622 Journal of Manipulative and Physiological Therapeutics
Volume 22 • Number 9 • November/December 1999
0161-4754/99/$8.00 + 0 76/1/102751 © 1999 JMPT
A Conservative Management Protocol for Calcific Tendinitis of the Shoulder
Paul A. Gimblett, BAppSc(chiro),a Jonathan Saville, BAppSc(chiro),b and Phillip Ebrall,
BAppSc(chiro)c
ABSTRACT
Objective: This paper presents a manage-
ment protocol for calcific tendinitis and
describes its effective application in 2 cases
of calcific tendinitis of the supraspinatus ten-
don in middle-aged women.
Clinical Features: Two patients presented to a
chiropractic clinic with previously diagnosed
calcific tendinitis of the supraspinatus tendon.
Both patients complained of chronic pain and ten-
derness in the shoulder region and had a limited
range of shoulder motion as a result of the pain. Radio-
graphs demonstrated calcific deposits in the region of the supra-
spinatus tendon.
Intervention and Outcomes: Both patients were admitted to a
treatment protocol involving approximately 20 sessions of
phonophoresis (driving of medication into tissue by ultrasound)
INTRODUCTION
The earliest evidence that calcific deposits may form in
the periarticular region of the shoulder was presented by
Painter1 in 1907 when he demonstrated, by radiograph, cal-
cific deposits in an area which he believed was the subacro-
mial bursa. The Codman2 text on the shoulder showed that
the calcific deposits were not in the subacromial bursa but in
the tendons that lie beneath it. Although most of the tendons
around the shoulder joint may be affected, those of the
supraspinatus, infraspinatus, teres minor, and subscapularis
(SITS) muscles are more often affected, with the supraspina-
tus muscle being the most common site.3,4
a
Private practice of chiropractic, New Zealand.
b
Private practice of chiropractic, Victoria, New South Wales,
Australia.
c ers when both shoulders were examined by radiography;
Senior lecturer in chiropractic, RMIT University, Melbourne,
Australia.
Submit reprint requests to: Phillip Ebrall, The Chiropractic Unit,
RMIT University, PO Box 71, Bundoora, Victoria 3083, Australia;
ebrallp@rmit.edu.au.
Paper submitted October 23, 1997; in revised form December
11, 1997; second revision November 23, 1998.
Conflict of interest statement: No benefits in any form have been
received or will be received from a commercial party related direct-
ly or indirectly to the subject of this article. The participation of
Phillip Ebrall in this work was made possible by fellowship fund-
ing from the Foundation for Chiropractic Education & Research
during 1993-94.
with Movelat cream followed by cross-friction
massage to the supraspinatus tendon and range
of motion exercises. A second set of radio-
graphs was requested. The calcific deposits,
clearly seen on the previous radiographs,
were no longer visible, and symptoms were
resolved. At 4-month follow up, both patients
continued to be symptom-free.
Conclusion: The result of these studies indicates
that the management of calcific tendinitis falls
within the scope of chiropractic practice and sup-
ports the use of a trial period of conservative man-
agement in cases of calcific tendinitis before consideration
of surgical treatment. (J Manipulative Physiol Ther 1999;
22:622-7)
Key Indexing Terms: Chiropractic; Calcific Tendinitis; Supra-
spinatus Muscle; Shoulder
Calcific tendinitis occurs in the shoulder region, in a num-
ber of other tendons throughout the body, and in the nucleus
pulposus of the intervertebral disc.3 A confusing array of
nomenclature has been applied to this condition, including
scapulohumeral periarthritis, calcified peritendinitis, hydroxy-
apatite rheumatism, hydroxyapatite deposition disease, calci-
fying tendinitis, and peritendinitis calcarea.3,5 This report
uses the term calcific tendinitis and describes the condition as
it affects the shoulder.
Incidence and Demographics
Calcific tendinitis is one of the most common causes of
nontraumatic pain in the shoulder.6,7 The incidence of radio-
graphically detectable calcific deposits in the rotator cuff
tendons of symptomatic and asymptomatic subjects has
been investigated by a number of authors. Bosworth4 report-
ed an incidence of 2.7% in 6061 asymptomatic office work-
Uhthoff and Sarkar5 reported that Welfing et al8 found an
incidence of 7.5% in 200 asymptomatic patients and 6.5% in
925 symptomatic patients.
Whereas Uhthoff and Sarkar5 and Kelley et al9 both
reported that women were more often affected than men, the
Bosworth4 study indicated that although there were more
women in the trial with supraspinatus calcific tendinitis, the
frequency was only 2.5% compared with 3.6% in men.
Calcific tendinitis is commonly found in people older than
age 30.3,9,10 Kelley et al9 reported a higher incidence of the

condition in the right shoulder and at least a 6% incidence of
the condition being bilateral.
Pathogenesis and Natural History
Codman2 described the natural history of calcific tendini-
tis as degeneration of the supraspinatus tendon, followed by
calcification and eventually rupture into the subacromial
bursa. The model used most frequently for the pathogenesis
of calcific tendinitis of the supraspinatus tendon is that of a
degenerative process with secondary calcification within the
tendon fibers.2,9 The localization of the calcific deposits in
the supraspinatus tendon is thought to most likely occur as a
result of 1 of 2 causes: (1) an early impingement syndrome
and longstanding impingement leading to the degeneration
of the tendon fibers, which then leads to calcification; or (2)
in patients without an impingement syndrome, the localiza-
tion of the calcium deposit may be related to the blood sup-
ply of the region.9
The stimulus for calcification in calcific tendinitis has
been the subject of some study.7,11 Steinbrocker7 proposed
that necrosis and fraying of the tendon fibers begins the
process, with the secondary formation of a fibrinoid mass
serving as a medium on which calcification occurs. Cailliet6
suggested that degeneration of the tendon caused the forma-
tion of small particles consisting primarily of calcium salts,
which would tend to coalesce as the vascularity of the acute
episode subsides.9
The degenerative nature of the process has been chal-
lenged by Uhthoff and Sarkar,5 who maintain that the
process is self-limiting. They suggested an alternative model
of pathogenesis that takes into account the proposed self-
healing nature of the disorder. They proposed that the evolu-
tion of the disease can be divided into 3 stages: precalcific,
calcific, and postcalcific. In the precalcific stage, the area
that will eventually calcify undergoes fibrocartilagenous
transformation. This initial fibrocartilagenous transforma-
tion takes place in the so-called critical zone of the supra-
spinatus tendon.
The concept of a critical portion of the supraspinatus ten-
don was first advanced by Codman.2 Moseley and Goldie12
later renamed the area the “critical zone” when they noted a
zone of diminished vascularity near the insertion of the supra-
spinatus. Rathbun and Macnab13 investigated the vascularity
of the region by injecting dye (micropaque) into the subcla-
vian artery of cadavers. They found that with the arm in the
position of adduction the vessels in the critical zone did not
fill. This method was repeated on the opposite arm with the
arm positioned in abduction, and the vessels of the critical
zone filled completely. The authors suggested that the avascu-
larity of the critical zone could be a result of the vessels being
wrung out by the constant pressure exerted by the head of the
humerus on the tendon when the arm is in a position of adduc-
tion. Uhthoff and Sarkar5 maintain that “focal hypoxia as a re-
sult of impaired perfusion may be an important triggering
mechanism for fibrocartilagenous transformation.”
Uhthoff and Sarkar5 have subdivided their calcific stage
into 3 phases: the formative, the resting, and the resorptive
Journal of Manipulative and Physiological Therapeutics 623
Volume 22 • Number 9 • November/December 1999
Calcific Tendinitis of the Shoulder • Gimblett et al
phases. Calcium crystals deposited primarily in matrix vesi-
cles, which coalesce to form large deposits during the for-
mative phase. The fibrocartilage is slowly eroded by the
expanding deposit. Radiographic diffraction studies of de-
hydrated specimens of the calcific deposits reveal hydroxy-
apatite [Ca10 (PO4)6 (OH)2] as the only inorganic constituent
in the deposits.14
The resting phase denotes a variable time period of local
inactivity; then the appearance of thin-walled vascular chan-
nels at the edge of the deposit heralds the beginning of the
resorptive phase. In this phase, the deposit is invaded by
macrophages, polymorphonuclear cells, and fibroblasts that
phagocytose the deposit. The trigger phenomenon for the
commencement of the resorptive phase has not yet been
elucidated.5
The postcalcific stage is characterized by granulation tis-
sue replacing the space left by the removal of the calcium
deposit. The postcalcific stage and the resorptive phase of
the calcific stage appear to occur concurrently. As the granu-
lation tissue matures to a scar, the collagen and fibroblasts
orient along the longitudinal axis of the tendon.
Presenting Symptoms and Differentials
The presenting symptoms depend on the stage of the
process. Presentation in the acute stage can resemble gout,9
with severe pain that increases with motion, especially
abduction, if the deposit is in the supraspinatus tendon. The
pain may also be felt at night.15 Uhthoff and Sarkar5 report
that the pain of the patient with an acute case can be severe
enough to almost completely incapacitate the arm. Rocks15
reports that the pain may radiate from the upper humerus to
the insertion of the deltoid muscle, upward to the occiput, or
down the arm into the fingertips. Pain in the chronic phase
may be persistent and nagging or only a soreness or aching
during abduction or rotary movements.15 The pain tends to
increase at night and the patient may report difficulty sleep-
ing on that side. These chronic symptoms may persist for
months and can be periodically interrupted by subacute peri-
ods when the pain is more intense.5
As a result of the high percentage (46.4%) of bilateral
presentations,4 it is recommended that radiographs are taken
of both shoulder complexes, even if only one shoulder is
symptomatic.5 The optimum view for demonstrating calcific
deposits in the supraspinatus tendon is an anteroposterior
view with the shoulder held in external rotation.3 Uhthoff
and Sarkar recommend that the initial radiographs for sus-
pected calcific tendinitis include the anteroposterior view in
neutral, internal, and external rotation.5
Bosworth16 reported that only 35% to 45% of people with
radiologically detectable calcific deposits in the supraspina-
tus tendon were symptomatic. In 1961, DePalma and Kru-
per17 developed a classification of the symptomatic patients
by allocating the patient into 1 of 3 groups: acute, subacute,
or chronic. The division of these groups was primarily based
on the duration and degree of the symptoms the patient had.17
Uhthoff and Sarkar5 believed it was more appropriate to
relate the symptoms to the pathogenetic mechanisms of the
624 Journal of Manipulative and Physiological Therapeutics
Volume 22 • Number 9 • November/December 1999
Calcific Tendinitis of the Shoulder • Gimblett et al
Fig 1. (Left shoulder, patient 1) Depicting the calcific deposit in
the supraspinatus tendon at initial consultation.
disease and correlated the symptomatic groupings outlined
by De Palma and Kruper17 with their model of the pathogen-
esis of calcific tendinitis. They maintained that chronic pain
was found in the formative phase of calcific tendinitis and
may also be present in the postcalcific stage, possibly in the
period before the collagen aligns with the long axis of the
tendon. They also maintained that acute pain could be expe-
rienced in the resorptive phase. The subacute symptoms may
follow the acute stage or appear as periods of transient inten-
sification of symptoms in the chronic stage. They believed
that subacute symptoms occurred as a result of inadequate
attempts at calcium resorption.5
The effective management of any condition requires a
knowledge of the site at which the condition is acting to elicit
the symptoms. The symptoms in the acute stage have been at-
tributed to an inflammation of the subacromial bursa, either
by way of the calcific material causing an inflammatory reac-
tion18 or by way of repeated motion or sudden stress resulting
in inflammation.10,15 Uhthoff and Sarkar5 attributed pain in
the acute stage to a consequence of the natural resorption of
the deposit. From a management standpoint, this argument
may be unimportant because the treatment of an inflamma-
tory process in the bursa is likely to affect the adjacent tendon.
Early methods of management emphasized the excision
of the calcific deposit, especially in the acute stage.4 The
general approach favored by physicians today is a trial peri-
od of conservative medical management with surgery advo-
cated in the approximately 10% of patients that do not
respond.9,19,20-22 Moll23 identifies the persistence of the con-
dition despite repeated local anaesthetic/corticosteroid
injections over a period of 8 weeks as the indication for
surgery. The typical conservative medical care for calcific
tendinitis is the use of steroids with local anesthetics.9,22-25
A number of studies have demonstrated the effectiveness
of physical modalities on calcific tendinitis.15,26-30 Manage-
ment depends on the stage of the disease. Table 1 summarizes
the various physical therapies that are effective or recom-
mended at each symptomatic stage of calcific tendinitis.
Table 1. Physical modalities recommended at various stages of
calcific tendinitis
Acute stage
Use Ice packs, ice massage, ice towels,15 TENS, and cryotherapy29,30
To Decrease inflammation, tendon compression pain, and muscle
spasm (if present)
Subacute stage
Use Luminous infrared, hot packs15
To Decrease inflammation, ischemic pain, and protective muscle
spasm
Chronic stage
Use Ultrasound3,15
To Decrease ischemic pain, muscle stretch pain, and protective
muscle spasm
Resorb calcium deposits
Increase extensibility of fibrous tissue
Use Deep-heating modalities28
Low-frequency TENS26,27
To Increase rate of resorption of calcific deposits (compared with
controls)
TENS, Transcutaneous electrical nerve stimulation.
CASE REPORT
Two patients with previously diagnosed calcific tendinitis
of the supraspinatus tendon visited the clinic of an author
(J.S.). Both had radiographs demonstrating calcific deposits
in the supraspinatus tendon.
The first patient was a 52-year-old woman with a constant
dull, throbbing pain in the anterolateral aspect of the left
shoulder, present for a 5-year period and aggravated by
abduction or flexion of the humerus. Physical examination
of the left arm produced pain at 90 degrees of active abduc-
tion and at 150 degrees of passive abduction. Palpation of
the shoulder region revealed tenderness over the left distal
deltoid, the greater tuberosity, and the bicipital groove. The
radiographs demonstrated a calcific deposit in the tendon of
the supraspinatus of the left shoulder (Figure 1).
The second patient was a 48-year-old woman who visited
6 months after what she reported as an excruciating episode
of right shoulder pain. At the time of presentation the shoul-
der pain was described as a constant dull ache, which result-
ed in disturbed sleep. Physical examination revealed
extreme tenderness over the greater tuberosity on the right,
with pain in the mid-arc of abduction and during internal
rotation of the humerus. The radiograph demonstrated a cal-
cific deposit in the tendon of the supraspinatus of the right
shoulder (Figure 2).
Both patients were admitted to a treatment protocol in-
volving 10 sessions of phonophoresis with Movelat (Searle),
a topical cream containing cortisone, and 7 minutes of 10%
pulsed ultrasound at 1.7 W/cm2. This was combined with
cross-friction techniques to the supraspinatus tendon and
range of motion exercises for the shoulder. The initial treat-
ment period consisted of 10 sessions over a 12-day period.
The frequency of treatment sessions then decreased to 2 per
week for a 3-week period, at the end of which a second set of
radiographs was requested (Figures 3 and 4). Treatment ses-
sions were then continued on a once weekly basis until the
symptoms had subsided. Patient 1 required weekly treatment
sessions for 4 weeks. However, patient 2 required weekly

Fig 2. (Right shoulder, patient 2) Depicting the calcific deposit in
the supraspinatus tendon at initial consultation.
sessions for 5 weeks with the protocol mentioned and an ad-
ditional 4 weeks of treatment sessions with ultrasound only
before becoming symptom-free.
A follow-up of the patients was conducted 4 months after
the initial resolution of symptoms and revealed no recur-
rence of the symptoms in either patient.
The above protocol has been used by one of the authors
(J.S.) without cortisone (with Difflam [3M Pharmaceuticals],
a topical antiinflammatory gel containing benzydamine hy-
drochloride 3.0% w/w), and there was no clinical reduction
in the deposit. Hence, cortisone would appear to be an inte-
gral part of the treatment protocol.
DISCUSSION
Calcific tendinitis is a reasonably common disorder and is
not limited to the shoulder girdle. The value of documenting
a management protocol lies in its availability for considera-
tion for future clinical guidelines and best practices docu-
mentation, and for providing a reference point from which
the clinician can build his or her management of the patient
with this symptom. The protocol described in this paper can
reasonably be considered useful in most regions where cal-
cific tendinitis may occur.
The management protocol used in these cases involves a
number of therapies and therefore cannot be seen as sup-
porting any single therapy out of this context. Therefore the
purpose of this paper is not to delineate which might be the
most effective single therapy for calcific tendinitis but to
document a management protocol drawn from the literature
that enables the clinician to achieve the goal of therapy in a
cost-effective manner. In the cases we report, the outcome
measure was improved quality of life as evidenced by the
resolution of pain and the return of full active and passive
ranges of motion. We do not advocate that this is the best
management protocol for every case; rather, we suggest that
this protocol is a good basis on which to start the conserva-
tive management of calcific tendinitis.
Journal of Manipulative and Physiological Therapeutics 625
Volume 22 • Number 9 • November/December 1999
Calcific Tendinitis of the Shoulder • Gimblett et al
Fig 3. (Left shoulder, patient 1) After treatment.
Fig 4. (Right shoulder, patient 2) After treatment.
The individual therapies of this management protocol
have been proposed in the literature as being indicated in the
management of calcific tendinitis.3,10,15 Ultrasound has been
used routinely in the management of calcific tendinitis15;
however, we found no study that reported the use of
phonophoresis in the management of this disorder. Steroids
have been used routinely for symptomatic relief by the med-
ical profession with good effect; however, this alone should
not affect the pathophysiologic features of the condition. We
believed that the combination of a topical steroid and ultra-
sound would allow symptomatic relief in combination with
increasing the extensibility of the collagen fibers. Stanton34
argued that cryotherapy was an effective analgesic and anti-
inflammatory agent that could replace the use of non-
steroidal antiinflammatory drugs.
Cross-friction has been advocated by a number of authors
in the management of chronic tendinitis.31-33 According to
Cryiax31 the transverse motion across the involved tissue
with the resulting hyperemia is the mechanism for healing in
cross-friction massage. In the acute stage, only light friction
massage is recommended to prevent abnormal orientation of
626 Journal of Manipulative and Physiological Therapeutics
Volume 22 • Number 9 • November/December 1999
Calcific Tendinitis of the Shoulder • Gimblett et al
the collagen fibers. Clinicians should note that it may take
up to 2 weeks for mature cross-links to form in collagen
fibers. In the chronic stage of the condition, a deep, stronger
friction is indicated.10 Cross-friction is not indicated in cases
if calcification is involved10; however, invariably with calcif-
ic tendinitis, a chronic bursitis occurs that is effectively
treated by cross-friction.32
The effect on the shoulder of cervical and thoracic spinal
manipulation has not yet been fully reported, but it would
seem a basic assumption that manipulation of these regions
would allow some relaxation of the shoulder girdle muscula-
ture and thus possibly contribute to pain relief. This is not
withstanding any hypothesized effects of spinal reflexes and
any remote myotomal response to segmental adjustment.
The persistence of the symptomatic picture in both
patients was of interest because it continued beyond the
point where the previously identified calcific deposits within
the supraspinatus tendon were no longer visible on radio-
graph. A possible explanation is that hydroxyapatite crystals
were still in the tendon, but their density was not sufficient
to attenuate the x-ray to the extent that it would be visible on
the radiograph. If this explanation is correct, there are nega-
tive implications for the use of radiographs as a diagnostic
aid; one implication is that pain around the shoulder with no
deposit seen on radiograph could possibly be a stage of cal-
cific tendinitis.
Uhthoff and Sarkar5 proposed that calcific tendinitis may
be a self-limiting condition. However, there are no known fac-
tors by which one may determine the progression of the stages
or even the transition from one stage to another. It is therefore
possible that any management protocol undertaken on the in-
volved tendon may simply trigger the transition from the cal-
cific phase into the resorptive phase, rather than actively re-
versing any pathological changes that have taken place.
Of value in the management of any condition is knowl-
edge of the reasons for its onset. Hammer32 points out that
the literature has identified 3 factors that may result in
pathologic change in the rotator cuff tendons: repetitive
overload and overuse, weakening and fatigue of the rotator
cuff and scapulothoracic muscles, and structural abnormali-
ties such as acromial enlargement.32 Our recommendation is
to address the living and work environments of the person to
eliminate repetitive tasks involving the shoulder.
An obvious question about this disorder asks if the cost of
intervention is justified by a significant shortening of the
natural history. The natural history is compounded by the
resorptive phase being variable in length with no prediction
of the time of likely onset. Patient 2 in this report had pre-
sented to a medical practitioner with the same symptom 4
years before her initial presentation to the chiropractor. The
radiographs of that time showed a calcific deposit in the
supraspinatus tendon of the right shoulder slightly smaller
than that shown in Figure 2. This suggests that the manage-
ment implemented at that time had no effect on reducing the
size of the deposit and that it actually continued to worsen.
Further, the fact that radiographs taken 3 months after the
start of the management protocol outlined in this paper
demonstrate no visible calcific deposit suggests that this
management protocol significantly shortens what may be
the natural history of the lesion.
The considerations for the management protocol de-
scribed in this paper are therefore 2-fold: (1) the natural his-
tory is at best ill-defined and may be significantly shortened;
and (2) psychosocial considerations suggest there is value in
responding with a therapy of likely success in cases in which
a patient reports chronic pain and discomfort with a reduced
quality of life, especially if a clinical alternative is an expen-
sive, invasive surgical procedure with the attendant risks of
hospitalization.
CONCLUSION
The results of these case studies demonstrate that the man-
agement of calcific tendinitis falls in the scope of chiroprac-
tic practice and support the use of a trial period of conserva-
tive management in all cases of calcific tendinitis before any
consideration of surgical removal of the deposit. The publi-
cation of this protocol may now serve (1) as a stimulus for
clinical research; (2) as a point for consideration in discus-
sions about clinical parameters; and (3) as a guide for the
clinical practice of chiropractic with these patients.
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