Many people are still unsure of the difference between keloid and hypertrophic scars, partly because both are caused by an overproduction of collagen.
What is the Difference Between a Keloid Scar and Hypertrophic Scar?
A keloid scar is a type of benign tumor that develops in the epidermis over wounds or at scars. A hypertrophic scar, on the other hand, is a type of raised and thickened scar tissue that results from injury to the skin.
A keloid can be described as an overgrowth of collagen that usually occurs in response to trauma to the skin. They are often seen as red patches that are raised from the surface of the skin and they can range in size from being very small to very large. Hypertrophic scars, on the other hand, are raised and thickened scars caused by injury to hairless skin. These scars have an appearance similar to keloids but they generally tend not be red like them.
Treatment Options for Keloids and Hypertrophic Scars
There are many ways to treat a keloid scar including removal of stitches with lasers or using exfoliation techniques such as peeling or dermabrasion to remove the excess tissue. It is important to keep in mind that each treatment has pros and cons so it is best to consult your
In addition, intravenously administered Verapamil, fluorouracil, bleomycin, interferon alfa 2b injection and topical imiquimod 5 cream (Aldara) are reasonable studies on alternative corticosteroid treatments for the postoperative prevention of keloids. Although the initial results appear promising, further studies of the treatment modalities are needed.
Radiotherapy is one of the most common adjuvant treatments for HT. It includes laser beams and light therapy to improve patient compliance and reduce physicians “ability to reduce hypertrophic scars and keloid sizes and the likelihood of relapse after surgery or excision. Radiotherapy has been reported to reduce scar size by inhibiting fibroblast reproduction after surgery and modulating humeral cellular factors that stimulate the production of these cells (Keeling et al. There is still speculation about the mechanism of action of radiotherapy, but its treatment could yield results.
Macrophages promote the transformation of fibroblasts into myofibro-blasts by secreting the transforming growth factor-B (TGF-B) and platelet-derived growth factor-CC (PDGF-CC), which facilitates collagen deposits and scarring [15, 16]. Radiotherapy has been shown to inhibit the proliferation and promote senescence of keloidal fibroblasts by disrupting the cell cycle [Xu et al.
This imbalance produces collagen degraded during the healing process, and as more collagen is produced and degraded, the scar spreads and remains elevated, becoming a keloid or hypertrophic scar. For example, hypertrophic scars form when the skin bursts, while keloids do not begin to form until years after injury, and the tissue structure can vary between hypertrophic and keeloid scars. With the right hypertrophic scar and keloid treatment, the healing process can be effective as a preventive measure.
Keloids and hypertrophic scars are characterized by disturbed growth and excessive collagen formation, which can be disturbing for the patient. The etiology of hypertrophic scars and keloids occurs after an injury or irritation of the skin deep enough to affect the skin layer. Both keloid scars and high blood pressure are the result of excess collagen produced at the wound site.
Hypertrophic scars do not extend beyond the line of the original wound, unlike keloid scars. Instead, they resemble keloids in appearance, but the wound remains within the wound area rather than expanding outside it. In contrast to a hypertrophic scar, the additional connective tissue that forms around the wound remains in the wound.
According to AARP, keloid scars can itch and lead to discomfort, tenderness and irritation in clothing or other forms of friction. Keloids tend to be larger than scars on the edges of the wound itself and can be described as buried edges. They can be unpleasant, itchy and go beyond the original wound.
A keloid scar is an overgrowth of tissue that occurs when too much collagen is produced at the wound site. The scar contracts as a result of the contractile wind, and the healing process occurs when the scar is epithelialized and healed again.
Excessive scarring is characterized by the disorganized and redundant accumulation of the ECM which leads to abnormal proliferation and differentiation of the fibroblasts. The transformation of wounds into clots and grains of tissue requires a delicate balance between deposition and degradation of ECM proteins, and when this balance is disturbed by abnormalities, scarring occurs as a result of keloid hypertrophic scarring. Excessive scarring has many negative consequences, including disfiguring pain, itching, contractures, and restricted movement inflicted on the injured.
Mancini (1962) and Peacock (1970) have distinguished for many years between excessive scarring and hypertrophic keloid scarring. The difference between hypertrophic scars and keloids lies in prognosis : the first develop closer to the original wound boundary and tend to regress over time while the latter grow faster, with limitations in this respect [1]. A study from the Netherlands wanted to find out how hypertrophic and keeloid scars develop and whether they retain the characteristics of young and immature scars or mature normally.
The clinical distinction between hypertrophic scar and keloid is problematic. According to the definition of Mancini (1962) and Peacock (1970), hypertrophic and keeloid scarring increases to the skin, but hypertrophic scarring does not extend beyond the original injury site, while keloids extend beyond the original wound edge [3, 4].
The skin tone of patients is decisive: keloids occur in darker skin tones more often and hypertrophic scars are present in all skin types. Patients with higher keloid risk are younger than 30 years and those with darker skin. Deterrence and patient education: Patients should be informed about the risk of keloid or hypertrophic scar formation during surgical procedures, prevention, and alternative treatments.
Control trial with intralesional recombinant interferon-gamma for the treatment of keloidal scar rings. Skin collagen biosynthesis in patients with rheumatoid arthritis treated with D-penicillamine. Mechanisms for confirmed upregulation of senescence-associated genes, including P21, P16 and P27.