Calcium apatite deposition disease: Difference between revisions
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{{CMG}} {{AE}} {{MKK}} | {{CMG}} {{AE}} {{MKK}} | ||
Synonyms: Calcific periarthritis, calcific bursitis, periarthritis | Synonyms: Calcific periarthritis, calcific bursitis, periarthritis Calcarea, periarthritis Calcarea, and hydroxyapatite rheumatism. | ||
==Overview== | ==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 most common site is shoulder mostly involving the supraspinatus and infraspinatus tendons. Next common is hip, followed by the spine. It occurs between the ages of 30–60 and usually asymptomatic. The patient also present with acute episodes of pain which is recurrent after one episode. Common symptoms are the pain, | 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 HLA1 gene, newly onset adult diabetes, estrogen and thyroid hormone disorder. The most common site is shoulder mostly involving the supraspinatus and infraspinatus tendons. Next common is hip, followed by the spine. It occurs between the ages of 30–60, 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== | ==Historical Perspective== | ||
Revision as of 20:23, 18 April 2018
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
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 HLA1 gene, newly onset adult diabetes, estrogen and thyroid hormone disorder. The most common site is shoulder mostly involving the supraspinatus and infraspinatus tendons. Next common is hip, followed by the spine. It occurs between the ages of 30–60, 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.[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.