Wound healing is a complex process that requires balanced regulation. However, when this regulation is disrupted, it can form undesirable scars, such as hypertrophic scars and keloids. These scars are characterized by an excess production of fibrinogen and collagen during the healing process, which leads to the development of raised, firm scars. Common symptoms of both hypertrophic scars and keloids include itchiness, pain, limited mobility, and cosmetic disfigurement.
It is worth noting that despite their similarities, the two have distinct differences. Hypertrophic scars are confined to the site of the initial injury and may regress over time, while keloids can spread beyond the borders of the initial injury and do not regress. Histologically, hypertrophic scars typically exhibit a wavy, regular pattern of collagen, whereas keloids lack any distinct pattern of collagen.
Keloid formation is believed to have a genetic predisposition and is more prevalent in individuals with darker skin complexions, particularly in African, Asian, and Hispanic populations. Twin studies and observations of familial inheritance suggest that keloid formation is influenced by genetics.
On the other hand, hypertrophic scars are not strongly associated with genetics but may be more common in populations with darker complexions. These scars typically form in areas of the skin that experience tension and are common after surgeries or burns, with reported incidence rates ranging from 39% to 68% after surgeries and 33% to 91% after burns. There is no significant difference in hypertrophic scarring between men and women.
Both keloids and hypertrophic scars tend to occur in younger individuals aged 11 to 30 due to increased collagen production and a higher epidermal turnover rate. This age group also has more tension on their skin and a more active immune system compared to older individuals with less elastic skin and a weakened immune response.
There are three stages in the process of wound healing: inflammatory, proliferative, and remodeling. The initial inflammatory phase plays a crucial role in determining the eventual outcome of the scar. This phase involves regulating inflammation through the activity of IL-6, IL-8, and IL-10. A disturbance in the expression of these pro-inflammatory and anti-inflammatory cytokines can lead to an increased incidence of hypertrophic scar and keloid formation.
During the proliferative phase, macrophages in the wound area release growth factors like transforming growth factor-beta (TGF-beta), which activates fibroblasts to generate collagen. Dysregulation of TGF-beta is thought to be responsible for forming hypertrophic scars and keloids.
TGF-beta 1 and 2 are responsible for activating fibroblasts, while TGF-beta 3 is a receptor antagonist that reduces fibroblast activity. Overexpression of TGF-beta 1 and 2 and decreased expression of TGF-beta 3 can lead to excessive extracellular matrix production, causing abnormal scars. Hypertrophic scars show a three-fold increase in collagen production, while keloids have a 20-fold increase, resulting in a more prominent, abnormal-looking scar.
During wound healing, various local factors can increase or prolong inflammation in the reticular dermis, which may increase the risk of pathological scarring. Infections, acne, and folliculitis also contribute to this risk. Additionally, secondary wounds caused by scratching, chicken pox can lead to scarring.
In the case of burn wounds, the risk of pathological scarring is higher if the wound is large or deep and if the duration of inflammation is prolonged. A burn wound that takes longer than 21 days to heal has a greater than 70% risk of developing into a hypertrophic scar.
Systemic factors such as adolescence and pregnancy may also increase the risk of pathological scarring, potentially due to the effects of sex hormones on inflammation. Hypertension has also been found to be a risk factor for severe keloid development. This is thought to be due to the damage to blood vessels caused by hypertension, which can increase inflammation in local tissue.
Compared to keloids, hypertrophic scarring has a more favorable outcome. Hypertrophic scars usually arise soon after injury, may initially increase in size, but often regress without treatment. They also tend to respond better to treatment, with a lower chance of recurrence, often requiring only one treatment modality.
In contrast, keloids have a poorer prognosis. They may have a hereditary component, and those at risk can develop multiple keloids from injuries or surgeries. Keloids may continue to grow for up to a year and do not regress spontaneously.
Treatment of keloids, especially surgical excision, often leads to a high recurrence rate, making it challenging to manage. Adjuvant therapies must be used in conjunction with surgery to help prevent a recurrence.
Clinical History
When evaluating a patient with a keloid or hypertrophic scar, the first step is to obtain a comprehensive patient history. It is essential to determine whether there was any associated trauma, as hypertrophic scars only occur after a traumatic event. In contrast, keloids can occur spontaneously or after minor trauma, typically in areas such as the earlobes, shoulders, chest, back, cheeks, and knees.
The presence of pain or pruritus is a crucial factor to consider, as keloids are more likely to cause discomfort and itching than hypertrophic scars. Keloids have a strong genetic predisposition, and individuals with a family history are more likely to develop keloids themselves. Keloids tend to develop about three months after an injury, persisting without improvement.
If the scar has been present for an extended period and has not increased in size, it may be a hypertrophic scar rather than a keloid. Keloids, however, do not regress and often continue to grow over time. Factors such as associated trauma, pruritus, pain, family history, and changes in scar size over time can provide valuable information in distinguishing between these two types of scars.
Physical Examination
Keloids and hypertrophic scars are raised, thickened scars with increased cellularity and collagen nodules. Differentiating between the two is important and can be done by examining the location of the scar. Keloids are typically found on areas such as the earlobes, chest, face, and back, while hypertrophic scars are more commonly located on extensor surfaces. Skin tone is also a factor, as keloids are more prevalent in darker skin tones, while hypertrophic scars can occur in all skin types.
One defining characteristic of keloids is their tendency to grow beyond the borders of the initial injury or occur spontaneously. In contrast, hypertrophic scars remain contained within the area of the injury. Additionally, keloids are more likely to occur in patients with a genetic predisposition and darker skin tones. It is worth noting that if a scar does not extend beyond the original scar’s borders, it is not considered a keloid.
Unfortunately, keloids are difficult to treat, and attempts to remove them often result in high recurrence rates. In contrast, hypertrophic scars are more common than keloids and tend to be confined to the original wound border. They typically occur in areas of high tension, such as extensor surfaces, and may begin to regress after about six months. While hypertrophic scars may appear within a month of injury, they have a lower recurrence rate following excision, making them easier to treat than keloids.
Differential Diagnoses
Cutaneous scleroderma
Giant cell fibroblastoma
Hair folliculitis
Keloidal basal cell carcinoma
Sclerotic neurofibroma
Trichilemmal carcinoma
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Wound healing is a complex process that requires balanced regulation. However, when this regulation is disrupted, it can form undesirable scars, such as hypertrophic scars and keloids. These scars are characterized by an excess production of fibrinogen and collagen during the healing process, which leads to the development of raised, firm scars. Common symptoms of both hypertrophic scars and keloids include itchiness, pain, limited mobility, and cosmetic disfigurement.
It is worth noting that despite their similarities, the two have distinct differences. Hypertrophic scars are confined to the site of the initial injury and may regress over time, while keloids can spread beyond the borders of the initial injury and do not regress. Histologically, hypertrophic scars typically exhibit a wavy, regular pattern of collagen, whereas keloids lack any distinct pattern of collagen.
Keloid formation is believed to have a genetic predisposition and is more prevalent in individuals with darker skin complexions, particularly in African, Asian, and Hispanic populations. Twin studies and observations of familial inheritance suggest that keloid formation is influenced by genetics.
On the other hand, hypertrophic scars are not strongly associated with genetics but may be more common in populations with darker complexions. These scars typically form in areas of the skin that experience tension and are common after surgeries or burns, with reported incidence rates ranging from 39% to 68% after surgeries and 33% to 91% after burns. There is no significant difference in hypertrophic scarring between men and women.
Both keloids and hypertrophic scars tend to occur in younger individuals aged 11 to 30 due to increased collagen production and a higher epidermal turnover rate. This age group also has more tension on their skin and a more active immune system compared to older individuals with less elastic skin and a weakened immune response.
There are three stages in the process of wound healing: inflammatory, proliferative, and remodeling. The initial inflammatory phase plays a crucial role in determining the eventual outcome of the scar. This phase involves regulating inflammation through the activity of IL-6, IL-8, and IL-10. A disturbance in the expression of these pro-inflammatory and anti-inflammatory cytokines can lead to an increased incidence of hypertrophic scar and keloid formation.
During the proliferative phase, macrophages in the wound area release growth factors like transforming growth factor-beta (TGF-beta), which activates fibroblasts to generate collagen. Dysregulation of TGF-beta is thought to be responsible for forming hypertrophic scars and keloids.
TGF-beta 1 and 2 are responsible for activating fibroblasts, while TGF-beta 3 is a receptor antagonist that reduces fibroblast activity. Overexpression of TGF-beta 1 and 2 and decreased expression of TGF-beta 3 can lead to excessive extracellular matrix production, causing abnormal scars. Hypertrophic scars show a three-fold increase in collagen production, while keloids have a 20-fold increase, resulting in a more prominent, abnormal-looking scar.
During wound healing, various local factors can increase or prolong inflammation in the reticular dermis, which may increase the risk of pathological scarring. Infections, acne, and folliculitis also contribute to this risk. Additionally, secondary wounds caused by scratching, chicken pox can lead to scarring.
In the case of burn wounds, the risk of pathological scarring is higher if the wound is large or deep and if the duration of inflammation is prolonged. A burn wound that takes longer than 21 days to heal has a greater than 70% risk of developing into a hypertrophic scar.
Systemic factors such as adolescence and pregnancy may also increase the risk of pathological scarring, potentially due to the effects of sex hormones on inflammation. Hypertension has also been found to be a risk factor for severe keloid development. This is thought to be due to the damage to blood vessels caused by hypertension, which can increase inflammation in local tissue.
Compared to keloids, hypertrophic scarring has a more favorable outcome. Hypertrophic scars usually arise soon after injury, may initially increase in size, but often regress without treatment. They also tend to respond better to treatment, with a lower chance of recurrence, often requiring only one treatment modality.
In contrast, keloids have a poorer prognosis. They may have a hereditary component, and those at risk can develop multiple keloids from injuries or surgeries. Keloids may continue to grow for up to a year and do not regress spontaneously.
Treatment of keloids, especially surgical excision, often leads to a high recurrence rate, making it challenging to manage. Adjuvant therapies must be used in conjunction with surgery to help prevent a recurrence.
Clinical History
When evaluating a patient with a keloid or hypertrophic scar, the first step is to obtain a comprehensive patient history. It is essential to determine whether there was any associated trauma, as hypertrophic scars only occur after a traumatic event. In contrast, keloids can occur spontaneously or after minor trauma, typically in areas such as the earlobes, shoulders, chest, back, cheeks, and knees.
The presence of pain or pruritus is a crucial factor to consider, as keloids are more likely to cause discomfort and itching than hypertrophic scars. Keloids have a strong genetic predisposition, and individuals with a family history are more likely to develop keloids themselves. Keloids tend to develop about three months after an injury, persisting without improvement.
If the scar has been present for an extended period and has not increased in size, it may be a hypertrophic scar rather than a keloid. Keloids, however, do not regress and often continue to grow over time. Factors such as associated trauma, pruritus, pain, family history, and changes in scar size over time can provide valuable information in distinguishing between these two types of scars.
Physical Examination
Keloids and hypertrophic scars are raised, thickened scars with increased cellularity and collagen nodules. Differentiating between the two is important and can be done by examining the location of the scar. Keloids are typically found on areas such as the earlobes, chest, face, and back, while hypertrophic scars are more commonly located on extensor surfaces. Skin tone is also a factor, as keloids are more prevalent in darker skin tones, while hypertrophic scars can occur in all skin types.
One defining characteristic of keloids is their tendency to grow beyond the borders of the initial injury or occur spontaneously. In contrast, hypertrophic scars remain contained within the area of the injury. Additionally, keloids are more likely to occur in patients with a genetic predisposition and darker skin tones. It is worth noting that if a scar does not extend beyond the original scar’s borders, it is not considered a keloid.
Unfortunately, keloids are difficult to treat, and attempts to remove them often result in high recurrence rates. In contrast, hypertrophic scars are more common than keloids and tend to be confined to the original wound border. They typically occur in areas of high tension, such as extensor surfaces, and may begin to regress after about six months. While hypertrophic scars may appear within a month of injury, they have a lower recurrence rate following excision, making them easier to treat than keloids.
Differential Diagnoses
Cutaneous scleroderma
Giant cell fibroblastoma
Hair folliculitis
Keloidal basal cell carcinoma
Sclerotic neurofibroma
Trichilemmal carcinoma
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
Wound healing is a complex process that requires balanced regulation. However, when this regulation is disrupted, it can form undesirable scars, such as hypertrophic scars and keloids. These scars are characterized by an excess production of fibrinogen and collagen during the healing process, which leads to the development of raised, firm scars. Common symptoms of both hypertrophic scars and keloids include itchiness, pain, limited mobility, and cosmetic disfigurement.
It is worth noting that despite their similarities, the two have distinct differences. Hypertrophic scars are confined to the site of the initial injury and may regress over time, while keloids can spread beyond the borders of the initial injury and do not regress. Histologically, hypertrophic scars typically exhibit a wavy, regular pattern of collagen, whereas keloids lack any distinct pattern of collagen.
Keloid formation is believed to have a genetic predisposition and is more prevalent in individuals with darker skin complexions, particularly in African, Asian, and Hispanic populations. Twin studies and observations of familial inheritance suggest that keloid formation is influenced by genetics.
On the other hand, hypertrophic scars are not strongly associated with genetics but may be more common in populations with darker complexions. These scars typically form in areas of the skin that experience tension and are common after surgeries or burns, with reported incidence rates ranging from 39% to 68% after surgeries and 33% to 91% after burns. There is no significant difference in hypertrophic scarring between men and women.
Both keloids and hypertrophic scars tend to occur in younger individuals aged 11 to 30 due to increased collagen production and a higher epidermal turnover rate. This age group also has more tension on their skin and a more active immune system compared to older individuals with less elastic skin and a weakened immune response.
There are three stages in the process of wound healing: inflammatory, proliferative, and remodeling. The initial inflammatory phase plays a crucial role in determining the eventual outcome of the scar. This phase involves regulating inflammation through the activity of IL-6, IL-8, and IL-10. A disturbance in the expression of these pro-inflammatory and anti-inflammatory cytokines can lead to an increased incidence of hypertrophic scar and keloid formation.
During the proliferative phase, macrophages in the wound area release growth factors like transforming growth factor-beta (TGF-beta), which activates fibroblasts to generate collagen. Dysregulation of TGF-beta is thought to be responsible for forming hypertrophic scars and keloids.
TGF-beta 1 and 2 are responsible for activating fibroblasts, while TGF-beta 3 is a receptor antagonist that reduces fibroblast activity. Overexpression of TGF-beta 1 and 2 and decreased expression of TGF-beta 3 can lead to excessive extracellular matrix production, causing abnormal scars. Hypertrophic scars show a three-fold increase in collagen production, while keloids have a 20-fold increase, resulting in a more prominent, abnormal-looking scar.
During wound healing, various local factors can increase or prolong inflammation in the reticular dermis, which may increase the risk of pathological scarring. Infections, acne, and folliculitis also contribute to this risk. Additionally, secondary wounds caused by scratching, chicken pox can lead to scarring.
In the case of burn wounds, the risk of pathological scarring is higher if the wound is large or deep and if the duration of inflammation is prolonged. A burn wound that takes longer than 21 days to heal has a greater than 70% risk of developing into a hypertrophic scar.
Systemic factors such as adolescence and pregnancy may also increase the risk of pathological scarring, potentially due to the effects of sex hormones on inflammation. Hypertension has also been found to be a risk factor for severe keloid development. This is thought to be due to the damage to blood vessels caused by hypertension, which can increase inflammation in local tissue.
Compared to keloids, hypertrophic scarring has a more favorable outcome. Hypertrophic scars usually arise soon after injury, may initially increase in size, but often regress without treatment. They also tend to respond better to treatment, with a lower chance of recurrence, often requiring only one treatment modality.
In contrast, keloids have a poorer prognosis. They may have a hereditary component, and those at risk can develop multiple keloids from injuries or surgeries. Keloids may continue to grow for up to a year and do not regress spontaneously.
Treatment of keloids, especially surgical excision, often leads to a high recurrence rate, making it challenging to manage. Adjuvant therapies must be used in conjunction with surgery to help prevent a recurrence.
Clinical History
When evaluating a patient with a keloid or hypertrophic scar, the first step is to obtain a comprehensive patient history. It is essential to determine whether there was any associated trauma, as hypertrophic scars only occur after a traumatic event. In contrast, keloids can occur spontaneously or after minor trauma, typically in areas such as the earlobes, shoulders, chest, back, cheeks, and knees.
The presence of pain or pruritus is a crucial factor to consider, as keloids are more likely to cause discomfort and itching than hypertrophic scars. Keloids have a strong genetic predisposition, and individuals with a family history are more likely to develop keloids themselves. Keloids tend to develop about three months after an injury, persisting without improvement.
If the scar has been present for an extended period and has not increased in size, it may be a hypertrophic scar rather than a keloid. Keloids, however, do not regress and often continue to grow over time. Factors such as associated trauma, pruritus, pain, family history, and changes in scar size over time can provide valuable information in distinguishing between these two types of scars.
Physical Examination
Keloids and hypertrophic scars are raised, thickened scars with increased cellularity and collagen nodules. Differentiating between the two is important and can be done by examining the location of the scar. Keloids are typically found on areas such as the earlobes, chest, face, and back, while hypertrophic scars are more commonly located on extensor surfaces. Skin tone is also a factor, as keloids are more prevalent in darker skin tones, while hypertrophic scars can occur in all skin types.
One defining characteristic of keloids is their tendency to grow beyond the borders of the initial injury or occur spontaneously. In contrast, hypertrophic scars remain contained within the area of the injury. Additionally, keloids are more likely to occur in patients with a genetic predisposition and darker skin tones. It is worth noting that if a scar does not extend beyond the original scar’s borders, it is not considered a keloid.
Unfortunately, keloids are difficult to treat, and attempts to remove them often result in high recurrence rates. In contrast, hypertrophic scars are more common than keloids and tend to be confined to the original wound border. They typically occur in areas of high tension, such as extensor surfaces, and may begin to regress after about six months. While hypertrophic scars may appear within a month of injury, they have a lower recurrence rate following excision, making them easier to treat than keloids.
Differential Diagnoses
Cutaneous scleroderma
Giant cell fibroblastoma
Hair folliculitis
Keloidal basal cell carcinoma
Sclerotic neurofibroma
Trichilemmal carcinoma
Keloids and hypertrophic scars can be treated with various methods as first-line therapy. Occlusive dressings, compression therapy, and steroids are the primary treatment options. Occlusive dressings reduce collagen synthesis by limiting the delivery of oxygen, blood and nutrients to the scar. Compression therapy involves applying pressure to the affected area to thin the skin and reduce collagen fibre cohesiveness. Steroids are effective in reducing collagen synthesis and proinflammatory mediators.
Triamcinolone injections are given every 4 to 6 weeks as monotherapy or in combination with other treatments. Surgical treatment involves removing the scar and ensuring a tension-free closure to prevent a recurrence. Although recurrence rates are high, adjuvant therapies such as radiotherapy, steroids and interferon therapy can reduce the risk. Cryotherapy is also used to induce cellular injury and reduce the size of the scar. Radiation therapy is often used after surgical excision for multiply recurrent keloids, with external-beam radiation therapy being the most common method. However, radiation therapy does carry a risk of subsequent malignancy.
Recently, various adjuvant and emerging therapies have been introduced to treat scarring, including interferon, 5-fluorouracil, bleomycin, tacrolimus, imiquimod, botulinum toxin A and retinoic acid. Interferon therapy can decrease collagen synthesis in vitro. In contrast, 5-fluorouracil acts as an antimetabolic agent to disrupt RNA, which inhibits fibroblast proliferation and TGF-beta expression, ultimately leading to decreased Type I collagen in scar tissue. Imiquimod induces apoptotic genes, causing cell death in keloidal tissue. Tacrolimus can reduce fibroblast proliferation by downregulating TGF-beta receptors.
Although bleomycin is primarily used to treat recalcitrant warts and keratoacanthomas in dermatology, in vitro administration to fibroblasts has reduced collagen synthesis. Retinoids, such as isotretinoin and tretinoin, can inhibit matrix metalloproteinases that overexpress in keloids and hypertrophic scars, reducing collagen synthesis and improving scar appearance. Tension is considered a factor that contributes to keloid and hypertrophic scar formation, and botulinum toxin A is believed to alleviate tension on the healing wound, resulting in better scarring outcomes.
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