What does it mean to have calcium deposits in tissues?

What Calcium Deposits in Tissues Mean

Calcium deposits in tissues represent abnormal accumulation of calcium salts outside the skeletal system, occurring through three distinct pathophysiological mechanisms: dystrophic calcification (damaged tissue with normal calcium metabolism), metastatic calcification (elevated calcium-phosphate levels depositing in normal tissue), or calcinosis (normal metabolism with subcutaneous/connective tissue deposition). 1

Understanding the Three Main Types

Dystrophic Calcification

• Occurs in damaged or devitalized tissues despite normal serum calcium and phosphate levels 1, 2
• The tissue injury itself triggers calcium deposition, not metabolic abnormalities 2
• Common examples include:
  • Atherosclerotic plaques in blood vessels 3
  • Damaged heart valves 4
  • Areas of prior inflammation or trauma 1
• In atherosclerosis, calcium granules begin microscopically in young people within lipid-rich lesion cores, eventually combining to form large calcified structures by the fourth decade of life 3

Metastatic Calcification

• Results from elevated calcium and/or phosphate levels in the blood, causing precipitation in otherwise normal tissues 1, 2
• Associated systemic conditions include:
  • Chronic kidney disease with mineral-bone disorder (most common cause) 4
  • Hyperparathyroidism 1
  • Hypervitaminosis D 1
  • Malignancies 1
  • Milk-alkali syndrome 1
• In chronic kidney disease, vascular calcification involves both intimal deposits (tied to traditional risk factors) and medial deposits (related to diabetes and hypertension) 4

Calcinosis

• Occurs in persons with normal calcium metabolism, primarily affecting subcutaneous tissues, skin, and connective tissue 1, 2
• Associated with autoimmune/connective tissue diseases:
  • Scleroderma 1
  • Dermatomyositis 1
  • Systemic lupus erythematosus 1
  • Calcinosis circumscripta or universalis 1

Special Clinical Entities

Calcium Pyrophosphate Deposition (CPPD)

• Represents crystal deposition in joints and cartilage, ranging from asymptomatic chondrocalcinosis to acute inflammatory arthritis 4
• Asymptomatic CPPD requires no treatment 4
• Acute attacks warrant joint aspiration with steroid injection, cool packs, and temporary rest 4

Calciphylaxis (Calcific Uremic Arteriolopathy)

• A severe, life-threatening condition involving calcification, fibrosis, and thrombosis of small-to-medium dermal vessels, primarily in end-stage kidney disease 5
• Diagnosis requires combining vascular calcification (detected by von Kossa stain) with subcutaneous small vessel thrombosis for optimal sensitivity (85%) and specificity (88%) 6
• First-line treatment includes sodium thiosulfate (12.5-25g per dialysis session, 2-3 times weekly for 3-6 months) and immediate discontinuation of vitamin K antagonists 5
• Carries extremely high mortality, primarily from sepsis of infected ulcers 5

Band Keratopathy

• Hydroxyapatite deposition in the anterior corneal surface from inflammation, local injury, or systemic hypercalcemia 4
• Generally asymptomatic; treatment reserved for cases causing glare, visual disability, or pain 4
• Managed with mechanical removal and/or EDTA chelation 4

Clinical Significance and Implications

Cardiovascular Risk

• Coronary artery calcification indicates atherosclerotic plaque burden and correlates with cardiovascular risk, though calcification itself does not determine plaque stability 4
• An Agatston score of 0 has nearly 100% negative predictive value for ruling out significant coronary stenosis 4
• Breast arterial calcification on mammography provides additional cardiovascular risk stratification beyond traditional calculators (net reclassification improvement 0.12) 4

Chronic Kidney Disease Context

• Vascular calcification in CKD represents a complex, multisystem disease requiring modification of multiple parameters 4
• Calcium-containing phosphate binders may increase vascular calcification risk, though evidence comparing calcium-free alternatives shows inconsistent benefits 4
• Currently, no direct methods exist to assess calcium balance or internal calcium fluxes, particularly calcium deposition in tissues 4

Critical Pitfalls to Avoid

• Do not assume all vascular calcification indicates unstable atherosclerotic disease—calcification can occur in stable plaques and does not necessarily predict rupture 4
• Recognize that fine calcium deposits visible only on von Kossa stain lack specificity without accompanying vessel thrombosis—this combination is needed to diagnose calciphylaxis 6
• Understand that calcium deposits in atherosclerosis persist despite aggressive lipid lowering—in primate studies, 3.5 years of drastic cholesterol reduction eliminated foam cells and lipid but left calcium deposits unchanged 3
• Avoid vitamin K antagonists in patients with end-stage renal disease—they increase calciphylaxis risk up to 11-fold 5
• Remember that bisphosphonates like alendronate inhibit bone resorption and can cause asymptomatic reductions in serum calcium (approximately 2%) and phosphate (approximately 4-6%) 7