Calcium apatite deposition disease
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]
Synonyms: Calcific periarthritis, calcific bursitis, periarthritis calcarea, periarthritis calcarea, and hydroxyapatite rheumatism.
Overview
Historical Perspective
- In 1966, McCarty and Gatten had found calcium hydroxyapatite as the crystal involved in “idiopathic” calcific periarthritis.
- In 2001 and 2006, Hamada has identified the calcium deposits of calcific tendinitis to be made up of carbonate apatite instead of hydroxyapatite.[1][2]
Classification
- Calcium apatite deposition disease is classified into two categories on the basis of symptoms:[3]
- Acutely symptomatic phase
- Chronic or asymptomatic phase
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: precalcific, formative, resorptive, and postcalcific.[4]
- Precalcific phase: In this stage, collagen fibers of the tendon is undergoing metaplasia into fibrocartilage tissue.
- Formative phase: Chondrocytes start depositing within the areas of fibrocartilage formation which further leads to the formation of calcified apatite crystals.
- After the formative phase sometimes it will go into the resting phase for long period of time.
- Resorptive phase: Calcification will further undergo to an inflammatory resorptive phase, which is characterized by the appearance 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.[5]
Differentiating [disease name] 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
Epidemiology and Demographics
- The prevalence of calcium apatite deposition disease is approximately 7.8% in asymptomatic patients and 42.5% in patients with subacromial pain syndrome.[3]
Age
- Calcium apatite deposition disease is more commonly observed among patients aged of 30–60 years old.[6]
- Calcium apatite deposition disease is also observed among 3 years old.[7]
Gender
- Women are more commonly affected with calcium apatite deposition disease than men.[6]
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:
- There is a genetic predisposition to the HLA-A1 gene and calcific tendinitis.[5]
- Adult-onset diabetes has the high risk of developing calcium apatite deposition disease.[8]
- Thyroid hormone and estrogen hormone disorder is associated increased risk of developing of calcium apatite deposition disease.[9]
Natural History, Complications and Prognosis
- The majority of patients with calcium apatite deposition disease 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 leads to joint destruction.
- Milwaukee shoulder syndrome if the shoulder joint is involved.
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.
- Patients usually experience acute episodes of pain to chronic mild pain.
- Acute episodes of pain usually resolve spontaneously but there are recurrent episodes after an initial episode.[10]
- Acute episodes are usually associated with swelling.
- Some patients also present with the symptoms of neuropathy.[11]
Physical Examination
- Patients with calcium apatite deposition disease usually appear fatigue and usually in pain.
- Physical examination of the involved joint is remarkable for:
Laboratory Findings
- There are no specific laboratory findings associated with calcium apatite deposition disease.
Imaging Findings
- MRI is the imaging modality of choice for calcium apatite deposition disease.
- On MRI, calcification is characterized by:
Other Diagnostic Studies
- [Disease name] may also be diagnosed using [diagnostic study name].
- Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
- There is the conservative treatment for the pain. Most of the calcifications resolve in size with conservative therapy.[12]
- Conservative treatment options are NSAIDS, hot compresses, and physiotherapy.
- Patients refractory to conservative therapy, following options are used:
Surgery
- Surgery is the choice of therapy for refractory cases of calcium apatite deposition disease. Following options are used:[13][14]
- Open resection
- Arthroscopic resection
- Ultrasound-guided needle lavage (barbotage)
- Extracorporeal shockwave therapy (ESWT)
Prevention
- There is no primary prevention for calcium apatite deposition disease.
References
- ↑ Hamada J, Ono W, Tamai K, Saotome K, Hoshino T (April 2001). "Analysis of calcium deposits in calcific periarthritis". J. Rheumatol. 28 (4): 809–13. PMID 11327256.
- ↑ Hamada J, Tamai K, Ono W, Saotome K (February 2006). "Does the nature of deposited basic calcium phosphate crystals determine clinical course in calcific periarthritis of the shoulder?". J. Rheumatol. 33 (2): 326–32. PMID 16465665.
- ↑ 3.0 3.1 Beckmann NM (2016). "Calcium Apatite Deposition Disease: Diagnosis and Treatment". Radiol Res Pract. 2016: 4801474. doi:10.1155/2016/4801474. PMC 5155096. PMID 28042481.
- ↑ Uhthoff HK, Loehr JW (July 1997). "Calcific Tendinopathy of the Rotator Cuff: Pathogenesis, Diagnosis, and Management". J Am Acad Orthop Surg. 5 (4): 183–191. PMID 10797220.
- ↑ 5.0 5.1 Sengar DP, McKendry RJ, Uhthoff HK (March 1987). "Increased frequency of HLA-A1 in calcifying tendinitis". Tissue Antigens. 29 (3): 173–4. PMID 3496685.
- ↑ 6.0 6.1 Louwerens JK, Sierevelt IN, van Hove RP, van den Bekerom MP, van Noort A (October 2015). "Prevalence of calcific deposits within the rotator cuff tendons in adults with and without subacromial pain syndrome: clinical and radiologic analysis of 1219 patients". J Shoulder Elbow Surg. 24 (10): 1588–93. doi:10.1016/j.jse.2015.02.024. PMID 25870115.
- ↑ Sakamoto K, Kozuki K (2002). "Calcific tendinitis at the biceps brachii insertion of a child: a case report". J Shoulder Elbow Surg. 11 (1): 88–91. doi:10.1067/mse.2002.119854. PMID 11845156.
- ↑ Mavrikakis ME, Drimis S, Kontoyannis DA, Rasidakis A, Moulopoulou ES, Kontoyannis S (March 1989). "Calcific shoulder periarthritis (tendinitis) in adult onset diabetes mellitus: a controlled study". Ann. Rheum. Dis. 48 (3): 211–4. PMC 1003723. PMID 2930276.
- ↑ Harvie P, Pollard TC, Carr AJ (2007). "Calcific tendinitis: natural history and association with endocrine disorders". J Shoulder Elbow Surg. 16 (2): 169–73. doi:10.1016/j.jse.2006.06.007. PMID 17188907.
- ↑ Kim JK, Park ES (May 2014). "Acute calcium deposits in the hand and wrist; comparison of acute calcium peritendinitis and acute calcium periarthritis". J Hand Surg Eur Vol. 39 (4): 436–9. doi:10.1177/1753193413478393. PMID 23422589.
- ↑ Garayoa SA, Romero-Muñoz LM, Pons-Villanueva J (December 2010). "Acute compartment syndrome of the forearm caused by calcific tendinitis of the distal biceps". Musculoskelet Surg. 94 (3): 137–9. doi:10.1007/s12306-010-0079-2. PMID 20936391.
- ↑ Cho NS, Lee BG, Rhee YG (March 2010). "Radiologic course of the calcific deposits in calcific tendinitis of the shoulder: does the initial radiologic aspect affect the final results?". J Shoulder Elbow Surg. 19 (2): 267–72. doi:10.1016/j.jse.2009.07.008. PMID 19800263.
- ↑ Rochwerger A, Franceschi JP, Viton JM, Roux H, Mattei JP (1999). "Surgical management of calcific tendinitis of the shoulder: an analysis of 26 cases". Clin. Rheumatol. 18 (4): 313–6. PMID 10468172.
- ↑ Louwerens JK, Sierevelt IN, van Noort A, van den Bekerom MP (August 2014). "Evidence for minimally invasive therapies in the management of chronic calcific tendinopathy of the rotator cuff: a systematic review and meta-analysis". J Shoulder Elbow Surg. 23 (8): 1240–9. doi:10.1016/j.jse.2014.02.002. PMID 24774621.