Botox For Scars and Keloids
Facial scar management is considered one of the difficult problems that cosmetic surgeons face. Several factors act to influence the final outcome of their management. The unique character of facial expression muscles which attach themselves to the dermis put the scar under continuous stress during the healing phase with subsequent complicated wound healing. The role of Botulinum toxin A in induction of facial muscle weakness is now well recognized in facial aesthetic procedures.
The skin has intricate features that affect relaxed skin tension lines. These lines develop as a result of underlying muscle activity and are related to visible lines on the skin surface. When a cut or incision runs across the skin tension lines, the wound is distorted every time the underlying muscle contracts. Muscle activity is more pronounced with a larger scar angle relative to the relaxed skin tension lines. The tension vectors acting on the wound edges are transmitted to immature collagen ﬁbres synthesised during the normal healing phase. Repeated microtrauma that’s caused by continuous displacement of the healing tissue of the wound induces a prolonged and strong inflammatory response and an increased metabolic activity during the healing process. This accounts for scar widening as well as hypertrophic and hyperpigmented scars due to increased extracellular collageneous and glycosaminoglycaneous deposits. An effective method to improve healing and reduce scar formation is to inject the musculature adjacent to a wound with botulinum toxin. This injection paralyzes the musculature and allows optimal healing to occur before muscle activity recovers.
Non Chemoimmobilization effects of Botox
Recent basic and clinical research has shown that botulinum toxin type A (BTXA) has antihypertrophic scar properties but the molecular mechanism for this action is unknown. BTXA effectively inhibited the growth of fibroblasts derived from hypertrophic scar and in turn caused a decrease in TGF-beta1 protein.
BoNT did not stimulate the proliferation of or show toxic effects on human dermal fibroblasts. Levels of PIP increased significantly in fibroblasts grown in the presence of BoNT, and BoNT upregulated the expression of type I collagen and decreased the production of some MMPs in fibroblasts that prevent collagen degradation.
For the histological findings on the H&E stain, the surgical wounds of the Botox group showed a significantly smaller number of fibroblasts and less fibrosis than the control wounds at the 4th week after surgery (P<0.05). The reason for the difference of the number of fibroblasts and the degree of fibrosis is presumed to be the decreased release of several cytokines, such as platelet-derived growth factor, TGF, epidermal growth factor, fibroblast growth factor and insulin-like growth factor, by the decreased inflammatory response and the short period of inflammation.
On the immunohistochemical staining, the wounds of the Botox group showed a lower expression of TGF-β 1 than that of the control group at the 4th week after surgery. TGF-βis one of major important cytokines in the wound healing process. This cytokine is produced by a host of cells, including platelets, fibroblasts, smooth muscle cells, endothelial cells, keratinocytes, lymphocytes and macrophages . It increases collagen synthesis and stimulates keratinocyte migration, angiogenesis and fibroplasias. TGF-β 1 is the most abundant isoform of TGF-β . The reason for the difference of the expression of TGF-β 1 is the decreased inflammation response at the surgical wounds of the Botox group.
In several in vivo studies, it was shown that BoNT increases blood supply, which accelerates the process of healing and prevents the collapse of the peripheral vessels in the cutaneous flap. Additionally, increased diameters of arterioles and venules were observed histologically.
Botox For Hypertrophic scars and Keloids
Several recent reports have demonstrated a possible action mechanism for botulinum toxin for hypertrophic scars. Shaarawy et al. recently reported that intralesional botulinum toxin was equally effective and better tolerated than an intralesional steroid for treating keloids in a randomized controlled trial. Botulinum toxin might effectively inhibit the growth of fibroblasts derived from scar contracture and reduce the expression of α-smooth muscle actin and myosin II. In addition, the botulinum toxin altered the expression levels of S100A4, TGF-β1, VEGF, MMP-1, and PDGFA genes in keloid fibroblasts, which provide useful clues for exploring the function of botulinum neurotoxin (BoNT)-A and finding a novel treatment for keloid scarring.
“Botulinum toxin reduces the size of keloids and also prevents recurrance.
LEVEL OF EVIDENCE 1″
In some patients, they may become unresponsive to treatment after one or more botulinum toxin type A injections. The formation of neutralizing antibodies has been implicated as the cause of treatment failure in most of these cases. The main risk factors for the development of neutralizing antibodies appear to be the injection of the neurotoxin at frequent intervals or at higher dose.