Acne Scarring , background , acne scars page 2 of the article
J AM ACAD DERMATOL
Even though this condition is widespread, patients do not always present to physicians for prompt diagnosis and treatment. Of those with acne, only approximately 16% seek appropriate medical treatment: 74% wait greater than 1 year before seeking evaluation, 12% wait 6 to 12 months, 6% wait 3 to 6 months, and only 7% waited less than 3 months to be seen.6
This is attributed to multiple factors that could include financial limitations, physician access, and patient delay, among others. The delay in treatment, though, increases the probability of secondary sequelae such as scarring. Educational efforts should be undertaken to informthe public and physicians as to the importance of preventative measures and urgency of early management. A good review of such treatments, including topical or systemic medication and lasers, was authored fairly recently.7
It has been written that ‘‘there is no single disease which causes more psychic trauma, more maladjustment between parent and children, more general insecurity and feelings of inferiority and greater sums of psychic suffering than does acne vulgaris.’’8
So too, and possibly more so through its permanence, is the effect of the resulting damage in the form of a physical scar. ‘‘Scar,’’ as a noun, is defined as ‘‘the fibrous tissue that replaces normal tissue destroyed by injury or disease’’ by the American Heritage Stedman’s Medical Dictionary.9
An impressive study involving the histology, pathology, and immunology of acne scarring found that ‘‘the cellular infiltrate was large and active with a greater nonspecific response (few memory T cells) in early lesions of NS [not prone to develop scarring] patients, which subsided in resolution. In contrast, a predominately specific immune response was present in S [prone to develop scarring] patients, which was initially smaller and ineffective, but was increased and activated in resolving lesions. Such excessive inflammation in healing tissue is conducive to scarring. . ..’’10
Collagen and other tissue damage from the inflammation of acne leads to permanent skin texture changes and fibrosis. Scars normally proceed through the specific phases of the wound-healing cascade: inflammation, granulation, and remodeling. However, even normal scars never reach the same level of strength as original skin, only about 80% at best.11
Dermal damage is more long lasting and results in an increase or decrease of tissue and often worsens in appearance with age as a result of normal skin changes. In contrast, damage limited to the epidermis or papillary dermis can heal without scar formation.12
Epidermal damage results in more transient erythema or pigmentary changes and not true scars as defined above. In one study of 185 patients (101 female and 84 male with various quantity, morphology, and severity of acne of the face, chest, or back), it was found that facial scarring affected 95% of both sexes to some degree. The truncal region of male patients showed significantly more total, hypertrophic, and keloidal scarring than the same region of female patients. The correlation with scar formation was related to those acne lesions with a time delay of up to 3 years between initial onset and sufficient treatment regardless of sex or location.13
A very touching and enlightening article by Koo14 discussed psychosocial effects primarily in regard to acne but it also applies to scars. They may both lead to emotional debilitation, embarrassment, poor self-esteem, social isolation, preoccupation, low confidence, altered social interactions, body image alterations, identity difficulties, anger, frustration, confusion, unemployment, lowered academic performance, exacerbation of psychiatric disease, anxiety, or depression. Although these effects are difficult to quantify in patient terms, health care effect, or social expense, the scarring that results from tissue damage and inflammation is a significant issue that requires attention and will be expanded. Now the focus will turn to the scars themselves; initially, the scar types are covered and then several of the treatment options currently available are discussed.
The two causes of acne scar formation can be broadly categorized as either a result of increased tissue formation or, the more common cause, loss or damage of tissue. Two examples of excess tissue presence are hypertrophic scars and keloids. Hypertrophic scars are confined within the margins of the original injury. These scars are most prevalent within the first couple of months postinjury, and then, in contrast to keloids, tend to normally mature with occasional spontaneous regression. However, some do also worsen. These scars are most often less bothersome and treatment may or may not be needed based on severity. Keloids are a human-specific phenomenon that is characterized by disproportionate creation and deposition of collagen with an excess outside of the original injury margins. They are commonly found on the chest, back, shoulders, and ears. These lesions are very persistent and are found almost equally among male and female patients, less commonly in the very young or old. There are familial and genetic influences with both autosomal dominant and recessive traits. Clinically, there may be pain, itching, burning, or limited range of motion. Surgery is sometimes done for debulking and multiple modality treatment is recommended because of the high recurrence with surgery alone; aggressive scars have a regrowth of 50% to 100%.
Acne Scarring A review and current treatment modalities BACKGROUND and ACNE SCARS ACNE SCARS page 2 ACNE SCAR TREATMENT and MEDICAL MANAGEMENT SURGICAL MANAGEMENT PROCEDURAL MANAGEMENT PROCEDURAL MANAGEMENT page 2 TISSUE AUGMENTATION TISSUE AUGMENTATION page 2 TISSUE AUGMENTATION page 3 TISSUE AUGMENTATION page 4 Light, laser, and energy therapy Light, laser, and energy therapy page 2 Light, laser, and energy therapy page 3 Light, laser, and energy therapy page 4 Conclusion and REFERENCES Manufacturers of brand name drugs mentioned in this article