Investigating Subclinical Elastosis in Long-Term Steroid Use and Its Contribution to Skin Thinning

¹University of Nevada, Reno School of Medicine, Reno, Nevada, USA

²Nova Southeastern University Dr. Kiran C. Patel College of Osteopathic Medicine, Tampa, FL, USA

³University of Missouri School of Medicine, Columbia MO, USA

⁴ A and T Still University School of Osteopathic Medicine in Arizona, Mesa, AZ, USA

⁵Idaho College of Osteopathic Medicine, Meridian ID, USA

⁶Department of Dermatology, Northwell Health, New Hyde Park, NY, USA

*Corresponding author: Kelly Frasier, DO, MS, Department of Dermatology, Northwell Health, New Hyde Park, NY, USA, Phone: 3105956882, Email: [email protected]

Received Date: February 09, 2025

Publication Date: February 28, 2025

Citation: Sataray-Rodriguez A, et al. (2025). Investigating Subclinical Elastosis in Long-Term Steroid Use and Its Contribution to Skin Thinning. Dermis. 5(1):31.

Copyright: Sataray-Rodriguez A, et al. © (2025).

ABSTRACT

Long-term corticosteroid use is a well-documented cause of skin thinning, with subclinical elastosis emerging as an important yet underexplored mechanism contributing to this phenomenon. Corticosteroids impact skin structure and function through multiple pathways, including inhibition of fibroblast activity, reduced collagen synthesis, and dysregulation of extracellular matrix remodeling. Recent evidence suggests that elastin metabolism is also significantly affected, leading to the accumulation of fragmented and non-functional elastic fibers, a condition referred to as subclinical elastosis. Abnormal elastin deposits disrupt the mechanical integrity and resilience of the dermis, exacerbating skin thinning and increasing susceptibility to tears and bruising. Corticosteroid-induced oxidative stress and impaired matrix metalloproteinase regulation amplify elastin degradation and remodeling defects, creating a pro-elastotic environment. Subclinical elastosis is particularly pronounced in chronic users of topical and systemic corticosteroids, with histological studies revealing early dermal changes that precede visible thinning. Diagnostic advancements, such as high-resolution imaging and elastography, are improving the detection of these subtle alterations, offering insights into the progression of steroid-induced skin changes. Therapeutic approaches aimed at mitigating subclinical elastosis focus on restoring extracellular matrix balance through agents that promote fibroblast activity, enhance collagen production, and modulate elastin synthesis. Adjunctive therapies, such as antioxidants and topical growth factors, show potential in counteracting oxidative damage and preserving dermal architecture. Understanding subclinical elastosis in steroid-induced skin thinning provides a foundation for developing targeted strategies to prevent and treat this condition, ultimately improving skin health outcomes in patients requiring long-term corticosteroid therapy.

Keywords: Corticosteroids, Skin Thinning, Subclinical Elastosis, Fibroblast Inhibition, Collagen Synthesis, Extracellular Matrix Remodeling, Elastin Metabolism