Calcinosis cutis is characterized by the deposition of calcium salts in the skin and underlying subcutaneous tissue. It is classified into five primary types: dystrophic, metastatic, iatrogenic, idiopathic, and calciphylaxis. The most common cause of calcinosis cutis is dystrophic calcification, which is associated with normal calcium and phosphorus levels in laboratory tests.
This type is often seen in conjunction with underlying diseases such as systemic sclerosis, dermatomyositis, mixed connective tissue disease, or lupus, which result in tissue damage and provide a site for calcification to occur. Metastatic calcification, conversely, is characterized by abnormal levels of calcium and phosphorus in the bloodstream.
Deposition of calcium salts takes place when the calcium phosphate product exceeds 70. Idiopathic calcification, which includes conditions like tumoral calcinosis, subepidermal calcified nodules, and scrotal calcinosis, occurs without any underlying tissue damage or abnormal laboratory values. Iatrogenic calcification is caused by administering medications or agents containing calcium or phosphate, leading to the precipitation of calcium salts.
The fifth type of calciphylaxis involves calcifying small and medium-sized blood vessels. It is typically associated with chronic renal failure and the need for dialysis. When the calcification is limited to a specific extremity or joint, it is classified as calcinosis circumscripta. However, when there is widespread involvement of subcutaneous tissue, muscles, and tendons, it is referred to as calcinosis universalis.
Epidemiology
Calcinosis cutis frequently manifests in individuals with systemic sclerosis, particularly those with the limited form known as CREST syndrome. Studies indicate that approximately 25% to 40% of patients with limited systemic sclerosis develop calcinosis cutis within ten years of onset.
Furthermore, this condition is observed in around 30% of adults and up to 70% of children and adolescents with dermatomyositis. In the case of systemic lupus erythematosus, approximately 33% of patients may exhibit periarticular calcification, while soft tissue calcification is reported in about 17% of cases.
Anatomy
Pathophysiology
Dystrophic Calcification
In dystrophic calcification, the most common form of calcinosis cutis, underlying tissue damage or inflammation provides a nidus or focal point for calcium salt deposition. This can occur in connective tissue diseases such as dermatomyositis, systemic sclerosis, mixed connective tissue disease, and lupus. Tissue injury leads to the release of pro-inflammatory cytokines and the formation of a local microenvironment that promotes the precipitation of calcium salts. The damaged tissues provide a scaffold for the deposition of calcium, forming calcific nodules.
Iatrogenic Calcification
Iatrogenic calcification occurs as a result of the administration of medications or agents containing calcium or phosphate. These substances can induce the precipitation of calcium salts at the injection site or in surrounding tissues, leading to calcinosis cutis.
Metastatic Calcification
Metastatic calcification occurs when there are abnormal calcium and phosphorus serum levels, leading to calcium salts deposition in various tissues, including the skin and subcutaneous tissue. It typically arises when the calcium-phosphate product exceeds the threshold of 70. Conditions associated with metabolic derangements, such as hyperparathyroidism, renal failure, or vitamin D imbalances, can contribute to the development of metastatic calcification.
Idiopathic Calcification
Idiopathic calcification refers to cases of calcinosis cutis without underlying tissue damage or abnormal laboratory values. It includes subtypes like tumoral calcinosis, subepidermal calcified nodules, and scrotal calcinosis. The exact mechanisms underlying idiopathic calcification remain uncertain, and further research is needed to elucidate the specific causes and triggers.
Etiology
The etiology of calcinosis cutis, or the underlying causes of the condition, can be diverse and multifactorial. The development of calcinosis cutis can be attributed to various factors and conditions, including:
Connective Tissue Diseases: Calcinosis cutis is commonly associated with connective tissue diseases such as systemic sclerosis, dermatomyositis, mixed connective tissue disease, and lupus. In these conditions, tissue damage, inflammation, and altered mineral metabolism create an environment conducive to calcium salt deposition.
Metabolic Disorders: Metabolic disorders can contribute to the development of calcinosis cutis. Examples include hyperparathyroidism, abnormalities in vitamin D metabolism, renal failure, and imbalances in mineral metabolism can also play a role.
Trauma or Tissue Injury: Local tissue trauma or injury can trigger the formation of calcinosis cutis. Surgical procedures, injections, and other forms of tissue damage can provide a site for calcium salt deposition.
Genetic Conditions: Certain genetic disorders can predispose individuals to calcinosis cutis. Examples include pseudoxanthoma elasticum, and tumoral calcinosis, an autosomal recessive condition characterized by the formation of large calcified masses in soft tissues.
Medications: Certain medications and therapeutic interventions can lead to calcinosis cutis. Prolonged use of calcium or phosphate-containing medications, such as antacids, can contribute to the deposition of calcium salts. Additionally, long-term intravenous therapy, including total parenteral nutrition (TPN), can increase the risk of calcinosis cutis.
Chronic Kidney Disease and Dialysis: Calcinosis cutis is often observed in individuals with chronic kidney disease, especially those requiring dialysis. Disturbances in calcium and phosphate metabolism and alterations in mineral regulatory factors can promote the development of calcinosis cutis in these patients.
Genetics
Prognostic Factors
Clinical History
Clinical History
The hallmark feature of calcinosis cutis is firm, palpable nodules or deposits in the skin and subcutaneous tissue. These nodules may range from small, millimeter-sized lesions to larger, several centimeters in diameter. They are typically firm or hard in consistency and may be visible or palpable under the skin. Calcinosis cutis can occur in various locations throughout the body.
The distribution may vary depending on the underlying condition. In systemic sclerosis, for example, calcinosis cutis is commonly found in the fingers, hands, forearms, and face. In dermatomyositis, it may involve the elbows, knees, and other extensor surfaces. The location and distribution of the calcinosis nodules can provide important clues for diagnosis and help differentiate it from other conditions. The presence of calcinosis cutis can cause changes in the overlying skin.
The skin may appear erythematous (red), indurated (hardened), or may have ulcerations or open wounds in severe cases. Skin texture and mobility may also be affected in the areas of calcinosis. Depending on the size, location, and extent of calcinosis cutis, individuals may experience pain or tenderness in the affected areas. This can range from mild discomfort to severe pain, significantly if there is associated inflammation or ulceration. In advanced calcinosis cutis cases, large or multiple nodules can lead to functional impairment.
It may restrict joint mobility, limit range of motion, or cause difficulty in performing activities of daily living. In cases where calcinosis cutis is associated with an underlying connective tissue disease or metabolic disorder, individuals may also present with symptoms related to the primary condition. For example, systemic sclerosis patients may have skin tightening, Raynaud’s phenomenon, or other signs of organ involvement.
Physical Examination
Physical Examination
The primary finding of calcinosis cutis is the presence of palpable nodules or deposits in the skin and subcutaneous tissue. These nodules are usually firm, hard, and can vary in size and number. They may be located in specific areas or be more widespread. The affected skin may show changes in texture. It may feel thickened, indurated (hardened), or have a peau d’orange appearance, resembling the skin of an orange. The overlying skin may also be erythematous (red) or appear normal, depending on the level of inflammation or secondary changes.
In some cases, the nodules of calcinosis cutis can lead to ulcerations or open wounds. These areas may be painful, prone to infection, and require appropriate wound care and management. The distribution pattern can vary depending on the underlying condition. For example, in systemic sclerosis, the fingers, hands, forearms, and face are commonly affected, while dermatomyositis may involve the extensor surfaces of the elbows and knees.
In cases where calcinosis cutis affects the periarticular areas or joints, there may be associated joint stiffness or limitation of movement. This can lead to functional impairment and difficulty with activities of daily living. The nodules or affected areas may be tender to touch. The degree of tenderness can vary from mild discomfort to severe pain, depending on the size and location of the calcinosis nodules.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnoses
Cutaneous mycetoma
Milia
Genital warts
Osteoma cutis
Xanthomas
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
In some cases, asymptomatic or small deposits may not require active treatment. Regular monitoring and preventive measures such as protecting the affected areas from trauma, avoiding cold exposure, and maintaining good skin hygiene are important. Physical therapy, including exercises and range-of-motion activities, may help improve joint mobility and reduce pain in some cases. Extracorporeal Shock Wave Lithotripsy uses shock waves to break down calcium deposits, showing promising results in some studies.
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Calcinosis cutis is characterized by the deposition of calcium salts in the skin and underlying subcutaneous tissue. It is classified into five primary types: dystrophic, metastatic, iatrogenic, idiopathic, and calciphylaxis. The most common cause of calcinosis cutis is dystrophic calcification, which is associated with normal calcium and phosphorus levels in laboratory tests.
This type is often seen in conjunction with underlying diseases such as systemic sclerosis, dermatomyositis, mixed connective tissue disease, or lupus, which result in tissue damage and provide a site for calcification to occur. Metastatic calcification, conversely, is characterized by abnormal levels of calcium and phosphorus in the bloodstream.
Deposition of calcium salts takes place when the calcium phosphate product exceeds 70. Idiopathic calcification, which includes conditions like tumoral calcinosis, subepidermal calcified nodules, and scrotal calcinosis, occurs without any underlying tissue damage or abnormal laboratory values. Iatrogenic calcification is caused by administering medications or agents containing calcium or phosphate, leading to the precipitation of calcium salts.
The fifth type of calciphylaxis involves calcifying small and medium-sized blood vessels. It is typically associated with chronic renal failure and the need for dialysis. When the calcification is limited to a specific extremity or joint, it is classified as calcinosis circumscripta. However, when there is widespread involvement of subcutaneous tissue, muscles, and tendons, it is referred to as calcinosis universalis.
Calcinosis cutis frequently manifests in individuals with systemic sclerosis, particularly those with the limited form known as CREST syndrome. Studies indicate that approximately 25% to 40% of patients with limited systemic sclerosis develop calcinosis cutis within ten years of onset.
Furthermore, this condition is observed in around 30% of adults and up to 70% of children and adolescents with dermatomyositis. In the case of systemic lupus erythematosus, approximately 33% of patients may exhibit periarticular calcification, while soft tissue calcification is reported in about 17% of cases.
Dystrophic Calcification
In dystrophic calcification, the most common form of calcinosis cutis, underlying tissue damage or inflammation provides a nidus or focal point for calcium salt deposition. This can occur in connective tissue diseases such as dermatomyositis, systemic sclerosis, mixed connective tissue disease, and lupus. Tissue injury leads to the release of pro-inflammatory cytokines and the formation of a local microenvironment that promotes the precipitation of calcium salts. The damaged tissues provide a scaffold for the deposition of calcium, forming calcific nodules.
Iatrogenic Calcification
Iatrogenic calcification occurs as a result of the administration of medications or agents containing calcium or phosphate. These substances can induce the precipitation of calcium salts at the injection site or in surrounding tissues, leading to calcinosis cutis.
Metastatic Calcification
Metastatic calcification occurs when there are abnormal calcium and phosphorus serum levels, leading to calcium salts deposition in various tissues, including the skin and subcutaneous tissue. It typically arises when the calcium-phosphate product exceeds the threshold of 70. Conditions associated with metabolic derangements, such as hyperparathyroidism, renal failure, or vitamin D imbalances, can contribute to the development of metastatic calcification.
Idiopathic Calcification
Idiopathic calcification refers to cases of calcinosis cutis without underlying tissue damage or abnormal laboratory values. It includes subtypes like tumoral calcinosis, subepidermal calcified nodules, and scrotal calcinosis. The exact mechanisms underlying idiopathic calcification remain uncertain, and further research is needed to elucidate the specific causes and triggers.
The etiology of calcinosis cutis, or the underlying causes of the condition, can be diverse and multifactorial. The development of calcinosis cutis can be attributed to various factors and conditions, including:
Connective Tissue Diseases: Calcinosis cutis is commonly associated with connective tissue diseases such as systemic sclerosis, dermatomyositis, mixed connective tissue disease, and lupus. In these conditions, tissue damage, inflammation, and altered mineral metabolism create an environment conducive to calcium salt deposition.
Metabolic Disorders: Metabolic disorders can contribute to the development of calcinosis cutis. Examples include hyperparathyroidism, abnormalities in vitamin D metabolism, renal failure, and imbalances in mineral metabolism can also play a role.
Trauma or Tissue Injury: Local tissue trauma or injury can trigger the formation of calcinosis cutis. Surgical procedures, injections, and other forms of tissue damage can provide a site for calcium salt deposition.
Genetic Conditions: Certain genetic disorders can predispose individuals to calcinosis cutis. Examples include pseudoxanthoma elasticum, and tumoral calcinosis, an autosomal recessive condition characterized by the formation of large calcified masses in soft tissues.
Medications: Certain medications and therapeutic interventions can lead to calcinosis cutis. Prolonged use of calcium or phosphate-containing medications, such as antacids, can contribute to the deposition of calcium salts. Additionally, long-term intravenous therapy, including total parenteral nutrition (TPN), can increase the risk of calcinosis cutis.
Chronic Kidney Disease and Dialysis: Calcinosis cutis is often observed in individuals with chronic kidney disease, especially those requiring dialysis. Disturbances in calcium and phosphate metabolism and alterations in mineral regulatory factors can promote the development of calcinosis cutis in these patients.
Clinical History
The hallmark feature of calcinosis cutis is firm, palpable nodules or deposits in the skin and subcutaneous tissue. These nodules may range from small, millimeter-sized lesions to larger, several centimeters in diameter. They are typically firm or hard in consistency and may be visible or palpable under the skin. Calcinosis cutis can occur in various locations throughout the body.
The distribution may vary depending on the underlying condition. In systemic sclerosis, for example, calcinosis cutis is commonly found in the fingers, hands, forearms, and face. In dermatomyositis, it may involve the elbows, knees, and other extensor surfaces. The location and distribution of the calcinosis nodules can provide important clues for diagnosis and help differentiate it from other conditions. The presence of calcinosis cutis can cause changes in the overlying skin.
The skin may appear erythematous (red), indurated (hardened), or may have ulcerations or open wounds in severe cases. Skin texture and mobility may also be affected in the areas of calcinosis. Depending on the size, location, and extent of calcinosis cutis, individuals may experience pain or tenderness in the affected areas. This can range from mild discomfort to severe pain, significantly if there is associated inflammation or ulceration. In advanced calcinosis cutis cases, large or multiple nodules can lead to functional impairment.
It may restrict joint mobility, limit range of motion, or cause difficulty in performing activities of daily living. In cases where calcinosis cutis is associated with an underlying connective tissue disease or metabolic disorder, individuals may also present with symptoms related to the primary condition. For example, systemic sclerosis patients may have skin tightening, Raynaud’s phenomenon, or other signs of organ involvement.
Physical Examination
The primary finding of calcinosis cutis is the presence of palpable nodules or deposits in the skin and subcutaneous tissue. These nodules are usually firm, hard, and can vary in size and number. They may be located in specific areas or be more widespread. The affected skin may show changes in texture. It may feel thickened, indurated (hardened), or have a peau d’orange appearance, resembling the skin of an orange. The overlying skin may also be erythematous (red) or appear normal, depending on the level of inflammation or secondary changes.
In some cases, the nodules of calcinosis cutis can lead to ulcerations or open wounds. These areas may be painful, prone to infection, and require appropriate wound care and management. The distribution pattern can vary depending on the underlying condition. For example, in systemic sclerosis, the fingers, hands, forearms, and face are commonly affected, while dermatomyositis may involve the extensor surfaces of the elbows and knees.
In cases where calcinosis cutis affects the periarticular areas or joints, there may be associated joint stiffness or limitation of movement. This can lead to functional impairment and difficulty with activities of daily living. The nodules or affected areas may be tender to touch. The degree of tenderness can vary from mild discomfort to severe pain, depending on the size and location of the calcinosis nodules.
Differential Diagnoses
Cutaneous mycetoma
Milia
Genital warts
Osteoma cutis
Xanthomas
In some cases, asymptomatic or small deposits may not require active treatment. Regular monitoring and preventive measures such as protecting the affected areas from trauma, avoiding cold exposure, and maintaining good skin hygiene are important. Physical therapy, including exercises and range-of-motion activities, may help improve joint mobility and reduce pain in some cases. Extracorporeal Shock Wave Lithotripsy uses shock waves to break down calcium deposits, showing promising results in some studies.
medtigo
Calcinosis Cutis
Updated :
September 4, 2023
Calcinosis cutis is characterized by the deposition of calcium salts in the skin and underlying subcutaneous tissue. It is classified into five primary types: dystrophic, metastatic, iatrogenic, idiopathic, and calciphylaxis. The most common cause of calcinosis cutis is dystrophic calcification, which is associated with normal calcium and phosphorus levels in laboratory tests.
This type is often seen in conjunction with underlying diseases such as systemic sclerosis, dermatomyositis, mixed connective tissue disease, or lupus, which result in tissue damage and provide a site for calcification to occur. Metastatic calcification, conversely, is characterized by abnormal levels of calcium and phosphorus in the bloodstream.
Deposition of calcium salts takes place when the calcium phosphate product exceeds 70. Idiopathic calcification, which includes conditions like tumoral calcinosis, subepidermal calcified nodules, and scrotal calcinosis, occurs without any underlying tissue damage or abnormal laboratory values. Iatrogenic calcification is caused by administering medications or agents containing calcium or phosphate, leading to the precipitation of calcium salts.
The fifth type of calciphylaxis involves calcifying small and medium-sized blood vessels. It is typically associated with chronic renal failure and the need for dialysis. When the calcification is limited to a specific extremity or joint, it is classified as calcinosis circumscripta. However, when there is widespread involvement of subcutaneous tissue, muscles, and tendons, it is referred to as calcinosis universalis.
Calcinosis cutis frequently manifests in individuals with systemic sclerosis, particularly those with the limited form known as CREST syndrome. Studies indicate that approximately 25% to 40% of patients with limited systemic sclerosis develop calcinosis cutis within ten years of onset.
Furthermore, this condition is observed in around 30% of adults and up to 70% of children and adolescents with dermatomyositis. In the case of systemic lupus erythematosus, approximately 33% of patients may exhibit periarticular calcification, while soft tissue calcification is reported in about 17% of cases.
Dystrophic Calcification
In dystrophic calcification, the most common form of calcinosis cutis, underlying tissue damage or inflammation provides a nidus or focal point for calcium salt deposition. This can occur in connective tissue diseases such as dermatomyositis, systemic sclerosis, mixed connective tissue disease, and lupus. Tissue injury leads to the release of pro-inflammatory cytokines and the formation of a local microenvironment that promotes the precipitation of calcium salts. The damaged tissues provide a scaffold for the deposition of calcium, forming calcific nodules.
Iatrogenic Calcification
Iatrogenic calcification occurs as a result of the administration of medications or agents containing calcium or phosphate. These substances can induce the precipitation of calcium salts at the injection site or in surrounding tissues, leading to calcinosis cutis.
Metastatic Calcification
Metastatic calcification occurs when there are abnormal calcium and phosphorus serum levels, leading to calcium salts deposition in various tissues, including the skin and subcutaneous tissue. It typically arises when the calcium-phosphate product exceeds the threshold of 70. Conditions associated with metabolic derangements, such as hyperparathyroidism, renal failure, or vitamin D imbalances, can contribute to the development of metastatic calcification.
Idiopathic Calcification
Idiopathic calcification refers to cases of calcinosis cutis without underlying tissue damage or abnormal laboratory values. It includes subtypes like tumoral calcinosis, subepidermal calcified nodules, and scrotal calcinosis. The exact mechanisms underlying idiopathic calcification remain uncertain, and further research is needed to elucidate the specific causes and triggers.
The etiology of calcinosis cutis, or the underlying causes of the condition, can be diverse and multifactorial. The development of calcinosis cutis can be attributed to various factors and conditions, including:
Connective Tissue Diseases: Calcinosis cutis is commonly associated with connective tissue diseases such as systemic sclerosis, dermatomyositis, mixed connective tissue disease, and lupus. In these conditions, tissue damage, inflammation, and altered mineral metabolism create an environment conducive to calcium salt deposition.
Metabolic Disorders: Metabolic disorders can contribute to the development of calcinosis cutis. Examples include hyperparathyroidism, abnormalities in vitamin D metabolism, renal failure, and imbalances in mineral metabolism can also play a role.
Trauma or Tissue Injury: Local tissue trauma or injury can trigger the formation of calcinosis cutis. Surgical procedures, injections, and other forms of tissue damage can provide a site for calcium salt deposition.
Genetic Conditions: Certain genetic disorders can predispose individuals to calcinosis cutis. Examples include pseudoxanthoma elasticum, and tumoral calcinosis, an autosomal recessive condition characterized by the formation of large calcified masses in soft tissues.
Medications: Certain medications and therapeutic interventions can lead to calcinosis cutis. Prolonged use of calcium or phosphate-containing medications, such as antacids, can contribute to the deposition of calcium salts. Additionally, long-term intravenous therapy, including total parenteral nutrition (TPN), can increase the risk of calcinosis cutis.
Chronic Kidney Disease and Dialysis: Calcinosis cutis is often observed in individuals with chronic kidney disease, especially those requiring dialysis. Disturbances in calcium and phosphate metabolism and alterations in mineral regulatory factors can promote the development of calcinosis cutis in these patients.
Clinical History
The hallmark feature of calcinosis cutis is firm, palpable nodules or deposits in the skin and subcutaneous tissue. These nodules may range from small, millimeter-sized lesions to larger, several centimeters in diameter. They are typically firm or hard in consistency and may be visible or palpable under the skin. Calcinosis cutis can occur in various locations throughout the body.
The distribution may vary depending on the underlying condition. In systemic sclerosis, for example, calcinosis cutis is commonly found in the fingers, hands, forearms, and face. In dermatomyositis, it may involve the elbows, knees, and other extensor surfaces. The location and distribution of the calcinosis nodules can provide important clues for diagnosis and help differentiate it from other conditions. The presence of calcinosis cutis can cause changes in the overlying skin.
The skin may appear erythematous (red), indurated (hardened), or may have ulcerations or open wounds in severe cases. Skin texture and mobility may also be affected in the areas of calcinosis. Depending on the size, location, and extent of calcinosis cutis, individuals may experience pain or tenderness in the affected areas. This can range from mild discomfort to severe pain, significantly if there is associated inflammation or ulceration. In advanced calcinosis cutis cases, large or multiple nodules can lead to functional impairment.
It may restrict joint mobility, limit range of motion, or cause difficulty in performing activities of daily living. In cases where calcinosis cutis is associated with an underlying connective tissue disease or metabolic disorder, individuals may also present with symptoms related to the primary condition. For example, systemic sclerosis patients may have skin tightening, Raynaud’s phenomenon, or other signs of organ involvement.
Physical Examination
The primary finding of calcinosis cutis is the presence of palpable nodules or deposits in the skin and subcutaneous tissue. These nodules are usually firm, hard, and can vary in size and number. They may be located in specific areas or be more widespread. The affected skin may show changes in texture. It may feel thickened, indurated (hardened), or have a peau d’orange appearance, resembling the skin of an orange. The overlying skin may also be erythematous (red) or appear normal, depending on the level of inflammation or secondary changes.
In some cases, the nodules of calcinosis cutis can lead to ulcerations or open wounds. These areas may be painful, prone to infection, and require appropriate wound care and management. The distribution pattern can vary depending on the underlying condition. For example, in systemic sclerosis, the fingers, hands, forearms, and face are commonly affected, while dermatomyositis may involve the extensor surfaces of the elbows and knees.
In cases where calcinosis cutis affects the periarticular areas or joints, there may be associated joint stiffness or limitation of movement. This can lead to functional impairment and difficulty with activities of daily living. The nodules or affected areas may be tender to touch. The degree of tenderness can vary from mild discomfort to severe pain, depending on the size and location of the calcinosis nodules.
Differential Diagnoses
Cutaneous mycetoma
Milia
Genital warts
Osteoma cutis
Xanthomas
In some cases, asymptomatic or small deposits may not require active treatment. Regular monitoring and preventive measures such as protecting the affected areas from trauma, avoiding cold exposure, and maintaining good skin hygiene are important. Physical therapy, including exercises and range-of-motion activities, may help improve joint mobility and reduce pain in some cases. Extracorporeal Shock Wave Lithotripsy uses shock waves to break down calcium deposits, showing promising results in some studies.
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