conformation, or that the differences of the incidence
of tendonitis between males and females may represent
di fferences in tendon fiber’s metabolism or
responsiveness of mechanoreceptors in the tendon to
exercise between the sexes as seen in orthopedic
disorders in human [13] and Thoroughbred
45
Fig. 6. Gender ratio in affected horses with
tendonitis.
racehorses [54, 55]. A comparison of body weights
revealed interesting results when tendonitis-affected
horses were compared with unaffected horses [35].
Fig. 7 compares the weight distribution during racing
in tendonitis-affected horses and unaffected horses.
The mean body weight of affected horses was 477.8 kg
for colts and 460.0 kg for fillies; affected colts were 17.8
kg heavier and fillies 12 kg heavier than unaffected
horses of their respective sexes. These were statistically
significant differences, that is, the probability level
exceeded 95% (p<0.05). However, it is still not
understood whether this indicates that only horses with
a particular conformation were susceptible to
tendonitis or whether heavier horses were susceptible
46 M. OIKAWA AND Y. KASASHIMA

Table 2. The mean run times of training in horses with tendinitis

and healthy horses*
No. of Course
Horses Woodchip Uphill
Horses that later become
afflicted with tendonitis 68 16.7 ± 2.4 sec 15.8 ± 3.2 sec
Healthy Horses 169 17.8 ± 1.5 sec 17.0 ± 1.8 sec
t-test P<0.037 P<0.059
*Ritto training center.

Table 3. The mean run times for the final 3 furlongs at trials (G1
entry racehorse)*
course Dirt course Turf course Woodchip course
Year
1990 38.98 sec 36.14 sec 39.68 sec
(n=154) (n=18) (n=9)
1997 38.72 sec 34.20 sec 38.23 sec
(n=14) (n=12) (n=192)
*Ritto training center.

In terms of run time, because only a small number of

Fig. 7. Relationship between body weight and
onset of tendonitis.
to tendonitis. Whereas nothing can be done to rectify
inborn conformation faults, it is best to play it safe by
paying close attention to proper conditioning of the
unaffected heavier horses.
To clarify further the relationship between
tendonitis and the types of training courses, a
retrospective comparison was made of affected horses
(52 horses at the Miho Training Center, 76 at the Ritto
Training Center) and healthy ones (175 at Miho and
180 at Ritto) during daily training and trials
(conducted 3 or 4 days before the major races). The
run times of these horses were also compared. In trials
at the Miho Training Center, affected horses were
found to have run less frequently on woodchip tracks
than unaffected horses. At the Ritto Training Center, it
was notable that the affected horses had trained more
on dirt tracks than had the healthy horses. Also, in
trials at the Ritto Training Center, the affected horses
had run less frequently on woodchip courses than had
the healthy ones, and so were more accustomed to
running on dirt [35].
effective samples was obtained at Miho Training
Center, only the data obtained at Ritto Training Center
were analyzed statistically. The run times on the
woodchip track of horses that later become afflicted
with tendonitis were significantly faster than those of
healthy horses, and they also ran faster over the uphill
course (Table 2) [35]. From the survey of the mean
run times for the final three furlongs at trial in Grade1
races entry racehorses over a period of 11 years, that is,
from 1987 to 1997, it was found that the use of
woodchip tracks and uphill tracks for training had
increased, and that mean times for the final 3 furlongs
of time trials had improved by 0.3 s on dirt, 2.1 s on turf,
and 0.5 s on woodchips (Table 3) [35]. The run times
on the woodchip track of horses that later became
afflicted with tendonitis were significantly faster than
those of healthy horses, and they also ran faster over the
uphill course. These findings suggest that subjecting
horses to higher speeds during training might be
associated with greater risk for the development of
tendonitis.
The hoof and tendonitis
As the saying goes “No hoof, No horse”. The
importance of the hoof in training horses has been
 TENDONITIS IN JAPANESE RACEHORSES
discussed for a long time. The hoof is not only an
important organ in sustaining the life of the horse as a
soliped, but also an important organ for high-speed
running.
The hoof has a peculiar shape. It was adapted from
the soliped’s physiology and biomechanics during the
process of evolution. It has long been known that a
long toe and low heel is one of the primary factors that
makes a horse susceptible to tendonitis. However, it is
not known how hoofs of different shapes affect the
racehorse’s biomechanics and athletic performance.
As part of a shoeing study, research has been
conducted on the relationships among shapes of hoofs,
malfunctions of the phalangeal joints, and standing
conformation. For details, see “American Farriers
Journal” May/June 1998, pp. 74–76 [45].
How are hoof shape and standing conformation related to ten-
donitis?
It was compared the healthy foot and the foot with
tendonitis (inflamed SDFT) in radiographs taken from
three directions (dorsally, laterally, and frontally). The
distances from a set reference point to the hoof wall
and to the coffin bone were measured (Fig. 8).
• From a lateral view, the distance from the reference
point to the front of the hoof was long, as was the
distance from the reference point to the rear of the
hoof with tendonitis.
• From a frontal view; the angle formed by the inside
and outside of the hoof wall was small, and the wall
was bent upward.
• From a dorsal view, the inside and outside of the
basilar margin were overhung in a base-wide toe-in
position, and the inside and outside of the heel
were unequal.
According to these data, racehorses that suffer from
tendonitis tend to have irregular hoof shapes, such as
low heels (Lh), long toes (Lt), or under-run heels
(Uh). Also, the base-wide toe-in position occurs
frequently in these horses. We assume that this
condition is similar to the spiral deformity of lower leg,
in which the fetlock is internally rotated.
What are the risks related to irregular hoof shape?
In Japan, Uh is regarded as a genetic problem and
has not been considered in relation to biomechanical
problems. However, in Europe, the risks of Uh have
attracted attention, and it is very common to adjust the
problem during shoeing.
In some racing circles, people believe that the
47
Fig. 8. Locations of measured variables in the hoof.
presence of a long tip on the hoof allows for longer
strides and increases speed. However, our preliminary
experiment, in which we artificially created Lt,
indicated that Lt did not give a longer stride and in fact
overburdened the leg [45].
The base-wide toe-in position with unevenness of the
outside or inside of the heel and Uh creates a delay
when the entire ground surface of the hoof is placed on
the ground. The break-over of the hoof with Lt takes
time. In Uh, for example, when a heel is lowered by
forward shifting, mechanical instability is generated
when a load is applied, adding significant stress to the
flexor tendons. The longer toe requires the flexor
tendons to take a greater load to enable the hoof to
break over.
Can tendonitis be prevented by shoeing treatment?
In shoeing racehorses it is very important to
understand irregular-shaped hoofs and their
relationship to conformation. To observe this
relationship, objective means, such as radiographs
taken in three planes, should be used.
Uh is seen in young horses. When Uh occurs with
incorrect standing conformation and/or offset knee,
close attention should be paid and any Lt with Lh and
Uh should be re-shaped by trimming and shoeing. If
the condition is serious, a four-point trim should be
done. When the horse is forced to rest when suffering
from tendonitis, it is important to correct any irregular
shape of the hoof, to make a complete angulus
parietalis, and to trim the tip of the hoof and the
longitudinal length of ground surface of the hoof to
move the break-over point backward.
Moreover, the use of egg-bar shoes stabilizes hoof
landing, reduces the burden on the SDFT, and means
that the tip of the hoof is trimmed to fit the shape of the
shoe. By this process, irregular hoof shapes are
48 M. OIKAWA AND Y. KASASHIMA
corrected, and the break-over of the hoof becomes
smoother.
Ultrasonographic diagnostic criteria
Can diagnostic criteria be unified by using ultrasound diag-
nosis?
Recently, ultrasound diagnosis has been widely used
to diagnose tendonitis. From a morphological
viewpoint, the presence of an anechoic area in
ultrasonography has proved to be an indicator of
collagen deposition in collagenase-induced tendonitis
[25, 38, 43]. With this method it is now possible to
ascertain the internal anatomy of the tendon; this was
difficult in the past with only tactile or visual means.
This means not only that there has been improved
progress in diagnostic capability, but also that standard
criteria can be applied to diagnostic staging, staging of
healing, assessment of healing techniques, and new
research. At JRA equine clinics, ultrasound diagnosis is
already being used for diagnosis of tendonitis, and this
diagnosis is based on diagnostic criteria widely
accepted in the United States [8]. These criteria
evaluate totally the status of tendons by visual
information. The superficial flexor tendon is divided
into 7 sections (4 cm each) from the carpus to the
fetlock joint. If the diagnostic criteria used by all
veterinary surgeons who are using ultrasound diagnosis
can be unified, we can expect to simplify the diagnostic
information and the accumulation of information.
However, there are still not enough reports that have
documented the use of diagnostic criteria for
formulating an accurate prognosis, optimum
treatment, and the diagnosis of tendonitis at an early
stage. This is one of the challenges that the Committee
will undertake.
What are the significant clinical and ultrasound imaging
parameters for diagnosing tendonitis?
To determine the clinical and sonographic
parameters that are useful for prognostic evaluation,
principal component analysis was used on data from
146 tendonitis cases to assess the diagnostic utility of 11
clinical and ultrasonographic parameters: swelling;
heat; pain; lameness at walk; lameness at trot; MIZ-SA
(cross-sectional area (csa) of the tendon at the
maximum injury zone); MIZ-HYP% (total lesion csa
(hypoechoic fiber tracts) in the maximum injury zone);
T-SA (sum of the cross-sectional areas of the SDFT in all
zones, normal or abnormal - in the forelimb, this
includes 7 measurement zones); T-HYP (sum of all
lesion csas (hypoechoic fiber tracts at all levels)); %T-
HYP (total percentage of hypoechoic fiber tracts); and
echogenicity (graded from 1 to 4 as defined by
Genovase et al.) [8]. The results indicated that the
statistically significant diagnostic parameters or
parameters indicating the extent and severity of
tendonitis were MIZ-HYP%, MIZ-SA, T-HYP, T-SA, and
%T-HYP (Fig. 9). The analysis also indicated that
clinical observation did not adequately indicate the
extent and degree of tendonitis [28].
How are ultrasonically detected lesions of tendonitis and the
prognosis of the condition related?
Based on imaging data from ultrasound diagnosis,
the lesions of tendonitis can be grouped into the
following three types: 1) Type A core lesion in the cross-
section of the SDFT bundle; 2) Type B peripheral or
border lesion situated dorsally, palmarly, medially, or
laterally in the rims and margins of the transverse
section of the SDFT bundle; 3) Type C diffuse lesion
that is hypoechogenic, giving a mottled appearance to
the internal architecture of the SDFT bundle. A chi-
squared statistical analysis of these three types of lesions
and their subsequent outcomes indicated that the
likelihood of horses making a comeback with Type A or
B lesions was low, while that of horses with Type C
lesions was high (Table 4) [5].
What does ultrasound imaging reveal of the prognosis for ten-
donitis cases?
There are not enough reports evaluating diagnostic
criteria in relation to prognosis and the presumption of
an adequate treatment period. This is one of the
challenges that the JRA has undertaken to meet. We
examined 105 horses that entered the JTA Hot Springs
Sanatorium in the 6 y from 1993 to 1998 with
ultrasonically diagnosed core lesions. A follow-up
survey was made to study whether or not the horses
returned to racing. At the time of entry into the
sanatorium, the extent of the core lesion injury was
calculated as MIZ-HYP%, that is, total lesion cross-
sectional area (hypoechoic fiber tracks) in the
maximum injury zone. The rehabilitation methods
employed were those developed by C. Gillis [10]. The
horses were classified into a group that returned to
racing and a group that was unable to do so. There was
a significant relationship between the extent of the
core lesion of tendonitis, as indicated by MIZ-HYP%,
 TENDONITIS IN JAPANESE RACEHORSES 49

Fig. 9. Clinical and sonographic parameters for prognostic evaluation.

Table 4. Relationship between lesion type and return to racing

Return to race Reoccurrence of tendinitis
Core type (N=80) 37.5% 43.3%
Border type (N=30) 17.09% * 33.33% *
* *
Diffuse type (N=29) 79.03% * 16.13% *

*Statistically significant; The significance of difference of the mean was assessed

using Chi-Square Test.

and the possibility of return to racing: that is, the

likelihood of horses making a comeback with a core
lesion of 17.3 ± 10.6%, as indicated by MIZ-HYP%, was
high, while that of horses with a core lesion of 25.6 ±
15.2% was low (Fig. 10). Linear regression analysis
indicated a positive correlation between the MIZ-HYP%
and the duration of the lay-up: length of resting period
(months) = 0.161 × (MIZ-HYP%) + 3.479, P<0.05,
r=0.581) (Fig. 11). The duration of the lay-up in
months had a slope of 0.16 times the MIZ-HYP%.
According to this equation, it is possible to estimate the
required duration of the lay-up for tendonitis.
However, as the correlation coefficient was only 0.8, it is
necessary to supplement this relationship with other Fig. 10. Relationship between the extent of the
parameters. core lesion in tendonitis and the possibility
of return to racing.
Can ultrasonography be useful for detecting subtle changes
that precede severe tendon injuries?
To reduce the treatment period and allow an early
50 M. OIKAWA AND Y. KASASHIMA
Fig. 11. Relationship between the duration of the lay-up
period and the extent of the core lesion in
tendonitis.
return to racing, we need a method to diagnose
tendonitis in its early stages. We tracked 26 racehorses
that had swollen front leg tendons but had no
abnormalities indicating tendonitis on diagnostic
ultrasound. The cross-sectional areas of the tendons in
the affected (A) legs and the non-affected (N) opposite
legs were measured, and their ratios (A/N) calculated.
These horses continued training, and were eventually
defined as two groups: those that developed
ultrasonographically discernible tendonitis, and those
that did not. A significant difference in A/N was
observed between the groups of horses. Horses that
developed tendonitis lesions tended to have an A/N >
1.2 in their prior ultrasound images, whereas in those
that did not develop tendonitis the A/N tended to be
smaller (Fig. 12) [21]. Therefore, we suggested that
horses whose front leg tendons were swollen to more
than 20% larger than normal cross-sectional areas of
the tendons had a high likelihood of developing
ultrasonographic evidence of tendonitis.
It is well known that magnetic resonance imaging
(MRI) has an advantages of excellent inherent soft
tissue contrast. But MRI has limited its applications in
equine practice due to high system cost, and the
requirement of general anesthesia. In the preliminary
examinations, to evaluate the high potential of MRI as
a diagnostic imaging tool for detecting subtle tendon
injuries, antemortem evaluation of equine flexor
tendons using MR was performed [22]. As a result, it
was possible by this method to take antemotem MR
images of equine tendon that distinguished features as
well as postmortem images described in previous
studies [47]. Further experimentation is needed in the
detection of subtle tendon injuries.
Fig. 12. Ratio of cross-sectional areas of tendons in affected legs
and unaffected opposite legs.
Fig. 13. Discolored lesion in the central region of
SDFT bundle.
Do lesions that predispose to tendonitis exist?
The opinions of researchers have been divided as to
whether predisposing lesions exist for tendonitis [12,
37, 48]. As mentioned below, we obtained research
results that support the opinion that sub-clinical
predisposing lesions for the onset of tendonitis exist
[23]. Two Thoroughbred racehorses with slight
swelling, inflammation, and enlarged cross-sectional
areas of their SDFT were dissected. Although no signs
of tendonitis had been found on ultrasonography,
discolored regions that stained dark brown were
observed in the central regions of the SDFT bundles in
both cases (Fig. 13) [23]. Histologically, bleeding and
edema were observed i n t he peri tendi neum
(endotendineum or epitendineum; loose connective
tissue containing blood vessels and nerves). In
addition, there was degeneration of the tendon fibers
around the discolored regions. Occasionally, there was
hyperplasia of the minute vessels in the peritendineum.
Compared with normal tendons, affected tendons had
 TENDONITIS IN JAPANESE RACEHORSES
enlarged cross-sectional areas and significant signals on
proton-spin echo imaging using nuclear magnetic
resonance (NMR) microscopy. The signals appeared
distinctively in the region of the peritendineum.
Recent studies have shown that immunopositive cells
for four cytokine antibodies (interleukin-1 α ,
interleukin-1β, tumor necrosis factor-α and interferon-
γ ) were lopcalized in peritendineum, vascular
endothelium and tenocytes near the peritendineum in
the inflamed tendons [15]. In vitro, we examined the
effects of transforming growth factor- β 1, β 2 and
β3(TGF-β) on the effect of mRNA for αI (XII) and αI
(XII) collagens in equine tenocyte cultures by using the
ribonuclease protection assay (RPA). From this
experiment, it was suggested that TGF-β promoted
collagen fibrogenesis in the tenocyte cultures [2]. It is
well known cytokines act in various manners: either to
activate or depress immune cells, cause degeneration of
tissues, promote and induce cellular differentiation,
and induce secretion of cytokines by other cells. These
findings suggest that the discolored lesions centered on
the transverse sections in the SDFT bundles were
related to edema that may have originally developed
from microvascular alterations in the peritendoneum,
resulting in mechanical weakening of the discolored
regions of the SDFT bundles. These circulatory
disturbances could have been primary or inciting
lesions contributing to the onset of tendonitis, or
alternatively secondary changes associated with the
progression of the tendonitis. As mentioned earlier, it
was found that if the cross-sectional area of a tendon
was swollen, there was a significant likelihood of
tendonitis developing. In such cases, there would be a
possibility that the flexor tendons had structural
abnormalities that could act as predisposing factors.
The location of greatest occurrence of tendon injury
is the mid-metacarpal region of SDFT. The mechanism
is not clear. To provide the need to explore the
functional implications, we preliminary observed the
distribution of a three dimensional network of the cell
processes of tendon cells, connexin and a component
of gap junctions of the tendon cells in the tendon
bundle in the direction of the longitudinal axis.
Between the mid-metacarpal and metacarpophalangeal
regions, there was a tendency of the difference of these
index which suggests the regional difference of
compressional or tensile forces applied to the tendon
cell [20, 24].
51
Therapeutic regimens
The goals of therapy for tendonitis are to decrease
inflammation, minimize the formation of scar tissue,
and promote restoration of normal tendon structure
and function. Despite the frequency of tendonitis and
the range of treatments currently used, there have been
no satisfactory controlled trials to determine the
efficacy of available treatments. Therefore, in spite of
our increased understanding of basic tendon biology,
the availability of new medical treatments, and the
ability to monitor healing with ultrasonography, there
is no evidence that the prognosis for tendonitis has
improved. As an emergency treatment, cold (with
either ice or iced water hydrotherapy) should be
applied. Afterward, there is a wide choice of surgical
treatments such as stabbing, splitting of the injured
tendon and section of the accessory ligament of the
SDFT, and medical treatments such as the use of
s yst e mi c or i nt r al es i onal pol ys ul phat ed
gl ycosami noglycan (PSGMG) [26, 41], beta-
aminopropionitrile (BAPN-F) [9, 39], or hyaluronic
acid [1, 6, 7, 42].
Is BAPN-F as non-surgical therapy a wonder drug?
Currently, the use of BAPN-F is gaining popularity
[8, 39]. BAPN-F has been evaluated as a scar-
remodeling drug. It inhibits the enzyme lysyl oxidase in
scars, thus blocking lysine deamination, an important
first step in the formation of strong scar collagen cross-
linking [3, 11]. The cross-linking between scar
collagen molecules formed after tendon injury results
in a decrease in mechanical strength of the healed
tendon, possibly resulting in the high incidence of
recurrence of tendonitis [11]. Therefore, the use of
BAPN-F can improve the arrangement of collagen
fibrils by briefly interrupting newly formed scar
collagen and delaying the cross-linking. In other
words, BAPN-F is considered effective in reducing the
production of undeveloped immature net-patterned
collagen fibrils, which occur at an early stage of tendon
recovery. It also promotes the construction of collagen
fibrils in a vertical direction if it is administered in
conjunction with appropriate rehabilitation [10].
However, because of this mode of action, one cannot
expect to reduce the duration of the healing period
with BAPN-F. Administration 1 to 3 months after
injury, when enzyme function is active, is most
beneficial. After this time it is hard to obtain the
desired result. According to our preliminary survey
52 M. OIKAWA AND Y. KASASHIMA
results, the use of BAPN-F medication, as compared
with placebo, was more effective in the alignment of
tendon fibers [unpublished data]. However, there was
no reduction in the length of the required treatment
period [unpublished data]. The efficacy of BAPN-F has
al so bee n ev al uat e d mo rphol o gi cal l y and
biomechanically in treating injuries to the SDFT in
horses [52]. BAPN-F was used to treat collagenase-
induced tendonitis [6, 40, 48, 49]. BAPN-F treated
tendons had many thin-diameter collagen fibrils that
might have been induced by the inhibition of collagen
cross-linking and a decrease in the collagen assembly,
reflecting a more regular orientation than that seen in
untreated collagenase-induced tendonitis [52]. In the
analysis of PSGMG in the matrix, levels of dermatan
sulphate, which modulates collagen fibrillogenesis,
increased markedly. These findings suggest that BAPN-
F allows collagen fibrils to take time remodeling and to
develop a normal fiber alignment [52]. When the
efficacy of BAPN-F and hyaluronic acid (HA) were
compared in the repair of collagenase-induced injury
of the rabbit achilles tendon, at 6 months the BAPN-
treated tendons had small-diameter fibrils that were
mechanically weaker than normal, large, regularly
arranged collagen fibrils [51]. The HA-treated
tendons, on the other hand, had large-diameter,
regularly arranged collagen fibrils compared with those
seen in untreated collagenase-induced tendonitis (Fig.
14). These results suggest that the diameters of the
collagen fibrils and the production of PSGMG in
collagenase-induced tendonitis would not have
returned to normal before 6 months after the injury
[51]. BAPN-F is of benefit to scar remodelling and is
capable of enhancing the function of healed tendons
through its anti-cross-linking properties [39]. By
contrast, HA is a PSGMG that has structural regulatory
roles in connective tissue [1]. HA promotes the tendon
healing and decreases adhesion formation [6, 7].
Thus, the results suggest that HA, unlike BAPN-F,
promotes the tendon healing process, and that
intralesional injection of HA is an effective treatment
[51].
Is section of the accessory ligament of the SDFT an effective
surgical therapy?
Section of the accessory ligament of the SDFT is a
surgical treatment for tendonitis. Proximally, most of
the superficial flexor tendon becomes superficial flexor
muscle. However, a portion of the tendon becomes a
ligamentous structure and attaches to the palmar
Fig. 14. Comparison of the efficacy of BAPN-F and HA in
collagenase-induced tendonitis in rabbits Achilles
tendon.
aspect of the radius. The surgeon must consider three
parts, the tendinous portion, the ligamentous portion,
and the muscular portion, as one weight-bearing
structure. Essentially, the purpose of the surgery is to
increase tendon flexibility by removing the inflexible
ligament and, thus, to decrease the ratio of load to
muscle when weight is placed on the joint. As a result,
it is surmised and expected that part of the tendon’s
burden is reduced to protect the recovery of the tendon
[14]. However, researchers have two different opinions
on the results of this operation. Although this
information is anecdotal, the effectiveness of the
operation has recently been called into question
because racehorses that have undergone it appear to
show increased susceptibility to suspensory desmitis.
Thus, we are considering forgoing the use of this
technique until its benefits are scientifically proven.
How effective is cold hydrotherapy?
Exercise-induced hyperthermia in the centers of
tendon bundles in athletic horses is a well-known
phenomenon that may contribute to tendon injuries
[50]. To confirm this relationship, we examined the
existing method reported by Wilson and Goodship
[50] for measuring the temperature of the centers of
tendon bundles in Thoroughbred horses, and
confirmed that the bundles reached over 42°C after a
run. We also found that when tenocytes isolated from
the SDFT of a Thoroughbred horse were cultured,
their survival rate decreases after 1 hr of exposure to a
temperature of 43°C [53]. Furthermore, we conducted
a morphological examination concerning histological
changes in the tendon caused by the treatment of
 TENDONITIS IN JAPANESE RACEHORSES
cooling and warming after exercise. From this
experiment, it was suggested that the damage to
tenocytes and the increase in small diameter collagen
fibrils observed in the warming limb possibly
predispose to subclinical lesions of SDFT injury [19].
Thus, in an effort to prevent tendonitis, we used
thermographic examination to compare the efficacy of
various cold modalities as daily therapies for cooling off
horses’ lower limbs. We used crushed ice, tap water,
isopropyl alcohol casts, or cooling gel to cool off the
legs after horses ran. Between crushed ice and tap
water, there were no remarkable differences in the time
it to cool down, or in the cooling temperature. The
other methods were not sufficiently effective to cool the
lower limbs immediately after exercise [18].
Conclusion
Finally, we will explain the future direction of our
research. The tendon is a highly differentiated tissue
from an embryological perspective, and it has a low
metabolic rate. The reason for this low metabolic rate
is that the collagen fibrils in the tendon are made by
protein that comes out of cells. Compared with protein
in the cells, this extracellular protein has a low
metabolic rate. Once tendonitis occurs, this
characteristic makes it difficult to regenerate normal
tissue, and thus it takes a long time to heal. In other
words, perfect regeneration after injury is unlikely to
occur, and irreversible structural alteration is unlikely
to be significantly altered by any therapy. Therefore,
research on tendonitis has gradually shifted from cure
to prevention, such as the optimization of training
regimens (distance, speed, frequency, etc.) to create a
strong tendon, as well as the determination of the
proper time to start training. A joint research project is
currently being carried out by the JRA and a group at
the Royal Veterinary College in London. This research
tests the hypothesis that conditioning of tendons from
a very early age will improve biological performance
and reduce the incidence of injury. We hope that a
new training regimen based on scientific knowledge
will be developed.
Areas for current and future study
1) Formulation of a training program based on
present scientific knowledge for evaluation of the
conditioning of tendons in commercially trained and
research horses.
53
It was hypothesized that if the number of tendon
fibers increases in response to functional demand over
a short period of time during development from the
intra-uterine period to after birth, as occurs in muscle
fibers, then an adequate amount of exercise
stimulation to the tendons of neonatal or young foals
may reinforce their tendons, thereby reducing the
likelihood that they will not be affected by tendonitis
when fully grown as racehorses. Joint research is
currently being carried out in conjunction with
Professor A. E. Goodship, Dr. R. K. W. Smith and Dr. H.
L. Birch of the Royal Veterinary College, University of
London, to test this hypothesis.
2) Continuation of a search for a tendon-specific
marker of tendon degeneration or early tendonitis.
3) Development of a gene therapy (vaccination)
method that reacts only with the target cells of tendons
(collaborative research with Professor M. Yamaguchi of
Ohio State University).
4) Structural analysis of the horse superficial digital
flexor myotendinous junction and exploration of
mechanoreceptors, with the aim of clarifying the roles
of s ens ory and mot or neuro ns such as t he
neurotendinal spindles and Vater-Pacini corpuscles as
reflex connections from muscle to tendon at the site of
the musculotendinous junction.
5) To clarify the effect of exercise on ultrastructure
of slow and fast skeletal muscle tendon fiber in SDFT.
6) Research into the possibility of using hyperbaric
oxygen therapy.
To examine whether intermittent exposure to
hyperbaric oxygen (HBO) is effective in enhancing
collagen synthesis and reducing the time needed for
healing tendonitis, Thoroughbred horses will receive
daily HBO sessions, at 2.5 atmospheres absolute and of
2 hr duration, in an equine HBO therapy chamber.
7) Development of a rehabilitation program for
reducing the treatment period for tendonitis and
setting up horses for early return to racing.
Acknowledgments
We thank the members of the Committee for the
Prevention of Accidents to Racehorses of the Japan
Raci ng Associ at i on. We al so thank Dr. Ryo
KUSUNOSE of the Equine Research Institute for his
support of statistical analysis on this manuscript. We
are also grateful to Dr. Roger K.W. SMITH, Equine
Referral Hospital, Royal Veterinary College, University
54 M. OIKAWA AND Y. KASASHIMA

of London, and Professor Allen E. GOODSHIP, 10. Gillis, C. 1996. Tendons and ligament
Orthopaedic Sciences, Institute of Orthopedics, Royal rehabilitation. In: Dubai International Symposium
National Orthopaedic Hospital and Royal Veterinary Proceedings. N.W. Rantanen and M.L. Hauser
College, University of London, for their valuable Eds., Mattew R. Rantanen Design, Bonsall,
suggestions. Their contributions are highly California, U.S.A., pp. 417–421.
appreciated. 11. Goodship, A.E. 1993. The pathophysiology of
flexor tendon injury in the horse. Equine vet Edu. 5:
23–29.
12. Goodship, A.E. and Birch, H.L. 1996. The
References pathophysiology of the flexor tendons in the
equine athlete. In: Dubai Equine International
1. Amiel, D., Ishizue, K., Billing, E., Wiig, M.,
Symposium Proceedings. N.W. Rantanen and
VandeBerg, J., Akeson, W.H., and Gelberman, R.
M.L. Hauser Eds., Mattew R. Rantanen Design,
1989. Hyaluronan in flexor tendon repair. J. Hand
Bonsall, California, U.S.A., pp. 83–107.
Surg. 14A: 837–843.
13. Heath III, H. and Sizemore, G.W. 1977. Plasma
2. Arai, K., Kasashima, Y., Kobayashi, A., Kuwano, A.,
calciton in normal man. J. Clin. Invest. 60: 1135–
and Yoshihara, T. 2002. TGF-β alters collagen XII
1140.
and XIX mRNA levels in cultured equine
14. Hogan, P.A. and Bramlage, L.R. 1995. Transection
tenocytes. Matrix Biol. 21: 243–250.
of the accessory ligament of the superficial digital
3. Boor, P.J., and Langford, S.D. 1997. Cardiovascular
flexor tendon for treatment of tendinitis: long
toxicology. In: Comprehensive Toxicology, 1st
term results in 61 Standardbred racehorses (1985–
Edn., Vol. 6, I.G. Sipes, C.A. McQueen and A.J.
1992). Equine vet. J. 27: 221–226.
Grandofi, Eds, Elsevier Sciences, Oxford, pp. 309–
15. Hosaka, Y., Kirisawa, R., Yamamoto, E., Ueda, H.,
332.
Iwai, H., and Takehana, K. Distribution of
4. Clunton, C., Kobluk, C., Robinson, A., and
cytokines in tendinocytes of the superficial digital
Gordon, B. 1991. Monitoring surface conditions
flexor tendon in horse. J.Vet. Med. Sci. (submitted).
of a Thoroughbred racetrack. J. Am. Vet. Med.
16. Kai, M., Takahashi, T., Aoki, O., and Oki, H. 1999.
Assoc. 198: 613–620.
Influence of rough track surface on components
5. Endo, Y., Sasaki, N., Morii, M., Koyama, S.,
of vertical forces in cantering Thoroughbred
Yoshihara, T., and Oikawa, M. 1999. Clinical and
horses. Equine vet. J., Suppl. 30: 214–217.
quantitative analysis of tendonitis in racehorses.
17. Kai, M., Aoki, O., Hiraga, A., Oki, H., and
Proc. 128th Ann Meeting Jpn. Soc. Vet. Sci. p. 252
Tokuriki, M. 2000. Use of an instrument
(written in Japanese without English Summary).
sandwiched between the hoof and shoe to
6. Forland, J.W., Trotter, G.W., Powers, B.E., Wrigley,
measure vertical ground reaction forces and three-
R.H., and Smith, F.W. 1992. Effect of sodium
dimensional acceleration at the walk, trot, and
hyaluronate in collagenase-induced superficial
canter in horses. Am. J. Vet. Res. 61: 979–985.
digital flexor tendinitis in horses. Am. J. Vet. Res.
18. Kasashima, Y., Eto, D., Kusano, K., and Hobo, S.
53: 2371–2376.
2001. Comparison of the method of cold therapy
7. Gaughan, E.M., Nixon, A.J., Krook, L.P., Yearger,
to equine limbs after training, with the aim of
A.E., Mann, K.A., Mohammed, H., and Bartel,
preventing tendinitis. J. Equine Sci. 12: 96.
D.L. 1991. Effect of sodium hyaluronate on
19 Katayama, Y. and Hobo, S. 2001. Morphological
tendon healing and adhesion formation in horses.
change in the superficial digital flexor tendon
Am. J. Vet. Res. 52: 764–773.
(SDFT) of racehorses in relation to cooling and
8. Genovase, R.L., Rantanen, N.W., and Simpson.,
warming after exercise. J. Equine Sci. 12: 63.
B.S. 1990. Clinical experience with quantitative
20. Kobayashi, A., Kasashima, Y., Katayama, Y.,
analysis of superficial digital flexor tendon injuries
Kuwano, A. , and Yoshi har a, T. 2001.
in thoroughbred and standardbred racehorses.
Ultrastructural analysis of tendon cells in the
Vet. Clin. North. Am. Equine Pract. 6: 129–145.
superficial digital flexor tendons of horses. J.
9. Genovese, R.L. 1992. Sonographic response to
Equine Sci. 12: 76.
intralesional therapy with beta-aminopropionitrile
21. Korosue, K., Satoh, H., Ueno, H., Yamamoto, J.,
fumarate for clinical tendon injuries in horses.
and Kasashima, Y. 1999. Can ultrasonography
Proc. 38th Annu. Conv. Am. Assoc. Equine Pract. pp.
detect tendonitis at early stage? Proc. 41st Annu.
265–272.
 TENDONITIS IN JAPANESE RACEHORSES
Meeting Invest. Res. Racehorses. Japan Racing
Association. p. 31 (written in Japanese without
English Summary).
22. Kotani, H., Taura, Y., Sakai, A., Tsuka, T.,
Kage yama, Y. , and Nakai chi, M. 2000.
Antemortem evaluation for magnetic resonance
imaging of the equine flexor tendon. J. Vet. Med.
Sci. 62: 81–84.
23. Kuwano, A., Sugimoto, M., and Manabe, N. 1999.
Clinical and pathomorphological approaches to
lesions predisposing to the onset of tendonitis.
Proc. 41st Annu. Meeting Invest. Res. Racehorses.
Japan Racing Association. p. 57 (written in
Japanese without English Summary).
24. McNeilly, C.M., Banes, A.J., Benjamin, M., and
Ralphs, J.R. 1996. Tendon cells in vivo form a
three dimensional network of cell processes linked
by gap junctions. J. Anat. 189: 593–600.
25. Marr, C.M., McMillan, I., Boyd, J.S., Wright, N.G.,
and Murray, M. 1993. Ultrasonographic and
histopathological findings in equine superficial
digital flexor tendon injury. Equine vet. J. 25: 23–
29.
26. Mair, C.M., Love, S., Boyd, J.S., and McKellar, Q.
1993. Factors affecting the clinical outcome of
injuries to the superficial digital flexor tendon in
national hunt and point-to-point racehorses. Vet.
Rec. 132: 476–479.
27. Mcllwraith, C.W., Clanton, C.J., and Clanton, C.N.
1987. Racetrack breakdown pilot study. In: Equine
Racet rack Breakdowns. A Col lect i on of
Cardiopulmonary and Musculoskeletal Research.
Grayson Jockey Club Research Foundation, Inc.,
Lexington, kentucky, U.S.A.
28. Morii, M. 2001. Ultrasonic quantitative evaluation
of t endoni ti s i n racehorses. MS Thesi s.
Department of Internal Medicine, School of
Veterinary Medicine, Nippon Veterinary and
Animal Science University, Musashino, Tokyo
(written in Japanese without English Summary).
29. Moyer, W., Spencer, P.A., and Kallish, M. 1991.
Relative incidence of dorsal metacarpal disease in
young Thoroughbred racehorses training on two
different surfaces. Equine vet. J. 23: 166–168.
30. Oikawa, M., Ueda, Y., Inada, S., Tsuchikawa, T.,
Kusano, H., and Takeda, A. 1994. Effect of
restructuring of racetrack on the occurrence of
racing injuries in thoroughbred horses. J. Equine
vet. Sci. 14: 262–268.
31. Oikawa, M. 1998. Cushioning fractures. Pacemakers
& Thoroughbred Breeder. March: 49–52.
32. Oikawa, M. and Goodship, A.E. 1999. Clinical and
55
investigational advances in the prevention of
tendonitis. Equine vet. J., Suppl. 30: 640–641.
33. Oikawa, M., Inada, S., Fujisawa, A., Yamakawa, H.,
and Asano, M. 2000. The use of a racetrack
hardness measurement system. Equine Pract. 22:
26–29.
34. Oikawa, M. 2000. The Japanese experience with
breakdowns. Proc. 13th Annu. Fall Sympo. Recent
Adv. Clin. Vet. Med. University of California, Davis.
pp. 63–67.
35. Oikawa, M. 2000. Japanese approaches to
tendinitis. Proc. 13th Annu. Fall Sympo. Recent Adv.
Clin. Vet. Med. University of California, Davis. pp.
68–73.
36. Oikawa, M. 2002. Epidemiological aspects of
training and racing injuries of Thoroughbred
racehorses, and corresponding countermeasures.
Japan Racing Journal. 10: 6–7.
37. Pool, R.R. 1996. Pathologic changes in tendonitis
of athletic horses. pp. 109–118. In: Dubai Equine
International Symposium Proceedings. N.R.
Rantanen and M.L. Hauser eds., Matthew R.
Rantanen Design., Bonsall, California, U.S.A.
38. Reef, V.B., Martin, B.B., and Stebbins, K. 1989.
Comparison of ultrasonographic, gross and
histologic appearance of tendon injuries in
performance horses. Proc. 35th Annu. Conv. Am.
Assoc. Equine Pract. p. 279.
39. Reef, V.D., Genovese, R.L., Byrd, J.W., Reed, K.P.,
and Davis, W.M. 1996. Treatment of superficial
digital flexor tendon injuries with beta-
aminoproprionitrile fumarate (BAPN-F):
sonographic evaluation of early tendon healing
and remodeling. In: Dubai International Equine
Symposium Proceedings. N.R. Rantanen and M.L.
Hauser eds., Matthew R. Rantanen Design,
Bonsall, California, U.S.A., pp. 423–430.
40. Silver, I.A. and Rossdale, P.D. 1983. Biochemistry
and pathology of tendon injury and healing.
Equine vet. J. Suppl. 1: 5–22.
41. Smith, R.K.W. 1992. A case of superficial digital
flexor tendinitis: ultrasonographic examination
and treatment with intralesional polysulphated
glycosaminoglycans. Equine vet. Educ. 4: 280–285.
42. Spurlock, G.H., Spurlock, S.L., and Parker, G.A.
1989. Evaluation of Hylartin V therapy for induced
tendonitis in the horse. J. Equine vet. Sci. 9: 242–
246.
43. Spurlock, G.H., Spurlock, S.L., and Parker, G.A.
1989. Ultrasonographic, gross and histologic
evaluation of a tendinitis disease model in the
horse. Vet. Radiol. 30: 184–188.
56 M. OIKAWA AND Y. KASASHIMA
44. Takahashi, T. and Stover, S. 2001. The
relationship of the modulus of elasticity and cross
sectional area of the superficial digital flexor
tendon in racehorses to their exercise history. J.
Equine Sci. 12: 62.
45. Tanaka, K. 1998. Tendinitis and the hoof.
American Farriers Journal, May/June: 74–76.
46. Ueda, Y. 1991. The safety sciences of safety. The
blood Horse. September 7: 4318–4320.
47. Wada, R., Oikawa, M., Yoshihara, T., Hasegawa,
M., and Kaneko, M. 1989. MR imaging of equine
tendonitis in vitro. Bull. Equine Res. Inst. No. 26: 65–
68.
48. Webbon, P.A. 1977. Post mortem study of equine
digital flexor tendons. Equine vet. J. 9: 61–67.
49. Williams, I.F., MaCullagh, K.G., Goodship, A.E.,
and Silver, I.A. 1984. Studies on the pathogenesis
of equine tendonitis following collagenase injury.
Res. Vet. Sci. 36: 326–338.
50. Wilson, A.M. and Goodship, A.E. 1994. Exercise
induced hyperthermia as a possible mechanism
for tendon degeneration. J. Biomech. 27: 899–905.
51. Yamamoto, E., Hata, D., Kobayashi, A., Ueda, H.,
Tangkawattama, P., Oikawa, M., and Takehana, K.
2002. Effect of beta-aminopropionitrile and
hyaluronic acid on repair of collagenase-induced
injury of the rabbit Achilles tendon. J. Comp. Path.
126: 161–170.
52. Yamamoto, E., Kobayashi, A., Yamashita, K., Ueda,
H., Prasong, B.P., Oikawa, M., and Takehana, K.
Beta-aminopropionitrile fumarate (BAPN)
evaluated morphologically and biochemically with
regard to efficacy in treating injuries to superficial
digital flexor tendon in horses. Vet. Pathol. (in
preparation).
53. Yamasaki, H., Goto, M., Yoshihara, T., Sekiguchi,
M., Konno, K., Momoi, Y., and Iwasaki, T. 2001.
Exercise-Induced superficial digital flexor tendon
hyperthermia and the effect of cooling sheets on
Thoroughbreds. J. Equine Sci. 12: 85–91.
54. Yoshikawa, H., Ueki, H., Muranaka, M., Oyamada,
T., and Yoshikawa, T. 2001. Distribution of C cells
in thyroids and association with age and sex in
racing horses. J. Equine Sci. 12: 39–45.
55. Yoshikawa, H., Oishi, H., Ueki, H., Muranaka, M.,
Oyamada, T., and Yoshikawa, T. 2002. Distribution
of C cells of fractured racehorses. J. Equine Sci. 13:
9–17.