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Calcific tendinitis of shoulder
CALCIFIC TENDINITIS OF SHOULDER
Introduction:
- It is form of tendinitis, characterized by deposits of hydroxyapatite in Rotator cuff
- Self limiting disease
- More common in females
- Age : 30 to 60 years
- Most commonly involved tendon is supraspinatus – 80% Infraspinatus – 15% Sub scapularis – 5%
- Bilateral – 13 to 47%
- Sedentary work > manual work
- Bursal side more common
Aetiology:
Two types :
- Type I – idiopathic
- Type II – Secondary ( endocrine, metabolic diseases or trauma)
Pathogenesis:
Many theories described for calcific tendinitis but still remains uncertain.
1. Ischemic theory – Mcnab microvascular injury, 1970,jbjs Booth RE Jr, Marvel JP Jr. Differential diagnosis of shoulder pain. OrthopClin North Am. 1975;6:353-379.
2. Degenrativetheory – they observed most of degenerative tendons have calcificatios . Refior H, Krödel A, Melzer C. Examinations of the pathology of the rotator cuff. Arch Orthop Trauma Surg. 1987;106:301308. Uhthoff HK, Loehr JW. Calcific tendinopathy of the rotator cuff: pathogenesis, diagnosis and management. J Am AcadOrthop Surg. 1997
3. Multiphasic disease theory – by uhthoff et al Widely accepted
- Calcific tendinitis is a multifocal, cell-mediated disease in which metaplastic transformation of tenocytes into chondrocytes induces subsequent calcification inside the This is followed by phagocytosis of the metaplastic areas in the tendons by multinucleated giant cells. Ultimately, the tendon remodels and reforms normal tendon.
- which suggests that deposition of calcium in the tissues is followed by spontaneous resorption of the calcific deposit (a cellmediated process)
4. Metaplasia theory – Ectopic bone formation from metaplasia of mesenchymal stem cells normally present in tendon tissue into osteogenic cells.
Genetic theory:
- A significantly increased expression of tissue transglutaminase (tTG)2 and its substrate, osteopontin
- 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 calcifi c area.
- BMP-2, collagen V and vascular endothelial growth factor (VEGF) did not show significant
- 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.
- Rotator cuff tear arthropathy was linked with mutations in ANK andTNA

Stages of calcific tendinitis

- Uhthoff and Loehr(1997)……. described a three-phase process: pre-calcific, calcific (divided into three subphases: formative, resting and resorptive), and post-calcific.
- Gosens and Hoftsee(2009) identified four phases (pre-calcific, formative, resorptive and recovery
Pre calcification stage
- FibrocartilagInous metaplasia
- Increased production of proteoglycans and FibrocartilagInous tissue
- Chondral metaplasia produce high quantities of collage type II and III.
Stages of calcification
- Formative phase :
- Hydroxyapatite crystals accumulate between the chondrocytes and FibrocartilagInous tissue – forming small Calcium deposits.
- These are primarily seperated by FibrocartilagInousseptae
- Merge with each other as disease progresses
- Resting phase :
- deposits of fibrocartilage are walled off
- No signs of inflammation
- Less pain
- Resorptive phase:
- during this phase calcifications are liquified and increase volume resulting spontaneous rupture of calcific deposits and lekage into the subacromial space
- Causes high inflammation
- Paunful
Post calcification stage
- Increased vascularity and macrophages, multinucleated giant cells
- Granuloma formation and migration of fibroblasts into the defect zone
- Formation of scar tissue (Primarily type III)
Remodelling ( type I)
Clinical features
- Typically present severe pain with out any trauma
- Commonly in night time
- Acute pain due to rupture of calcific deposits into subacromial bursa Causing inflammatory bursitis
- Some patients may have chronic pain
Diagnosis
- X rays
- Usg
- Ct scan
- Mri
x ray:
- Most commonly usedExtent and density
- Ap view
- Rotational views Axillary view
- Ct scan
- Rarely used
- Best for assessing consistency
- Soft or semi liquid – heterogeneous
- Hard or solid – more homogeneous and higher density
- Many authors have tried to classify the deposits in terms of size or morphology ( mainly based on conventional radiographs)

Usg:
- Both diagnostic and treatment
- Its accuracy has been reported to be similar to that of MRI in calcific deposits detection
- Doppler examination during the nodular or cystic phase shows increased vascularity around the deposits , which correlates well with the histopathological findings of Uhthoff et al.
Classification based on usg
- Farin et al. divided the deposits into three types:
- hyperechoic focus with a well-defined shadow
- hyperechoic focus with a faint shadow
- hyperechoic focus with no shadow
- Chiou et al classified calcific plaques, into the following five types:
- arc-shape (echogenic arc with clear shadowing),
- fragmented (at least two separated echogenic plaques with or without shadowing)
- punctuated (tiny calcific spots without shadowing),
- nodular (echogenic nodule without shadowing),
- cystic (bold echogenic wall with echo-free content.
- Sansone et al adopted the following terminology:
- “granular”, calcifications with partially defined margins and irregular echogenicity (encompassing the previously defined “arc-shaped”, “nodular”, and “fragmented” calcifications);
- “nodular”, cystic appearance with a sediment-type content (previously “cystic” calcifications);
- “linear”, slight thickening following the course of the collagen fascicle.


MRI:
- MRI is an additional but not essential imaging
- have low signal intensity in all MRI sequences, although areas of increased signal intensity can be found around deposits in T2 images.
- The accuracy of MRI in identifying calcific deposits is around 95 %, but it is more useful in cases of chronic CT, which may be associated with RC tears.
- Loewet
- Type A: compact and homogeneous one-part structure, clearly defined outline
- Type B: subdivided homogeneous structure, clearly defined outline
- Type C: diffuse area of low-signal intensity, no defined outline in the tendon

Arthroscopic classification
- The French society of arthroscopy divided the condition into four types:
- Type A (20%) with homogenous deposits with well defined edges;
- Type B (45%) with heterogeneous fragmented deposits with well defined edges;
- Type C (30%) with heterogeneous deposits with ill defined edges
- Type D which is not calcific tendinitis but degenerative dystrophic calcifications at the rotator cuff
Treatment
-
- NSAIDS
- REST
- PHYSIOTHERAPY
- CORTICOSTEROID INJECTION
- ULTRASOUND GUIDED NEEDLING AND LAVAGE
- PRP INJECTION
- EXTRACARPORIAL SHOCK WAVE TREATMENT
- SURGICAL TREATMENT
- Galletti S, Magnani M, Rotini R, et al. The echo-guided treatment of calcific tendinitis of the shoulder. ChirOrgani Mov. 2004
de Witte et described the differences observed between a group of patients treated with USguided percutaneous needling and lavage and a group of patients treated with simple subacromial injection of corticosteroid; at one year after treatment the group of patients treated with needling showed better recovery of shoulder function (Constant score: 86/100) with respect to those treated with steroid injection; furthermore, complete resorption occured more frequently in the patients treated with needling (13 out of 23 patients) than in those treated with corticosteroid injection (6 out of 25 patients). - Galletti et , in a series of patients followed up for around two years, reported resolution of the symptoms after percutaneous needling in nearly 90%, and complete radiographic resolution of the calcific tendinopathy in 54%.
- Galletti S, Magnani M, Rotini R, et al. The echo-guided treatment of calcific tendinitis of the shoulder. ChirOrgani Mov. 2004 del Cura et al. reported complete resolution of calcific tendinopathy in Joints 78.1% of shoulders at one year after aspiration and lavage.

AjR,2007

PRP
A 44-year-old woman with calcific tendinitis of the shoulder treated with platelet-rich plasma injection. Prior to this, she had no improvement of the symptoms after 6 weeks of ultrasound treatment, Codman exercises, and anti-inflammatory treatment. Platelet-rich plasma was injected into the subacromial area 3 times at 2-week intervals. She had progressive improvement of pain after 2 weeks, and was asymptomatic at week 6. The patient then underwent the previous protocol of rehabilitation. At the one-year follow-up, the patient was pain-free and had complete resolution of calcific tendinitis.
ESWT
- Low and medium energy is effective
- Less than 0.28mj/mm2
- local neoangiogenesis associated with an increase in antiinflammatory cytokines and growth factors after shock wave administration, followed by cell proliferation and increased metabolism
- lead to a cell-mediated reabsorption of calcification Daecke et al. published long-term follow-up of patients managed with ESWT

- 20 % of all patients required surgery,
- 70 % of patients were treated successfully and no longterm complications
- JSES,2002 Krasny et al.

- compared ESWT alone and ESWT combined with UGN, f inding that the combined treatment was more effective in relieving symptoms and that fewer patients in the combined treatment group required surgery Kim et al. carried out a comparative study between UGN and ESWT, finding better radiological and clinical outcomes in the UGN group, though both groups showed improvement relative to initial findings.


Arthroscopic removal
- Surgery is indicated in patients with severe symptoms persisting for more than six months
- Porcellini et considered the question of whether or not to suture the tendon after removal of the calcific deposits: in the authors’ view suturing is indicated in the presence of a complete or partial lesion larger than 1 cm, and not indicated in the presence of a partial lesion of less than 1 cm





