Summary of theories for the pathophysiology of calcinosis cutis.
| Mechanism | Evidence |
|---|---|
| Chronic inflammation | Increased production of TNF, IL-1, IL-6, and other proinflammatory cytokines |
| Vascular hypoxia (ischemia) | Hypoxia-induced imbalance between angiogenic factors (such as VEGF, platelet-derived growth factors) and antiangiogenic factors (such as angiostatin, endostatin) Increased expression of the hypoxia-associated GLUT-1 Hypoxia-induced osteoclast activity |
| Recurrent trauma | Presence or history of digital ulcers Calcification occurs at sites of chronic trauma/stress, suggesting a role of pressure or recurrent trauma |
GLUT-1: glucose transporter 1; IL: interleukin; TNF: tumor necrosis factor; VEGF: vascular endothelial growth factor.