Calcium apatite deposition disease
Synonyms and Keywords: Calcific periarthritis; calcific bursitis; periarthritis calcarea; hydroxyapatite rheumatism

# Overview
Calcium apatite deposition disease is a chronic condition usually characterized by deposition of calcium apatite crystals within and around connective tissues and tendons, most commonly around the periarticular location. The risk factors for calcium apatite deposition disease are the genetic predisposition to HLA-A1 gene, newly onset adult diabetes, estrogen, and thyroid disorders. The most common site of involvement is shoulder, mostly involving the supraspinatus and infraspinatus tendons. Next common location is hip, followed by the spine. It occurs between the ages of 3060, most common in females and usually asymptomatic. The patient also present with acute episodes of pain, which is recurrent after one episode. Common symptoms are the pain and swelling of the involved joint. Physical examination shows restricted joint movements and swelling. Diagnosis is made by radiography. MRI is the gold standard for the diagnosis of calcification. Treatment is usually conservative such as NSAIDS, physiotherapy, and hot compresses. Those are refractory to conservative treatment are referred to surgical treatment like open resection, arthroscopic resection, ultrasound-guided needle lavage (barbotage), and extracorporeal shockwave therapy (ESWT).

# Historical Perspective
- In 1966, McCarty and Gatten had found calcium hydroxyapatite as the crystal involved in idiopathic calcific periarthritis.
- In 2001 and 2006, Hamada had identified the calcium deposits of calcific tendinitis to be made up of carbonate apatite instead of hydroxyapatite.

# Classification
- Calcium apatite deposition disease may be classified into two phases based on symptoms:
Acutely symptomatic phase
Chronic or asymptomatic phase
- Acutely symptomatic phase
- Chronic or asymptomatic phase
- Based on the duration of symptoms, calcium apatite deposition disease may be classified as either acute or chronic.

# Pathophysiology
- The pathogenesis of calcium apatite deposition disease is not clear. Various authors have formulated the different hypothesis about the pathophysiology of calcium apatite deposition disease.
- Uhthoff and Loebr described the pathogenesis in four phases which include:
Precalcific phase: In this phase, fibrocartilage tissue is formed due to the metaplasia of collagen fibers of the tendon.
Formative phase: In this phase, in the areas of fibrocartilage formation, chondrocytes start depositing which further leads to the formation of calcified apatite crystals. Sometimes calcified apatite crystal will go into the resting phase for long period of time.
Resorptive phase: In this phase, calcification will further undergo to an inflammatory resorptive phase, which is characterized by the prsence of leukocytes, lymphocytes, and giant cells leading to the formation of a calcium granuloma.
Postcalcific phase: Reparative process allows new capillary and collagen fiber formation that is when calcification enters the postcalcific phase.
- Precalcific phase: In this phase, fibrocartilage tissue is formed due to the metaplasia of collagen fibers of the tendon.
- Formative phase: In this phase, in the areas of fibrocartilage formation, chondrocytes start depositing which further leads to the formation of calcified apatite crystals. Sometimes calcified apatite crystal will go into the resting phase for long period of time.
- Resorptive phase: In this phase, calcification will further undergo to an inflammatory resorptive phase, which is characterized by the prsence of leukocytes, lymphocytes, and giant cells leading to the formation of a calcium granuloma.
- Postcalcific phase: Reparative process allows new capillary and collagen fiber formation that is when calcification enters the postcalcific phase.
- The HLA-A1 gene has been associated with the development of calcium apatite deposition disease.

# Differentiating Calcium Apatite Deposition Disease from other Diseases
- Calcium apatite deposition disease must be differentiated from the following disease:
Calcium pyrophosphate dihydrate deposition disease (CPPD)
Dystrophic calcification
Renal osteodystrophy
Hyperparathyroidism
Hypoparathyroidism
Collagen vascular disease
Milk-alkali syndrome
Hypervitaminosis D
- Calcium pyrophosphate dihydrate deposition disease (CPPD)
- Dystrophic calcification
- Renal osteodystrophy
- Hyperparathyroidism
- Hypoparathyroidism
- Collagen vascular disease
- Milk-alkali syndrome
- Hypervitaminosis D

# Epidemiology and Demographics

## Prevalence
- The prevalence of calcium apatite deposition disease is approximately 7.8% in asymptomatic patients and 42.5% in patients with subacromial pain syndrome.

## Age
- Calcium apatite deposition disease has a bimodal pattern which affects both children around 3 years of age and adult between 3060 years old.

## Gender
- Women are more commonly affected with calcium apatite deposition disease than men.

## Race
- There is no racial predilection for calcium apatite deposition disease.

# Risk Factors
- Common risk factors in the development of calcium apatite deposition disease are:
Genetic predisposition to the HLA-A1 gene 
Adult-onset diabetes mellitus
Thyroid disorders
Estrogen hormone disorder
- Genetic predisposition to the HLA-A1 gene 
- Adult-onset diabetes mellitus
- Thyroid disorders
- Estrogen hormone disorder

# Natural History, Complications and Prognosis
- The majority of patients with calcium apatite deposition disease may remain asymptomatic for an indefinite period of time.
- Early clinical features include acute pain or chronic mild pain.
- If left untreated, intraarticular calcification may progress to develop joint destruction.
- Common complications of calcium apatite deposition disease
Intraarticular calcification
Joint destruction
Milwaukee shoulder syndrome
- Intraarticular calcification
- Joint destruction
- Milwaukee shoulder syndrome

# Diagnosis

## Diagnostic Criteria
According to the American association of rheumatology, there is no diagnostic criteria of calcium apatite deposition disease.

## Symptoms
- Patients with calcium apatite deposition disease are usually asymptomatic. However, patients might experience following symptoms:
Acute episodes of pain which might be:
Spontaneously resolved
Recurrent
Associated with swelling
Chronic mild pain
- Acute episodes of pain which might be:
Spontaneously resolved
Recurrent
Associated with swelling
- Spontaneously resolved
- Recurrent
- Associated with swelling
- Chronic mild pain
- Some patients also present with the symptoms of neuropathy such as: 
Weakness
Tingling
Numbness
- Weakness
- Tingling
- Numbness
- If it involves longus colli muscle, following symptoms are experienced by the patient which include:
Neck pain
Decreased range of motion
Neck stiffness
Odynophagia
Dysphagia
- Neck pain
- Decreased range of motion
- Neck stiffness
- Odynophagia
- Dysphagia

## Physical Examination
- Patients with calcium apatite deposition disease usually appear tired and in pain.
- Physical examination of the involved joint is remarkable for:
Redness
Swelling
Warmth
Restricted range of movement
- Redness
- Swelling
- Warmth
- Restricted range of movement
- Some patients show signs of neuropathy such as:
Weakness
Decreased sensation
Hyporeflexia
- Weakness
- Decreased sensation
- Hyporeflexia

## Laboratory Findings
- There are no specific laboratory findings associated with calcium apatite deposition disease.
- Some of the general tests indicating inflammation are abnormal which includes:
Increased ESR
Increased CRP
- Increased ESR
- Increased CRP

## Imaging Findings
- X-ray is used to see calcification in affected joint.
- CT scan is not used to diagnose, but it is used to find out deep tissue infections and soft tissue edema.
- Ultrasound is not used for diagnosis, but it is used in image-guided treatment of the calcifications.
- MRI is the imaging modality of choice for calcium apatite deposition disease.
- On MRI, calcification is characterized by:
Homogeneous and discrete calcifications
Ill-defined inhomogeneous calcifications
Soft tissue edema
- Homogeneous and discrete calcifications
- Ill-defined inhomogeneous calcifications
- Soft tissue edema

# Treatment

## Medical Therapy
- There is the conservative treatment for the pain. Most of the calcifications resolve in size with conservative therapy.
- Conservative treatment options are NSAIDS, hot compresses, and physiotherapy.
- Patients refractory to conservative therapy, following options are used:
Platelet-rich plasma injection
Steroid injection
- Platelet-rich plasma injection
- Steroid injection

## Surgery
- Surgery is the choice of therapy for refractory cases of calcium apatite deposition disease. Following options are used:
Open resection
Arthroscopic resection
Ultrasound-guided needle lavage (barbotage)
Extracorporeal shockwave therapy (ESWT)
- Open resection
- Arthroscopic resection
- Ultrasound-guided needle lavage (barbotage)
- Extracorporeal shockwave therapy (ESWT)

## Prevention
- There is no primary prevention for calcium apatite deposition disease.