Extensive CD34-to-CD90 Fibroblast Transition Defines Regions of Cutaneous Reparative, Hypertrophic, and Keloidal Scarring.

BACKGROUND

CD90 fibroblasts have been described arising from and replacing the homeostatic CD34 network in scleroderma, but have not been specifically examined in other forms of cutaneous fibrosis.

OBJECTIVES

To address expression, timelines, and spatial relationships of CD90, CD34, and smooth muscle actin (SMA) expressing fibroblasts in scars and to examine for the presence of a CD34-to-CD90 transition.

METHODS

One hundred and seventeen scars (reparative/hypertrophic/keloidal) were evaluated for CD90, CD34, and SMA expression. Double-staining immunohistochemistry for CD90/CD34 was performed to identify CD90/CD34 transitioning cells, confirmed by double-color immunofluorescence. In addition, some scars were double-stained with CD90/SMA, CD90/procollagen-1, or SMA/procollagen-1 to evaluate spatial relationships and active collagen synthesis. Expression was graded as diffuse, minority, and negative.

RESULTS

Most scars demonstrate a CD90/CD34 pattern, and dual CD90/CD34 fibroblasts were observed in 91% of scars. In reparative scars, CD90 expression reverses to a CD34/CD90 state with maturation. Pathologic scars exhibit prolonged CD90 expression. Both CD90 and SMA fibroblasts collagenize scars, although CD90 fibroblasts are more prevalent.

CONCLUSIONS

CD90 fibroblasts likely arise from the resting CD34 fibroblastic network. Actively collagenizing scar fibroblasts exhibit a CD90/CD34 phenotype, which is prolonged in pathologic scars. CD90 fibroblasts are likely important players in cutaneous scarring.