Tendinitis, calcification, chemical carbuncle, soft tissue calcification,

1. Calcific Tendinitis
Vinod Naneria
Girish Yeotikar
Arjun Wadhwani
Choithram Hospital & Research Centre, Indore
India

3. Calcific tendinitis
• It is a form of tendinitis, characterized by
deposits of hydroxyapatite in any tendon of
the body.
• Most commonly in the tendons of the rotator
cuff of shoulder, causing pain and
inflammation.

4. Clinical
• Usually females aged 30 to 60 years.
• Calcifications within Supraspinatus tendon
80% of cases,
• Infraspinatus - 15% of cases
• Subscapularis - 5% of cases. tendons;
• Bilateral in 10 to 25%.
• Asymptomatic shoulders - 5% or more of in
healthy adults.

5. Clinical Types
• Type I - Idiopathic
• Type II – Secondary - endocrine-related
disorders of thyroid, estrogen and glucose
metabolism.

6. Three main theories
A
• Reactive calcification and involves an active
cell-mediated process, usually followed by
spontaneous resorption by phagocytosing
multinucleated cells showing a typical
osteoclast phenotype.

7. Three main theories
B
• Calcium deposits are formed by a process
resembling endochondral ossification.
• The mechanism involves regional hypoxia,
which transforms tenocytes into
chondrocytes.

8. Three main theories
C
• Ectopic bone formation from metaplasia of
mesenchymal stem cells normally present in
tendon tissue into osteogenic cells.
• As no single theory is satisfactory to explain all
cases, calcific tendinopathy is currently
believed to be multifactorial.

9. Stages of Calcification
Calcification stage
• It can be divided into the following phases:
– Formative phase,
– Resting phase,
– Resorptive phase.
or
• Pre-calcification stage,
• Calcification stage,
• Post-calcification stage.

10. Stages of Calcification
Pre-calcification stage
• This stage is initiated by chondral metaplasia
of tenocytes within the tendon. This causes
increased production of proteoglycans and
formation of fibrocartilaginous tissue at the
predilection sites.
• chondral metaplasia produce abnormally high
quantities of collagen type II and III.

11. Stages of Calcification
Pathology
• The actual mechanisms that initiate these
stages are still not fully known.
• Local hypoxia caused by tissue hypoperfusion,
which triggers the transformation of tenocytes
into chondrocytes.
• The number of vessels found at the
predilection sites of calcification is very low .

12. Stages of Calcification
Calcification stage - formative phase
• Hydroxyapatite crystals accumulate between the
chondrocytes and the fibrocartilaginous tissue,
forming small calcium deposits.
• These are primarily separated by fibrocartilaginous
septa, but merge with each other as the disorder
progresses.
• In this phase, the calcifications have a chalk-like,
crumbly consistency.
• The deposits with fibrocartilage are walled off, but
there are no signs of an inflammatory process.

13. Stages of Calcification
Calcification stage- resting phase
• During this process, the calcifications are
liquefied and change to a toothpaste-like
consistency.
• The histo-morphological changes give rise to
an increase in volume resulting in higher
pressure which may cause spontaneous
perforation of the calcific deposit and leakage
into the subacromial space.

14. Stages of Calcification
Post-calcification stage
• The resorptive phase is initiated by increased
vascularization of the encapsulated deposit. The
macrophages and multinucleated giant cells
surrounding it form granuloma in which the calcific
deposits are reabsorbed.
• It is characterized by the migration of fibroblasts into
the defect zone.
• This leads to the formation of scar tissue consisting
primarily of type III collagen which is replaced by type I
collagen in the course of the remodeling process.

16. Clinical symptoms
• Severe, acute pain is typically seen in the
resorptive phase.
• Patients will describe waking up with a sharp,
stabbing pain in the shoulder at night
• There is absence of any inciting trauma or
overuse.

17. Pain due to -
• Acute pain due to rupture of calcific deposits
into the subacromial bursa causing an
inflammatory bursitis.
• The resorptive phase causes local edema and
cyto-proliferation leads to increase pressure
within the tendon substance, directly
triggering pain.

18. Investigations
• A standard shoulder x-ray series, including
antero-posterior (AP), Grashey, scapular-Y, and
axillary views, remains the primary imaging
modality.
• The standard AP x-ray will show calcium
deposition within the tendon, usually 1.5 to
2cm away from the supraspinatus tendon
insertion on the greater tuberosity.

19. X-rays
• The arm can be rotated to optimize
visualization of the different tendons.
• Mineral deposits within the Supraspinatus
best seen in neutral rotation.
• Mineral deposition in Infraspinatus and Teres
Minor can be viewed in internal rotation.

21. Internal Rotation view

22. Non–Operative Management
• Rest,
• Physical therapy,
• NSAIDs,
• Subacromial cortisone injections,
• Extracorporeal shock wave therapy (ESWT),
• Ultrasound guided needle lavage.

23. Needle Therapy
• Needling and lavage has been reported to
augment the relief of acute pain.
• Multiple perforations of the lesion can decrease
pressure within the tendon substance.
• A two-needle technique which facilitates lavage
and deposit outflow can be performed.
• During the procedure, lidocaine can be injected,
followed by administration of a corticosteroid.

24. Calcific Tendinopathy of the Rotator Cuff:
Pathogenesis, Diagnosis, and Management.
Uhthoff HK1, Loehr JW.
J Am Acad Orthop Surg. 1997 Jul;5(4):183-191.
• Calcific tendinopathy, or calcifying tendinitis, is
a disease characterized by multifocal, cell-
mediated calcification of living tissue. After
spontaneous disappearance of the calcific
deposits or, less frequently, surgical removal,
the tendon reconstitutes itself.

25. Rui YF, Lui PP, Chan LS, Chan KM, Fu SC, Li G. Does
erroneous differentiation of tendon-derived stem cells
contribute to the pathogenesis of calcifying
tendinopathy? Chin Med J (Engl) 2011;124(4):606–610
• One of the key histopathological features of
calcifying tendinopathy is the presence of
chondrocyte phenotype which surrounds the
calcific deposits, suggesting that the formation of
calcific deposits was cell-mediated. Although the
origin of cells participating in the formation of
chondrocyte phenotype and ossification is still
unknown, many evidences have suggested that
erroneous tendon cell differentiation is involved
in the process.

26. Rui YF, Lui PP, Chan LS, Chan KM, Fu SC, Li G. Does
erroneous differentiation of tendon-derived stem cells
contribute to the pathogenesis of calcifying
tendinopathy? Chin Med J (Engl) 2011;124(4):606–610
• Recent studies have shown the presence of
stem cells with self-renewal and multi-
differentiation potential in human, horse,
mouse and rat tendon tissues. We
hypothesized that the erroneous
differentiation of tendon-derived stem cells
(TDSCs) to chondrocytes or osteoblasts leads
to chondrometaplasia and ossification and
hence weaker tendon, failed healing and pain,
in calcifying tendinopathy.

27. Gene expression analysis in calcific tendinopathy of
the rotator cuff.
Oliva F, Barisani D, Grasso A, Maffulli N.
Eur Cell Mater. 2011 Jun 20;21:548-57.
A significantly increased expression of tissue transglutaminase
(tTG)2 and its substrate, osteopontin, was detected in the calcific
areas compared to the levels observed in the normal tissue from
the same subject with calcific tendinopathy, whereas a modest
increase was observed for catepsin K. There was also a significant
decrease in mRNA expression of Bone Morphogenetic Protein
(BMP)4 and BMP6 in the calcific area. BMP-2, collagen V and
vascular endothelial growth factor (VEGF) did not show significant
differences. Collagen X and matrix metalloproteinase (MMP)-9 were
not detectable. A variation in expression of these genes could be
characteristic of this form tendinopathy, since an increased level of
these genes has not been detected in other forms of tendon
lesions.

28. Basic morphologic structures of calcified tendopathy
and their significance for pathogenesis.
Mohr W1, Bilger S. Z
Rheumatol. 1990 Nov-Dec;49(6):346-55.
• it is deduced that calcifying tendopathy is
initiated by injury to cells with subsequent
intracellular calcification followed by necrosis
and eliberation of the microspheroliths and,
thereafter, extracellular calcification with
increase of the calcifying areas, in part due to
further injury to the cells.

29. Case presentation
• A 50 years old Female
• Acute onset pain right shoulder 1 day duration
• Localised tenderness over deltoid
• Restriction of shoulder movements
• X-ray – classical appearance
• Blood investigations for infection, thyroid, DM
negative.

30. May 2012

31. June 2012

32. May 2013

33. DISCLAIMER
Information contained and transmitted by this presentation is
based on personal experience and collection of cases at
Choithram Hospital & Research centre, Indore, India, during
last 40 years.
It is intended for use only by the students of orthopaedic
surgery.
Views and opinion expressed in this presentation are personal
opinion. Depending upon the x-rays and clinical presentations
viewers can make their own opinion.
Authors are not responsible for any controversies arise out of
this presentation.
For any correction or suggestion please contact
naneria@yahoo.com