What is Calcific Tendonitis?

Calcific Tendonitis, as the name suggests, is the deposition of calcium in the rotator cuff of shoulders. Rotator Cuff is a group of muscles and tendons that surround the shoulder joint. When there is build up of calcium, it puts pressure on the rotator cuff which causes inflammation and pain. In fact, it is one of the worst pains in the shoulder. This calcium deposit also reduces the space between rotator cuff and the acromion (acromion is a bony process on the shoulder blade, scapula). This affects the normal functioning of rotator cuff thus creating a subacromial impingement between the acromion and the calcium deposit in the rotator cuff, while lifting the arm overhead. This condition is quite common and generally affects people over the age of 40.

Types of Calcific Tendonitis

There are two types of Calcific Tendonitis of the Shoulder – Degenerative Calcification and Reactive Calcification.

Calcific Shoulder Tendonitis

Causes

The exact cause of Calcific Tendonitis is not known. The wear and tear of shoulder due to aging is considered to be the primary cause of Degenerative Calcification. Some experts consider damage exerted by pressure on tendons to be the cause of calcium deposits. Others feel that calcium deposit forms because there is not enough oxygen to the tendons of rotator cuff. The cause of Reactive Calcification is unclear. It is not related to aging. It is the type which causes great deal of pain in the shoulder.

Symptoms

Symptoms include pain and stiffness in the shoulder. Lifting your arm can become quite painful. At advanced stages, it can cause loss of motion in your shoulder.

Diagnosis

X-rays are the best way to detect calcium deposits. In some cases, ultrasound scan may be needed as small calcium deposits might get missed on x-rays.

Treatment of Calcific Tendonitis

Treatment is normally started with non-surgical methods as follows:

  1. Rest and anti-inflammatory medicines
  2. Steroids in case of severe pain
  3. Insertion of needles and rinsing with sterile saline(called Lavage)
  4. Physiotherapy
  5. Shock Wave Therapy

In most cases, your body will reabsorb the calcium buildup once they are fully formed, though there is the risk of a relapse.  Medically there are surgical and non-surgical treatment modalities.  The first-line of treatment is as always conservative with anti-inflammatory medications like ibuprofen and naproxen.  If that does not yield the required benefit, as a little more effective way of dealing with the pain, the doctor may go for a cortisone injection.  A cortisone shot is likely to reduce the inflammation in the short term.

If the calcium tendonitis is a little serious in nature, the doctor may go in for a procedure called lavage where two needles are inserted into your tendon and then the area is rinsed with saltwater solution.  This technique can break the calcium particles and ameliorate the pain.  Some doctor may go in for another form of treatment called “barbotage” or “fine-needling”, where calcium deposits are sucked out of the tendon through fine needles.  If the pain is recalcitrant to all of the above treatment modalities, your condition may warrant an operative intervention, though the chance of resorting to an operative intervention is still rare.

When the non-surgical methods do not help in controlling the inflammation and severe pain, doctor may advise a surgery. Most of the surgeries performed for treating Calcific Tendonitis are arthroscopic surgeries. In rare cases, open surgery is required. In both cases, calcium deposits are removed from the tendons and the area is rinsed to get rid of calcium crystals.

Arthroscopic removal of calcium deposits (surgical intervention):

Arthroscopic surgery is the most preferred surgical intervention if it is decided to remove the calcium deposits via surgically.  A small cut is made into your area of calcific tendonitis and a small instrument that looks like a tube is inserted into your joint.  This way calcium deposits are removed and the area is rinsed.

However, in rare cases, open surgery is also adopted.  Here, a large cut is made to get to the calcium deposits out.

Importance of physiotherapy:

Whichever treatment route is pursued, post treatment you are likely to have physiotherapy rehabilitation to help regain your range of motion.  Physiotherapy includes a set of stretching and strengthening exercises to strengthen the affected area.  Your doctor will explain to you in detail what this means for you and how good it is for a speedy recovery.

If you have had conservative treatment for your calcific tendonitis, your physiotherapist will teach you a series of range-of-motion workouts to help regain flexibility in the affected body part.  Physiotherapy will start with gentle exercises and work up to isometric and light-weight bearing exercises over time.

However, if you had surgery, type of physiotherapy exercises can be very subjective.  In some cases, full recovery can take three or more months.  If the surgery was done arthroscopically, recovery time is shorter compared to open method.  Be it arthroscopic surgery or open surgery, post surgical procedure, your doctor may advise you wear a sling to protect the shoulder area.  A complete physiotherapy protocol may range from six to eight months.

Rehabilitation for Calcific Tendonitis

Your case may need a surgery or not, you will have to undergo a rehabilitation program. Your doctor may recommend you work with a physical/occupational therapist. Your therapist will suggest some exercises which will help ease the pressure on the calcium deposits. He might also suggest changes in your posture which can help avoid further problems.

In case you have undergone a surgery, your surgeon might advise you to wear a sling for couple of weeks (depending on the severity of the condition).  Patient has to undergo physiotherapy post surgery as well.

Relationship between calcium deposits and tendons?

As you may be aware, tendons connect muscles to the bones.  Sometimes there can be calcium deposits in them.  Calcium deposits are like toothpaste.  They can be found in one particular spot or they can spread around the tendons.  Medical fraternity still does not know what exactly causes calcific tendonitis.  Its onset is generally around middle age.  Medical studies show that there is a relationship between calcium deposits in tendons, diabetes and thyroid disorders.

In the beginning calcium deposits are not troubling, but when they come bigger and inflamed, it can trigger intense pain.  It may take years for one to feel pain arising out of calcific tendonitis as the process of calcium being deposited in tendons is gradual and slow.  The reason behind feeling pain only at the advanced stage is that calcium deposit goes through three stages.  The final stage known as resorption is considered to cause intense pain.  Our shoulder joint is vulnerable to calcific tendonitis.   Apart from shoulder joint, it can also be found in Achilles tendon, wrist, hip, thigh, knees, ankle and foot.  The patient affected with calcium tendonitis may feel it more troublesome in the morning, especially with movement.  Lifting the affected body part gets very difficult and it affects the patient’s sleep quality as well.  In order to zero in on the diagnosis, your doctor may go for a series of images to see clearly the calcific changes in your joint.

Am I at risk of developing calcific tendonitis?

As already mentioned, the exact reason for the development of calcium deposits in some people is not discovered, it is believed that calcium build up stems from:

  • genetic predisposition
  • abnormal cell growth
  • abnormal thyroid gland activity
  • bodily production of anti-inflammatory agents
  • metabolic diseases, such as diabetes 

People who are sporty and raising the arm consistently up and down as part of their work are more at risk. The condition is prevalent among females than in males, especially between the age bracket of 40 and 60.

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

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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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