Abstract
Psoriasis is a chronic inflammatory disease of the skin and joints. More recent data emphasize an association with dysregulated glucose and fatty acid metabolism, obesity, elevated blood pressure and cardiac disease, summarized as metabolic syndrome. TNF-α and IL-17, central players in the pathogenesis of psoriasis, are known to impair bone formation. Therefore, the relation between psoriasis and bone metabolism parameters was investigated. Two serum markers of either bone formation—N-terminal propeptide of type I procollagen (P1NP) or bone resorption—C-terminal telopeptide of type I collagen (CTX-I)—were analyzed in a cohort of patients with psoriasis vulgaris. In patients with psoriasis, P1NP serum levels were reduced compared to gender-, age-, and body mass index-matched healthy controls. CTX-I levels were indistinguishable between patients with psoriasis and controls. Consistently, induction of psoriasis-like skin inflammation in mice decreases bone volume and activity of osteoblasts. Moreover, efficient anti-psoriatic treatment improved psoriasis severity, but did not reverse decreased P1NP level suggesting that independent of efficient skin treatment psoriasis did affect bone metabolism and might favor the development of osteoporosis. Taken together, evidence is provided that bone metabolism might be affected by psoriatic inflammation, which may have consequences for future patient counseling and disease monitoring.
Highlights
Bone is a dynamic tissue that is constantly being remodeled in a lifelong process with about 10% of bone material being renewed each year [1]
Serum was collected from 64 patients with psoriasis vulgaris and 49 healthy controls which have been group-matched for age, sex and body mass index (BMI) (Table 1)
Since P1NP and CTX-I are preferred for clinical use as a marker of bone formation and resorption, respectively, we measured both in serum of patients with psoriasis vulgaris and age/gender matched healthy subjects [17,18,19]
Summary
Bone is a dynamic tissue that is constantly being remodeled in a lifelong process with about 10% of bone material being renewed each year [1]. It involves the concerted action of osteocytes, osteoclasts, and osteoblasts. An imbalance in bone resorption and bone formation may occur under certain pathological conditions, which lead to abnormal bone remodeling and the development of bone disorders. Primary osteoporosis is caused by postmenopausal estrogen deficiency or by age-related changes. Secondary osteoporosis is related to secondary complications such as vitamin D or calcium deficiency, changes in physical activity, or therapeutic interventions like long-term glucocorticoid treatment [1].
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