Cath Lab Digest

The management of scars has come a long way over the years but still poses a significant problem both to the physician and the patient. This author reviews the clinical presentation of abnormal scars as well as the development of numerous treatments for the management of hypertrophic and keloid scars.

   Understanding the science of how a scar forms has allowed the development of numerous treatments for the management of these scars. (See “A Brief Overview On Scar Formation” on page 46.) Product development with well-controlled clinical studies provides evidence-based outcomes for the physician to be able to make knowledgeable decisions on how best to manage and treat abnormal scar formation.

   Most normal scars are flat and become less noticeable with time. However, there are often situations in which the body produces too much fibrous tissue, leading to an extra thick or raised scar. This is an abnormal and overly proliferative response to the remodeling phase of the wound healing cascade that results in the formation of problematic scars. Such scars include two distinct types (hypertrophic scars and keloid scars) that differ both morphologically and histologically.

   Hypertrophic scars. These are prominent red areas located inside the borders of the original injury. The collagen formation is in a disorganized and skewed arrangement rather than the normal parallel orientation. The hypervascularity gives rise to the erythematous appearance. Hypertrophic scars tend to be quite inelastic in nature and are often associated with pruritus and pain. In some cases, hypertrophic scars may shrink and fade on their own.

   Keloid scars. These are raised, deep red areas that tend to cover much more area than that of the original injury. Even when one surgically removes keloids, they tend to recur and do not subside over time. People may refer to keloids as “scars that do not know when to stop.” Previous research provides evidence that keloids have a genetic basis with researchers reporting both autosomal dominant and recessive genes, especially in those individuals with multiple lesions.^3,4

   Biologically, keloids are characterized by a collection of atypical fibroblasts with excessive deposition of extracellular matrix components, especially collagen, fibronectin, elastin and proteoglycans. Oliver and co-workers and Babu and colleagues found that keloid-derived fibroblasts exhibit as much as a fourfold increase in the rate of fibronectin biosynthesis compared to fibroblasts from normal dermis and normal scars.⁵

   Researchers also believe this pathologic process is influenced by certain growth factors.⁶ Transforming growth factor beta (TGF-b) and platelet-derived growth factors (PDGF) are the key factors in modulating contraction in normal skin fibroblasts. TGF-b is also a possible contributor to keloid formation. TGF-b promotes the chemotaxis of fibroblasts to the site of inflammation in order to induce extracellular matrix proteins. The messaging sequence and activity of TGF-b should then turn off upon completion of tissue repair. If this function does not turn itself off, abnormal fibrosis may result.

   Generally, keloids contain relatively acellular centers and thick, abundant collagen bundles that form nodules in the deep dermal portion of the lesion. Research has found that collagen synthesis in these scars is 20 times greater than normal skin and three times greater than hypertrophic scars. In addition, the type 1 collagen is present at significantly higher levels in comparison to type III collagen.