Calcium apatite deposition disease: Difference between revisions
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==Classification== | ==Classification== | ||
*Calcium apatite deposition disease is classified into two categories on the basis of symptoms:<ref name="pmid28042481">{{cite journal |vauthors=Beckmann NM |title=Calcium Apatite Deposition Disease: Diagnosis and Treatment |journal=Radiol Res Pract |volume=2016 |issue= |pages=4801474 |date=2016 |pmid=28042481 |pmc=5155096 |doi=10.1155/2016/4801474 |url=}}</ref> | *Calcium apatite deposition disease is classified into two categories on the basis of symptoms:<ref name="pmid28042481">{{cite journal |vauthors=Beckmann NM |title=Calcium Apatite Deposition Disease: Diagnosis and Treatment |journal=Radiol Res Pract |volume=2016 |issue= |pages=4801474 |date=2016 |pmid=28042481 |pmc=5155096 |doi=10.1155/2016/4801474 |url=}}</ref> | ||
**Acutely symptomatic phase | **Acutely [[symptomatic]] phase | ||
**Chronic or asymptomatic phase | **[[Chronic]] or asymptomatic phase | ||
==Pathophysiology== | ==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. | *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.<ref name="pmid10797220">{{cite journal |vauthors=Uhthoff HK, Loehr JW |title=Calcific Tendinopathy of the Rotator Cuff: Pathogenesis, Diagnosis, and Management |journal=J Am Acad Orthop Surg |volume=5 |issue=4 |pages=183–191 |date=July 1997 |pmid=10797220 |doi= |url=}}</ref> | *Uhthoff and Loebr described the pathogenesis in four phases: precalcific, formative, resorptive, and postcalcific.<ref name="pmid10797220">{{cite journal |vauthors=Uhthoff HK, Loehr JW |title=Calcific Tendinopathy of the Rotator Cuff: Pathogenesis, Diagnosis, and Management |journal=J Am Acad Orthop Surg |volume=5 |issue=4 |pages=183–191 |date=July 1997 |pmid=10797220 |doi= |url=}}</ref> | ||
**Precalcific phase: In this stage, collagen fibers of the tendon is undergoing metaplasia into fibrocartilage tissue. | **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. | **Formative phase: [[Chondrocytes]] start depositing within the areas of [[fibrocartilage]] [[Formation matrix|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. | **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. | **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. | **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.<ref name="pmid3496685">{{cite journal |vauthors=Sengar DP, McKendry RJ, Uhthoff HK |title=Increased frequency of HLA-A1 in calcifying tendinitis |journal=Tissue Antigens |volume=29 |issue=3 |pages=173–4 |date=March 1987 |pmid=3496685 |doi= |url=}}</ref> | *The [[HLA-A1]] [[gene]] has been associated with the development of calcium apatite deposition disease.<ref name="pmid3496685">{{cite journal |vauthors=Sengar DP, McKendry RJ, Uhthoff HK |title=Increased frequency of HLA-A1 in calcifying tendinitis |journal=Tissue Antigens |volume=29 |issue=3 |pages=173–4 |date=March 1987 |pmid=3496685 |doi= |url=}}</ref> | ||
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. | *On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. | ||
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. | *On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. | ||
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*Calcium apatite deposition disease must be differentiated from the following disease: | *Calcium apatite deposition disease must be differentiated from the following disease: | ||
**Calcium pyrophosphate dihydrate deposition disease (CPPD) | **Calcium pyrophosphate dihydrate deposition disease (CPPD) | ||
**Dystrophic calcification | **[[Dystrophic calcification]] | ||
**Renal osteodystrophy | **[[Renal]] [[osteodystrophy]] | ||
**Hyperparathyroidism | **[[Hyperparathyroidism]] | ||
**Hypoparathyroidism | **[[Hypoparathyroidism]] | ||
**Collagen vascular disease | **[[Collagen vascular diseases|Collagen vascular disease]] | ||
**Milk-alkali syndrome | **[[Milk-alkali syndrome]] | ||
**Hypervitaminosis D | **[[Hypervitaminosis D]] | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
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==Risk Factors== | ==Risk Factors== | ||
*Common risk factors in the development of calcium apatite deposition disease are: | *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.<ref name="pmid3496685">{{cite journal |vauthors=Sengar DP, McKendry RJ, Uhthoff HK |title=Increased frequency of HLA-A1 in calcifying tendinitis |journal=Tissue Antigens |volume=29 |issue=3 |pages=173–4 |date=March 1987 |pmid=3496685 |doi= |url=}}</ref> | **There is a genetic predisposition to the HLA-A1 gene and [[calcific tendinitis]].<ref name="pmid3496685">{{cite journal |vauthors=Sengar DP, McKendry RJ, Uhthoff HK |title=Increased frequency of HLA-A1 in calcifying tendinitis |journal=Tissue Antigens |volume=29 |issue=3 |pages=173–4 |date=March 1987 |pmid=3496685 |doi= |url=}}</ref> | ||
**Adult-onset diabetes has the high risk of developing calcium apatite deposition disease.<ref name="pmid2930276">{{cite journal |vauthors=Mavrikakis ME, Drimis S, Kontoyannis DA, Rasidakis A, Moulopoulou ES, Kontoyannis S |title=Calcific shoulder periarthritis (tendinitis) in adult onset diabetes mellitus: a controlled study |journal=Ann. Rheum. Dis. |volume=48 |issue=3 |pages=211–4 |date=March 1989 |pmid=2930276 |pmc=1003723 |doi= |url=}}</ref> | **Adult-onset [[diabetes]] has the high risk of developing calcium apatite deposition disease.<ref name="pmid2930276">{{cite journal |vauthors=Mavrikakis ME, Drimis S, Kontoyannis DA, Rasidakis A, Moulopoulou ES, Kontoyannis S |title=Calcific shoulder periarthritis (tendinitis) in adult onset diabetes mellitus: a controlled study |journal=Ann. Rheum. Dis. |volume=48 |issue=3 |pages=211–4 |date=March 1989 |pmid=2930276 |pmc=1003723 |doi= |url=}}</ref> | ||
**Thyroid hormone and estrogen hormone disorder is associated increased risk of developing of calcium apatite deposition disease.<ref name="pmid17188907">{{cite journal |vauthors=Harvie P, Pollard TC, Carr AJ |title=Calcific tendinitis: natural history and association with endocrine disorders |journal=J Shoulder Elbow Surg |volume=16 |issue=2 |pages=169–73 |date=2007 |pmid=17188907 |doi=10.1016/j.jse.2006.06.007 |url=}}</ref> | **[[Thyroid hormone]] and estrogen hormone disorder is associated increased risk of developing of calcium apatite deposition disease.<ref name="pmid17188907">{{cite journal |vauthors=Harvie P, Pollard TC, Carr AJ |title=Calcific tendinitis: natural history and association with endocrine disorders |journal=J Shoulder Elbow Surg |volume=16 |issue=2 |pages=169–73 |date=2007 |pmid=17188907 |doi=10.1016/j.jse.2006.06.007 |url=}}</ref> | ||
== Natural History, Complications and Prognosis== | == Natural History, Complications and Prognosis== | ||
*The majority of patients with calcium apatite deposition disease remain asymptomatic for an indefinite period of time. | *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. | *Early clinical features include acute [[pain]] or chronic mild pain. | ||
*If left untreated, intraarticular calcification may progress to develop joint destruction. | *If left untreated, [[intraarticular]] calcification may progress to develop [[joint]] destruction. | ||
*Common complications of calcium apatite deposition disease | *Common complications of calcium apatite deposition disease | ||
**Intraarticular calcification leads to joint destruction. | **Intraarticular calcification leads to joint destruction. | ||
**Milwaukee shoulder syndrome if the shoulder joint is involved. | **Milwaukee shoulder syndrome if the [[shoulder joint]] is involved. | ||
== Diagnosis == | == Diagnosis == | ||
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=== Symptoms === | === Symptoms === | ||
*Patients with calcium apatite deposition disease are usually asymptomatic. | *Patients with calcium apatite deposition disease are usually [[asymptomatic]]. | ||
*Patients usually experience acute episodes of pain to chronic mild pain. | *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.<ref name="pmid23422589">{{cite journal |vauthors=Kim JK, Park ES |title=Acute calcium deposits in the hand and wrist; comparison of acute calcium peritendinitis and acute calcium periarthritis |journal=J Hand Surg Eur Vol |volume=39 |issue=4 |pages=436–9 |date=May 2014 |pmid=23422589 |doi=10.1177/1753193413478393 |url=}}</ref> | *Acute episodes of [[pain]] usually resolve spontaneously but there are recurrent episodes after an initial episode.<ref name="pmid23422589">{{cite journal |vauthors=Kim JK, Park ES |title=Acute calcium deposits in the hand and wrist; comparison of acute calcium peritendinitis and acute calcium periarthritis |journal=J Hand Surg Eur Vol |volume=39 |issue=4 |pages=436–9 |date=May 2014 |pmid=23422589 |doi=10.1177/1753193413478393 |url=}}</ref> | ||
*Acute episodes are usually associated with | *[[Acute]] episodes are usually associated with [[swelling]]. | ||
*Some patients also present with the symptoms of neuropathy.<ref name="pmid20936391">{{cite journal |vauthors=Garayoa SA, Romero-Muñoz LM, Pons-Villanueva J |title=Acute compartment syndrome of the forearm caused by calcific tendinitis of the distal biceps |journal=Musculoskelet Surg |volume=94 |issue=3 |pages=137–9 |date=December 2010 |pmid=20936391 |doi=10.1007/s12306-010-0079-2 |url=}}</ref> | *Some patients also present with the symptoms of [[neuropathy]].<ref name="pmid20936391">{{cite journal |vauthors=Garayoa SA, Romero-Muñoz LM, Pons-Villanueva J |title=Acute compartment syndrome of the forearm caused by calcific tendinitis of the distal biceps |journal=Musculoskelet Surg |volume=94 |issue=3 |pages=137–9 |date=December 2010 |pmid=20936391 |doi=10.1007/s12306-010-0079-2 |url=}}</ref> | ||
=== Physical Examination === | === Physical Examination === | ||
*Patients with calcium apatite deposition disease usually appear fatigue and usually in pain. | *Patients with calcium apatite deposition disease usually appear [[fatigue]] and usually in [[pain]]. | ||
*Physical examination of the involved joint is remarkable for: | *Physical examination of the involved [[joint]] is remarkable for: | ||
**Redness | **[[Redness]] | ||
**Swelling | **[[Swelling]] | ||
**The restricted range of movement | **The restricted range of movement | ||
**Some patients show signs of neuropathy such as | **Some patients show signs of [[neuropathy]] such as [[weakness]], decreased [[sensation]] and [[reflexes]]. | ||
=== Laboratory Findings === | === Laboratory Findings === | ||
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===Imaging Findings=== | ===Imaging Findings=== | ||
*MRI is the imaging modality of choice for calcium apatite deposition disease. | *MRI is the imaging modality of choice for calcium apatite deposition disease. | ||
*On MRI, | *On MRI, calcification is characterized by: | ||
** | ** | ||
** | ** | ||
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== Treatment == | == Treatment == | ||
=== Medical Therapy === | === Medical Therapy === | ||
*There is the conservative treatment for the pain. Most of the calcifications resolve in size with conservative therapy.<ref name="pmid19800263">{{cite journal |vauthors=Cho NS, Lee BG, Rhee YG |title=Radiologic course of the calcific deposits in calcific tendinitis of the shoulder: does the initial radiologic aspect affect the final results? |journal=J Shoulder Elbow Surg |volume=19 |issue=2 |pages=267–72 |date=March 2010 |pmid=19800263 |doi=10.1016/j.jse.2009.07.008 |url=}}</ref> | *There is the conservative treatment for the [[pain]]. Most of the calcifications resolve in size with conservative therapy.<ref name="pmid19800263">{{cite journal |vauthors=Cho NS, Lee BG, Rhee YG |title=Radiologic course of the calcific deposits in calcific tendinitis of the shoulder: does the initial radiologic aspect affect the final results? |journal=J Shoulder Elbow Surg |volume=19 |issue=2 |pages=267–72 |date=March 2010 |pmid=19800263 |doi=10.1016/j.jse.2009.07.008 |url=}}</ref> | ||
*Conservative treatment options are NSAIDS, hot compresses, and physiotherapy. | *Conservative treatment options are [[NSAIDS]], hot compresses, and [[physiotherapy]]. | ||
*Patients refractory to conservative therapy, following options are used: | *Patients refractory to conservative therapy, following options are used: | ||
**Platelet-rich plasma injection | **[[Platelet]]-rich plasma injection | ||
**Steroid injection | **[[Steroid]] injection | ||
=== Surgery === | === Surgery === | ||
*Surgery is the choice of therapy for refractory cases of calcium apatite deposition disease. Following options are used:<ref name="pmid10468172">{{cite journal |vauthors=Rochwerger A, Franceschi JP, Viton JM, Roux H, Mattei JP |title=Surgical management of calcific tendinitis of the shoulder: an analysis of 26 cases |journal=Clin. Rheumatol. |volume=18 |issue=4 |pages=313–6 |date=1999 |pmid=10468172 |doi= |url=}}</ref><ref name="pmid24774621">{{cite journal |vauthors=Louwerens JK, Sierevelt IN, van Noort A, van den Bekerom MP |title=Evidence for minimally invasive therapies in the management of chronic calcific tendinopathy of the rotator cuff: a systematic review and meta-analysis |journal=J Shoulder Elbow Surg |volume=23 |issue=8 |pages=1240–9 |date=August 2014 |pmid=24774621 |doi=10.1016/j.jse.2014.02.002 |url=}}</ref> | *Surgery is the choice of therapy for [[refractory]] cases of calcium apatite deposition disease. Following options are used:<ref name="pmid10468172">{{cite journal |vauthors=Rochwerger A, Franceschi JP, Viton JM, Roux H, Mattei JP |title=Surgical management of calcific tendinitis of the shoulder: an analysis of 26 cases |journal=Clin. Rheumatol. |volume=18 |issue=4 |pages=313–6 |date=1999 |pmid=10468172 |doi= |url=}}</ref><ref name="pmid24774621">{{cite journal |vauthors=Louwerens JK, Sierevelt IN, van Noort A, van den Bekerom MP |title=Evidence for minimally invasive therapies in the management of chronic calcific tendinopathy of the rotator cuff: a systematic review and meta-analysis |journal=J Shoulder Elbow Surg |volume=23 |issue=8 |pages=1240–9 |date=August 2014 |pmid=24774621 |doi=10.1016/j.jse.2014.02.002 |url=}}</ref> | ||
**Open resection | **Open [[resection]] | ||
**Arthroscopic resection | **[[Arthroscopic]] [[resection]] | ||
**Ultrasound-guided needle lavage (barbotage) | **[[Ultrasound]]-guided needle lavage (barbotage) | ||
**Extracorporeal shockwave therapy (ESWT) | **[[Extracorporeal shockwave therapy]] (ESWT) | ||
Revision as of 16:40, 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
Historical Perspective
- [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
- In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
- In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].
Classification
- Calcium apatite deposition disease is classified into two categories on the basis of symptoms:[1]
- 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.[2]
- 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.[3]
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
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.[1]
Age
- Calcium apatite deposition disease is more commonly observed among patients aged of 30–60 years old.[4]
- Calcium apatite deposition disease is also observed among 3 years old.[5]
Gender
- Women are more commonly affected with calcium apatite deposition disease than men.[4]
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.[3]
- Adult-onset diabetes has the high risk of developing calcium apatite deposition disease.[6]
- Thyroid hormone and estrogen hormone disorder is associated increased risk of developing of calcium apatite deposition disease.[7]
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.[8]
- Acute episodes are usually associated with swelling.
- Some patients also present with the symptoms of neuropathy.[9]
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.[10]
- 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:[11][12]
- 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
- ↑ 1.0 1.1 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.
- ↑ 3.0 3.1 Sengar DP, McKendry RJ, Uhthoff HK (March 1987). "Increased frequency of HLA-A1 in calcifying tendinitis". Tissue Antigens. 29 (3): 173–4. PMID 3496685.
- ↑ 4.0 4.1 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.