CASE
For 2 years, a 14-year-old baseball player had experienced right medial foot pain without
identifiable causes. The patient visited several outpatient clinics, where he was diagnosed
with flat feet, painful os tibiale externum, and calcareous deposition in the medial side of
the right foot (Fig. 1). He underwent the
following conservative treatments: analgesics, avoidance of weight-bearing and sports
activities, using arch support, and local injection of corticosteroids for 3 months.
However, the patient complained of persistent pain. Subsequently, redness and swelling
developed on the medial side of the right foot. The patient experienced gradual exacerbation
of pain and experienced difficulty in exercising and walking. Therefore, he was referred to
our outpatient clinic 2 years after the first onset of symptoms. Upon physical examination
of the right foot, we observed redness, swelling, a feeling of warmth, and significant
tenderness on the posterior tibial tendon (PTT), rather than the os tibiale externum. The
visual analog scale (VAS) score was 85 mm. The patient’s score was 48 points and 48 points,
respectively, using the Japanese Society of Surgery for Foot (JSSF) score1,2) and the American Orthopaedic Foot and Ankle Society (AOFAS)
score.3) The radiographs
showed os tibiale externum and calcareous deposition in the right medial foot at the
insertion point of the PTT (Fig. 2). Magnetic
resonance imaging (MRI) showed a reduction in signal intensity as a result of calcification
at the insertion of the PTT and bone marrow edema at the navicular region (Fig. 3). Initial treatment involved restricted
activity and load bearing, administration of nonsteroidal anti-inflammatory drugs (NSAIDs,
loxoprofen, two 100-mg tablets per day, for 1 month), and the wearing of arch support for 2
months. However, extracorporeal shock wave therapy (ESWT) was performed because the pain
continued and the patient was unable to walk. ESWT was started from 0.03 mJ/mm2
(the lowest energy level) and increased to 0.36 mJ/mm2, which was the maximal
level. Treatment was completed when the gross radiation energy reached 1300
mJ/mm2. The pain improved on the second day and the gait pain disappeared
within 1 week after ESWT. The VAS score improved to 10 mm in 4 weeks. However, the pain
recurred 3 months after ESWT. During the patient’s visit to our outpatient clinic, the VAS
score was 57 mm. Therefore, a second course of ESWT was performed with the same protocol as
the first course of ESWT. The pain quickly disappeared after the second course of ESWT and
the patient was able to walk on the second day. He was able to play tennis without pain
after 3 months. The calcareous deposition had disappeared on radiographs taken 6 months
after the second course of ESWT (Fig. 4). At
present (2 years after the two courses of ESWT), the patient is able to exercise. The VAS
score has improved to 5 mm and the JSSF and AOFAS scores both increased to 95 points. Arch
support can be worn without pain. Informed consent for the publication of this case report
was obtained from the patient and his parent.
DISCUSSION
In the literature, calcific tendinopathy has been reported under various names, e.g.,
calcific peritendinitis, calcific bursitis, periarticular calcarea, and hydroxylapatite
rheumatism.4) Generally,
calcific tendinopathy occurs in the tendons around the shoulder and affects approximately 3%
of adults.5) This condition
occurs in both men and women and has been observed mainly in the past 40–60 years.6) Moreover, calcific tendinopathy has
been reported in many parts of the body other than the shoulder, but it rarely occurs in the
foot, which reportedly accounts for approximately 1% of all cases.4) The flexor tendon of the forefoot is the most common
site of this disorder, when arising in the foot. Reports on similar cases in which calcific
tendinopathy occurred in the insertion of PTT are extremely rare. To date, only four such
cases have been reported, to the best of our knowledge (Table 1).7,8,9,10) Differential diagnoses of calcific tendinopathy of the
insertion of PTT include local infection, fracture, gout, pseudogout, and painful accessory
navicular. The diagnosis of calcific tendinopathy is straightforward, and calcareous
deposition in the insertion of PTT can be confirmed through plain radiographs. Such images
of the calcareous deposition in symptomatic patients show cloudy calcium hydroxyapatite
crystals in common calcific tendinopathy.
Table 1.
Reports of calcific tendinopathy of the posterior tibial tendon
| Author |
Age (years), sex |
Image findings |
Treatment |
Therapeutic outcomes |
| Delmi M (1995) |
38, female |
None |
Surgical removal |
Walk for 1 hour without a limp |
| Kirschner S (1998) |
55, female |
X-ray: calcific shadow MRI-T2WI: high signal intensity
in PTT |
Surgical removal |
Pain free, full ROM of ankle |
| Jakhere SG (2011) |
40, male |
X-ray: calcific shadow MRI-T1WI: thickening of PTT
with loss of normal hypointense signal MRI-STIR: edema with overlying subcutaneous
tissues |
Pain killers, rest, immobilization |
Resorption after 1 month |
| Harries L (2011) |
42, female |
X-ray: calcific shadow Ultrasound: hyperechoic
structure in distal portion of PTT |
NSAIDs, steroid injection, rest, crutches |
Pain free after 2 weeks |
| This report |
14, male |
X-ray: calcific shadow MRI-T1WI: thickening of PTT
with loss of normal hypointense signal MRI-STIR: edema with overlying subcutaneous
tissues |
NSAIDs, rest, immobilization, ESWT |
Play tennis 6 months later |
MRI-T2WI, magnetic resonance imaging T2-weighted image; MRI-STIR, magnetic resonance
imaging – short tau inversion recovery; ROM, range of motion.
We observed similar findings in our patient during the subacute phase with relevant
symptoms of calcific tendinopathy. This disorder is extremely rare, especially in a
14-year-old boy and in the part of the foot involved. It is possible that chronic
inflammation in the accessory navicular bone may have induced calcific tendinopathy, because
os tibiale externum was present as a developmental mechanism.
Conservative treatment strategies are commonly used for the treatment of calcific
tendinopathy. In particular, local steroid injections are effective and surgery is generally
not required. However, the optimal therapy has not yet been established because of the
extreme rarity of this condition. We sequentially administered sufficient conservative
treatments for the disorder using previously recommended medicines, but the symptoms did not
improve.
ESWT may be more efficacious in treating calcific tendinopathy in the shoulder compared
with initial conservative treatments.11,12,13) Shock waves are acoustic waves associated with a sudden rise
in pressure. They may be generated by electrohydraulic, electromagnetic, or piezoelectric
devices. However, their interactions with tissues are not completely understood. The amount
of energy released by the sonic pulse per unit area is expressed as an energy flux density
in mJ/mm2.14)
Although there is no universal agreement on the threshold values, low-energy extracorporeal
shock waves have an energy flux density below 0.08 mJ/mm2, medium-energy shock
waves are from 0.08 to 0.28 mJ/mm2, and high-energy shock waves are from 0.28 to
0.60 mJ/mm2.15)
The effects of ESWT on calcific tendonitis are currently unknown. However, its effects on
focal regions include desensitization by the induction and enhancement of absorption due to
microinjury, which in turn causes the destruction of free nerve endings. This effect of ESWT
relieved the pain from calcific tendinopathy in the current patient. In addition, bone
formation and angiogenic promotion occur as a result of the mechanical irritation of cells
in the boundary region during the tendon repair response.15) This explains why the absorption of calcific
deposits did not occur immediately.
Because the symptoms had continued for over 2 years despite conservative treatments using
previously prescribed medicines, we anticipated that the patient would benefit from the same
ESWT treatment as had been administered to a different patient with calcific tendinopathy of
the shoulder. Consequently, we pursued the case for ESWT treatment after consultation with
the patient and his family. The treatment was very effective: the symptoms mostly
disappeared after two sessions of ESWT, and the calcareous deposition had disappeared on
x-ray images taken 6 months later. Therefore, ESWT was effective in treating calcific
tendinopathy of the PTT. In this case, the symptoms persisted for about 2 years. Therefore,
a long period elapsed between irradiation and calcium deposit absorption, and the symptoms
recurred. In addition, we believe that the irradiation energy required for absorbing calcium
deposits was the reason for requiring two irradiation courses. To minimize the possibility
of recurrence and to reduce the load on the PTT after the second round of ESWT, the patient
wore insoles with a medial wedge and refrained from exercise until the calcium deposits were
absorbed.
A possible side effect of ESWT includes osteonecrosis at the head of the humerus in the
shoulder, as described in two reports.16,17) Osteonecrosis occurs between 6 months and 2 years after
treatment. It is also important to pay attention to osteonecrosis of the navicular bone.
However, we observed no evidence of osteonecrosis to a radiale on radiographic images in our
case even 2 years after treatment. Indeed, careful observations in the future are necessary.
In conclusion, ESWT was effective in treating the disorder in this case of calcific
tendinopathy of the insertion of PTT that occurred in a 14-year-old boy, even though the
patient was resistant to conservative treatment.
