Impaired collagen remodelling following injury is the main contributor for formation of scars. In an scarred tissue organization of collagen fibers is disrupted and there is an imbalance between collagen insertion and removal in the injured skin. The result is too much disorganized fibers, a feature particularly seen in aging acne scars. As we discuss later in the following this disorganization becomes more apparent with aging.
Aging skin appears more thin, smooth, dry with less elasticity and number of pores.
1- Decrease in connective tissue matrix, its fibers, collagen and elastin and its cells, fibroblasts. decrease in GAGs, glycosaminoglycans, which is the main ingredient of connective tissue matrix. GAGs normally bound to associated proteins such as fibronectin and laminin. This binding diminshes substantially in aging. Organization of collagen and elastin fibers is also impaired. This is to a great extent due to breakdown of assoicated protiens. This decrease includes chondritinf sulfate and hyaluronic acid. Hyaluronic acid requires zinc and magnesium for its synthesis. Deficiencies of these elements can results in hyaluronic acid abnormalities, seen in Marfan and Ehler Danlos syndromes. Keratin sulfate increases. Decrease in collagen and elastin could be as a result of either loss of these fibers or a decrease in their production and solubility. The net result is less support for uppermost layer, epidermis. Skin scarring becomes more pronounced. Aging-related atrophy of subcutaneous muscles aggravates the situation.
2- Anti oxidant generation and direct skin damages due to free radical formation. oxidative stress associated with free radicals can cause lipid peroxidation and cell membrane disruption. this process could be triggered by UV rays as well as aging acne scars. Many lipid soluble vitamins, vitamin C and gluthantione, known antioxidants, may reduce oxidative stress. Reactive oxygen species may directly affect cell organells such as mitochondria and endoplasmic reticulum leading to cellular dysfunctions.
3- Role of cytokines such as interlukin1 and TNF as inflammatory mediators. UV in particular can induce cytokine and growth factors cell surface receptors. These mediators in turn involve in generation of reactive oxygen species which cause collagen destruction and thymine-thymine dimer formation in DNA, more damage to skin connective tissue. Cytokines may directly target type I and type III procollagen and diminish their concentration in extracellular matrix. This result in skin thinning, loss of elasticity and aggravation of skin scars.
4- Chronic high levels of glucose and formation of advanced glycosylation products are among other changes in pathology as a result of skin aging in prolonged untreated acne scars. This leads to cell swelling and disruption of the membrane. Proper glycemic control may delay formation of these molecules and prevent oxidative stress. Growing evidence indicates that severe spikes in postprandial blood sugar care a major problem for non-diabetic as well. Formation of advanced glycation end products and increased generation of free radicals are two main mechanisms by which post-meal hyperglycemia can causes serious aging-related problems such as arterial wall damage.
5- Polyunsaturated fatty acids are a major component of cell membranes and their deterioration can cause interruption in many of the cellular functions.
How these changes affect aging acne scars requires further investigation and research. Regression in collagen fibers accumulated in scarring seem to lessen the appearance of acne scars, however, decrease in extracellular matrix and its support for epidermis counteract this effect. Scars become more pronounced and may appear as wrinkles. Some shallow acne scars and spots may improve over time. Scar treatment in its early course benefit the patients most by resurfacing the skin and improving its tone and elasticity. Resurfacing treatments do not affect the dermis at a significant level. However, the degree of improvement in overall skin appearance and its tone is substantial.