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Keloid and hypertrophic scars are when scars rather than healing normally, grow thick and large.
How do I know if I am going to keloid?
A sign is if you have keloids or hypertrophic scars already. Other signs can be if family members have a history of keloiding or hypertrophic scars. And sometimes, you just don't know.
How do you treat keloids and hypertrophic scars?
Serial steroid injections are the most common method. Adjunctive measures include, silicone sheeting or gel, Codran tape. If these measures are ineffective finally excision can be used along with postoperative steroids.
What causes keloids?
Its not sure why some areas keloid and others don't, but keloids result from trauma to the fibroblasts resulting in abnormal scar response.
Keloid and hypertrophic scar histopathologic differences
Clinical differences become more apparent as lesions mature. The most consistent histologic difference is the presence of broad, dull, pink bundles of keloid collagen in keloids, which is not present in hypertrophic scars
The collagen fibrils in keloids are more irregular, abnormally thick, and have unidirectional fibers arranged in a highly stressed orientation. Biochemical differences in collagen content in normal hypertrophic scars and keloids have been examined in numerous studies. Collagenase activity, ie, prolyl hydroxylase, has been found to be 14 times greater in keloids than in both hypertrophic scars and normal scars. Collagen synthesis in keloids is 3 times greater than in hypertrophic scars and 20 times greater than in normal scars. Type III collagen, chondroitin 4-sulfate, and glycosaminoglycan content are higher in keloids than in both hypertrophic and normal scars. Collagen cross-linking is greater in normal scars, while keloids have immature cross-links that do not form normal scar stability.
Disagreement exists about whether hypertrophic scars can be differentiated from keloids using light microscopy. Blackburn and Cosman described eosinophilic refractile hyaline collagen fibers, an increase in mucinous ground substance, and a lack of fibroblasts in keloids. Scanning electron microscopy findings clearly demonstrate the randomly organized sheets of collagen with no obvious relationship to the skin surface in keloid scar formation.
Keloids have the clinical appearance of a raised amorphous growth and are frequently associated with pruritus and pain (see Images 1-2). Scanning electron microscopy reveals a number of distinguishing features, including randomly organized collagen fibers in a dense connective tissue matrix. In normal scars, the collagen bundles are arranged parallel to the skin surface (see Image 3).
What happens to a hypertrophic scar w/ triamcinolone injection?:
The triamcinolone down regulates the pro-alpha 1 collagen gene. Less collagen, smaller scar. Associated complications include atrophy of subcutaneous layer and decreased pigmentation.
What’s most common complication of intralesional (scar) triamcinolone (atrophy)
Atrophy most common complication (skin appears thin and shiny)
Telangiectasia, necrosis ulceration, visible deposition of steroid in the form of white flecks in the scar are also potential complications
Injection given too deeply or in doses greater than 75 mg per week may lead to cushingoid habitus.
Keloids are dermal fibrotic lesions that are a variation of the normal wound healing process. They usually occur during the healing of a deep skin wound. Hypertrophic scars and keloids are both included in the spectrum of fibroproliferative disorders. These abnormal scars result from the loss of the control mechanisms that normally regulate the fine balance of tissue repair and regeneration. The most important risk factor for the development of abnormal scars such as keloids is a wound healing by secondary intention, especially if healing time is greater than 3 weeks. Wounds subjected to a prolonged inflammation, whether due to a foreign body, infection, burn, or inadequate wound closure, are at risk of abnormal scar formation. Areas of chronic inflammation, such as an earring site or a site of repeated trauma, are also more likely to develop keloids. Intralesional steroid injections apparently act by diminishing collagen synthesis, decreasing mucinous ground substance, and inhibiting collagenase inhibitors that prevent the degradation of collagen, thus significantly decreasing dermal thickening. This is accomplished by uniform injection of 40 mg/mL of triamcinolone acetonide (Kenalog) into the fresh site of scar excision with a 25- to 27-gauge needle at 4- to 6-week intervals until the scar flattens and discomfort is controlled.
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