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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

 

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