About strawberry, crab claws, and the Sir James Black's invention. Hypothesis: can we battle keloids with propranolol?

The cutaneous hemangiomas of infancy or infantile hemangiomas are the most common benign tumor of childhood. They were formerly known as strawberry hemangiomas in reason of its typical appearance although uncommon morphologic variations can be found. Usually hemangiomas are harmless growths that are the result of proliferation of endothelial cells during early childhood. Involution of the lesion occurs at 12-18 months and can last up to 7 years. Occasionally, infantile hemangiomas suffer dramatic overgrowth causing esthetical damages, as well compromises to vital structures that requires prompt intervention. Propranolol, a beta-adrenergic receptor antagonist that was invented by Sir James Black in 1960s, appears to be an effective treatment for infantile hemangiomas and should now be used as a first-line treatment in hemangiomas when intervention is required. Keloids (that resembles crab claws) and hypertrophic scars are fibrous tissue outgrowths that result from a derailment in the normal wound-healing process. Systemic or intralesional propranolol may play a role in the amelioration of keloids and hypertrophic scars due to their potential to induce vasoconstriction of over proliferating tissues, triggering apoptosis of endothelial cells and also to their effect as modulator of inflammatory process during wound healing. In adding the propranolol to the melting pot of abnormal (or supra-normal) wound healing, we hypothesized that we can battle keloids with propranolol.

Effect of imiquimod on partial-thickness burns.

BACKGROUND: Burns can result in substantial morbidity through fibroblast proliferation and contracture. Imiquimod (IMQ), an immune response modifier and upregulator of endogenous cytokine expression, has been shown to suppress fibroblast proliferation. It is widely used in the treatment of viral, neoplastic and non-neoplastic skin conditions and has recently been tested in the reduction of hypertrophic scarring and keloids. To our knowledge, no other study has so far evaluated the effect of IMQ on cutaneous burns. METHODS: Partial-thickness burns were produced on the dorsum of 32 Wistar rats. Right-sided wounds received saline and left-sided wounds received 5% IMQ cream three times/week following injury. Photographs taken on post-burn days (PBD) 4, 7, 14 and 21 were evaluated for wound appearance using a clinical assessment scale and a visual analog scale. Scars were measured by digital planimetry. Samples stained with hematoxylin-eosin were submitted to conventional histological analysis. Samples stained with Sirius Red were analyzed under polarized light for collagen morphometry. RESULTS: Visual scores were higher in the saline group on PBD 21 (p<0.05). Wound edge migration rates were lower (p<0.05) and conventional histology showed accentuated inflammation and delayed reepithelialization in the IMQ group. Type-I and type-III collagen deposition increased in the saline group and decreased in the IMQ group. Conversely, the proportion between type-I and type-III collagen differed significantly between treatments on PBD 4 and 21 (p<0.05 in both cases). CONCLUSIONS: Short-term topical imiquimod treatment of partial-thickness burns in rats did not improve clinical appearance and scarring but rather decreased fibrosis. Significant differences in collagen deposition were observed between the treatments.