Health ConditionsScars are areas of fibrous tissue that replace normal tissue destroyed by a wound. Scar tissue is not identical to the normal tissue it replaces and is often of inferior functional quality; for example, scars in the skin can be less resistant to ultraviolet radiation and may contain no sweat glands or hair follicles.
Scars are a result of the natural healing process that occurs when the skin repairs itself after wounds, trauma, burns, surgical incision, or disease. Normal skin tissue is replaced with scar tissue to close open wounds and prevent infection. Scars can be painful, cause itching, and limit mobility. Many scars are primarily a cosmetic concern, but their presence may have a significant negative impact on the affected individual's self-esteem.
Scars lack elastin and consist of poorly reconstituted collagen matrix in dense parallel bundles rather than the mechanically efficient basket-weave meshwork of collagen in unwounded dermis. During the maturation phase, the wound continues to gain tensile strength — up to approximately 80% of the original skin — but there is no further increase in collagen content. During this maturation phase the wound tends to become less cellular and vascular until a quiescent, white scar is formed.
Scars can be classified into immature scars and mature scars. Mature scars can be "normal," atrophic, or hypertrophic. Keloids occur in patients with a genetic predisposition and behave differently than hypertrophic scars, although there can be a continuum in terms of appearance.
In a typical wound, anabolic and catabolic processes achieve equilibrium approximately 6–8 weeks after the original injury. At this stage, the strength of the wound is approximately 30–40% that of healthy skin. As the scar matures, the tensile strength improves as a result of progressive cross-linking of collagen fibers. The scar is usually hyperemic initially, and it may be thickened, but it tends to subside gradually over months until a flat, white, pliable, possibly stretched, mature scar has developed.
When collagen continues to accumulate, the scar widens and becomes elevated or ropy in appearance and erythema fails to resolve. In a hypertrophic scar, the period of collagen accumulation is prolonged up to 6–12 months, resulting in a scar that is elevated, thickened, and very stiff. Erythema will be prolonged and the scars are often intensely pruritic or even painful. Hypertrophic scars are defined as raised scars that remain within the boundaries of the original lesion and often regress spontaneously after the initial injury, rarely recurring after surgical excision.
Keloids are the result of an overgrowth of dense fibrous tissue that usually develops after healing of a skin injury. The tissue extends beyond the borders of the original wound, does not usually regress spontaneously, and tends to recur after excision. A keloid, unlike a hypertrophic scar, behaves more like a tumor in that growth can occur even years after the original injury and extend far beyond the confines of the original scar. The keloid often has a mushroom or cauliflower type of appearance.
The overexpression of TGF-beta 1 and 2 and decreased expression of TGF-beta 3 is believed to lead to increased extracellular matrix production causing these abnormal scars. There is a 3-fold increase of collagen production in hypertrophic scars and a 20-fold increase in keloids, leading to a larger, abnormal-appearing scar.
Atrophic scars represent the opposite extreme, characterized by a lack of growth which leads to indentations, craters, or pits in the skin. This is due to a loss of dermal tissue and not enough collagen to heal the wound. Atrophic scars are common sequelae of acne, chickenpox, and certain surgical procedures.
The cutaneous wound healing process closes skin gaps by inducing the formation of granulation tissue and epithelialization, which re-establishes an effective epidermal barrier. The complex biochemical events that underlie wound closure can be categorized into four overlapping processes: coagulation, inflammation, proliferation, and remodeling. Coagulation and the inflammatory process begin immediately after injury, while the proliferative phases start within a few days. The remodeling phase commences within a week of injury and continues for months.
Coagulation / Hemostasis: Immediately after tissue injury, blood vessel disruption leads to the extravasation of blood and concomitant platelet aggregation and blood coagulation resulting in fibrin clot formation. Activated platelets trapped within the fibrin clot degranulate and release a variety of cytokines and growth hormones. These cytokines and growth hormones help to recruit inflammatory cells to the site of injury, to stimulate angiogenesis, and to initiate the tissue movements associated with re-epithelialization and connective tissue contraction.
Inflammation: In the inflammatory phase, increased numbers of blood cells such as granulocytes, macrophages, and lymphocytes are brought to the area at or near the wound. The blood cells clean the wound by taking up exogenous materials and tissue detritus and breaking them down enzymatically. An abnormal course of the inflammatory phase at the beginning of the healing process can have effects long after scar formation.
Proliferation: After the inflammatory phase, there is a rapid increase in collagen content in the incision that is associated with a rapid increase in tensile strength. This phase is called the proliferative or collagen phase. Two key events occur during this phase: the deposition of the extracellular matrix (ECM) and the ingrowth of new vessels. The inflammatory response is followed by the formation of fibrous tissue by proliferation of fibroblasts, and differentiation of fibroblasts to myofibroblasts, which produce collagen, mucopolysaccharides, and glycosaminoglycans at the wound site.
Remodeling: The type III collagen deposited during the proliferative phase is slowly degraded and replaced with stronger type I collagen. This type of collagen is oriented as small parallel bundles, which differs drastically from the basket-weave orientation of collagen present in normal dermis. Towards the later stages of healing, the wound undergoes a contractile response through the action of myofibroblasts; these actin-rich cells contract and reduce the surface area of the scar.
When remodeling goes wrong: During the remodeling phase, formation of granulation tissue normally ceases through apoptosis of the responsible cells. This process is important, because its aberration leads to hypertrophic scarring and keloids.
Myofibroblasts are pivotal cells for the control of extracellular matrix deposition and remodeling during normal repair and are also important in pathological conditions such as excessive scarring. Myofibroblasts definitively represent an essential target in any approach designed to modulate tissue repair.
The balance between extracellular matrix synthesis and degradation determines the degree of scarring after wounding. Studies using second-harmonic generation microscopy imaging of fibrillar collagens have been employed to characterize collagen organization in wounded and repaired skin, lung, cardiovascular tissue, tendons, ligaments, and eye tissue, underscoring the cross-system relevance of ECM regulation in scarring.
Immunologic alterations are implicated in abnormal scars. Specifically, irregular immunoglobulin and complement levels, increased transforming growth factor-beta, and mast cells are found in abnormal scars. Additionally, decreased tumor necrosis factor and interleukin-1 levels are found in these abnormal scars.
In keloids, several histological findings help to distinguish the condition from other types of scarring. Increased numbers of mast cells are present in keloid scar tissue compared with normal scar tissue. An increase in keratinocytes in the epidermis may account for the thicker epidermal layer seen in keloids.
Keloid formation has a genetic basis, as demonstrated by its predilection for persons of certain races and in certain families. Keloids occur in patients with a genetic predisposition. Abnormal scarring is 15 times more likely to occur in darker-skinned individuals.
Keloids are more prevalent in persons aged 10–30 years, while hypertrophic scars occur in persons of any age. Because keloids tend to demonstrate accelerated growth during puberty or pregnancy and tend to resolve with menopause, hormones — both androgen and estrogen — have been implicated in keloid formation. Other hormones linked to keloid formation include thyroid hormone alterations and melanocyte-stimulating hormones.
Skin tension is frequently implicated in hypertrophic scar formation. Abnormal scar healing commonly involves areas of high skin tension, such as the anterior chest, shoulders, and upper back. Other factors implicated in the etiology of abnormal scar formation include wound infection or anoxia, a prolonged inflammatory response, and wound orientation different from the relaxed skin tension lines.
There is significant evidence in the literature that diabetic patients are at a higher risk for increased wound infections, wound dehiscence, and pathological scarring. Factors such as nutritional status and glycemic control also significantly influence diabetic wound outcomes. Diabetes results in several pathological changes that impair almost all phases of wound healing. Diabetic wounds are often characterized by excessive inflammation and reduced angiogenesis.
Obesity has been shown in a number of studies to impair wound healing, and chronic nonhealing wounds in obesity and diabetes are a major cause of limb amputations in the United States. Recent evidence indicates that aberrant wound site inflammation may be an underlying cause for delayed healing. Obesity, diabetes, and other conditions such as stress and aging can result in a chronic low-level inflammatory state, thereby potentially affecting wound healing negatively.
The presence of chronic ulcers and wounds can be associated with malnutrition, vitamin C deficiency, dehydration, autoimmune disorders, diabetes, arterial obstruction, and/or venous congestion.
Smoking, with its plethora of harmful substances — notably nicotine — induces vasoconstriction and disrupts microcirculation, thereby impairing wound healing. The inhibition of cellular migration and neutrophil activity during the inflammatory phase further exacerbates wound complications in smokers compared with nonsmokers. The consumption of alcohol, including chronic abuse and acute intoxication, has been linked to an elevated incidence of surgical wound infections and impaired wound healing.
Physical exercise training has been shown to speed healing in both aged and obese mice and in older adults. Exercise is a relatively low-cost intervention strategy that may be able to be used clinically to prevent or treat impairments in the wound-healing process.
Wound healing is an energy-intensive process, requiring an array of macronutrients and micronutrients to restore skin integrity efficiently. Macronutrients, including carbohydrates, fats, proteins, and fluids, along with micronutrients such as vitamins and minerals, collectively orchestrate the seamless progression of wound healing. The caloric demands for protein synthesis, a cornerstone in forming granulation tissue, underscore the heightened nutritional requirements during the reparative phases. The impact of nutrition on the aesthetic outcomes of wound healing is substantial; an appropriate supply of nutrients is crucial for reducing scar formation and supporting the intricate process of skin remodeling.
Protein provides the amino acids necessary for the synthesis of new tissue, enzymes, and immune cells. Protein-energy malnutrition can significantly impair wound healing, leading to delayed healing times and increased risk of infection. Ensuring adequate protein intake is vital for patients with wounds, especially those with chronic wounds or those recovering from surgery.
Adequate protein intake is required during the inflammatory phase to produce the enzymes and antibodies necessary for immune function. In the proliferative phase, amino acids, B vitamins, lipids, zinc, and iron play key roles. Insufficient carbohydrates and/or fats force the body to look for alternate forms of energy, leading to excess oxidation of amino acids to satisfy caloric needs. Following injury, obese patients preferentially oxidize proteins and carbohydrates. Amino acid use further perpetuates protein malnutrition and its adverse effects on wound healing.
Vitamin C, also known as ascorbic acid, is involved in all phases of wound healing. In the inflammatory phase it is required for neutrophil apoptosis and clearance. During the proliferative phase, ascorbic acid contributes towards the synthesis, maturation, secretion, and degradation of collagen. Deficiencies affect the maturation phase by altering collagen production and scar formation. The body strives to maintain homeostasis of ascorbic acid, thereby ensuring availability for collagen synthesis.
A deficiency in vitamin C yields less-than-optimally hydroxylated collagen with low tensile strength. Topical application of vitamin C may increase local skin concentrations, potentially supporting collagen synthesis and improving scar quality.
Scientific evidence: Clinical studies provide evidence that wound healing in subjects judged not deficient in vitamin C can be significantly accelerated with supplements of this nutrient above the recommended daily allowance (RDA). Studied daily dosages ranged from 500 to 3,000 mg, roughly 8 to 50 times the RDA of 60 mg, in subjects recovering from surgery, other injuries, decubital ulcers, and leg ulcers.
A dose-response analysis between scar strength and vitamin C intake suggests that the daily vitamin C intake needed to prevent collagen-related pathologies is in the range recommended by the National Academy of Medicine and the European Food Safety Authority (75 to 110 mg/d), not the WHO recommendation (45 mg/d). Separately, a vitamin C intake averaging 65 mg/d over a mean follow-up of 6.5 months failed to restore the normal wound-healing capacity of vitamin C-depleted tissues, which had 49% weaker scar strength compared with non-depleted tissues (P < 0.05). Thus, average daily vitamin C intakes approximately 50% higher than the WHO recommends may fail to treat existing collagen-related pathologies.
Much of the data surrounding vitamin C in wound healing derives from multiple, concomitant nutritional interventions in patients with existing nutritional deficiencies. Many studies and reviews found unclear benefits to vitamin and mineral supplementation unless patients had confirmed or suspected nutritional deficiencies. Overall, the evidence supports vitamin C's essential mechanistic role, but the evidence base for supplementation above physiological needs in nutritionally replete individuals remains limited and mixed.
Studies dating back to 1970 and earlier have shown the importance of zinc concentrations towards healing wounds in patients with thermal injuries or surgical stress. Zinc is especially important in skin. Skin contains a relatively high zinc content, primarily associated within the epidermis (50–70 μg/g dry weight). Mild zinc deficiency is noted to lead to roughened skin and impaired wound healing.
Zinc deficiency is known to retard wound healing by preventing cellular mitosis and by disturbance of fibroblast function and collagen synthesis. About two or three days after the wound occurs, fibroblasts begin to enter the wound site, marking the onset of the tissue proliferative phase. Fibroblast infiltration is associated with collagen and ECM deposition, which serves as a temporary scaffold for repair.
Scientific evidence: The function of zinc in the normal wound-healing process is acknowledged as being evident throughout the inflammatory and proliferative stages. However, the evidence regarding oral zinc supplementation is generally inconclusive. Findings suggest that further research could demonstrate a place for supplementation in zinc-deficient patients, but more rigorous patient-centred trials are necessary to support a significant change in clinical practice. Excessive zinc levels may hinder macrophage migration and phagocytosis and thus impair wound healing.
Vitamin A has been recognized for its contributions to epithelial growth, angiogenesis, collagen synthesis, wound strength, and epithelialization. Vitamin A deficiency leads to impaired wound healing. During the inflammatory phase of wound healing, vitamin A has been noted among the key micronutrients required alongside calcium, vitamin K, vitamin E, zinc, and proteins.
Vitamin E is a family of essential micronutrients with strong antioxidant activity, composed of lipid-soluble tocopherols and tocotrienols. Vitamin E may assist in wound healing through direct effects on tissue repair and regeneration.
Scientific evidence: The most commonly cited form is vitamin E (tocotrienol). One review concluded that evidence for its efficacy in wound healing was lacking. Vitamin E appears to negatively affect collagen synthesis, antioxidant response, and the inflammatory process. Hobson's 2016 literature review echoed these findings while recommending further research owing to the limited literature on this topic. The evidence for topical or oral vitamin E in scar improvement is weak and in some analyses suggests potential for harm to collagen synthesis; current evidence does not consistently support its use for scar reduction.
Emerging evidence of vitamin D deficiency has underscored its potential implication in the wound-healing process. A case series found that vitamin D binds with vitamin D receptors via calcitriol, regulating the production of several receptors and upregulating the innate immune system. However, further research is necessary to gain a comprehensive understanding of its complex mechanics and to establish a causative or correlative relationship.
Omega-3 fatty acids, found in fish oils, have anti-inflammatory properties that can help modulate the inflammatory response, reducing excessive inflammation and promoting healing. Evidence specific to scar formation — as distinct from general wound healing — remains preliminary, with no large-scale clinical trials specifically targeting omega-3 fatty acid supplementation and scar quality outcomes identified in the current literature.
Traditional use: Centella asiatica is a small perennial herbaceous plant belonging to the Apiaceae family and widely spread in Southeast Asian countries. It has been used to treat a variety of diseases in Asiatic traditional medicine for thousands of years. Due to its medicinal properties, Centella asiatica is traditionally used to treat a variety of dermatological conditions, such as wounds, burn injuries, scars, lupus, leprosy, eczema, psoriasis, and varicose ulcers. Traditional preparations include poultices of fresh crushed leaves applied directly to wounds and oral decoctions made from the whole herb.
Active constituents: The medicinal plant and its triterpenes include asiaticoside, madecassoside, and their aglycones, asiatic acid and madecassic acid. Preliminary findings have shown that asiatic acid is one of the main active constituents of Centella asiatica, directly associated with its healing activity.
Scientific evidence: Studies have shown that Centella asiatica extracts display activity in tissue regeneration, cell migration, and wound repair processes by promoting fibroblast proliferation and collagen synthesis. In human clinical research, topical application with Centiderm ointment made from Centella asiatica ethanol extract significantly improved objective signs (pliability, vascularity, pigmentation, height, and visual acuity scores) and subjective signs (dryness, itching, and irritation) in patients with second-degree burn wounds on their limbs. The means of re-epithelialization and complete healing were significantly better in the Centiderm group than in the control group. These beneficial effects are linked to the ability to accelerate wound contraction by stimulating fibronectin and collagen synthesis. However, there is currently a lack of large clinical trials regarding its effect on wound healing parameters, and no systematic review or quantitative synthesis had been conducted in this area at the time of one key review, highlighting the need for an evidence base. The available human evidence is promising but predominantly derived from small trials with limited follow-up; evidence strength is currently preliminary to moderate.
Traditional use: Onion (Allium cepa) has a longstanding use in folk medicine across European, Middle Eastern, and Asian traditions, applied topically as poultices and extracts to wounds and scars, with the intention of softening and fading scar tissue.
Active constituents and proposed mechanisms: Quercetin from onion extract is found in various scar treatment products. It has anti-inflammatory, bacteriostatic, and collagen down-regulatory properties.
Scientific evidence: Owing to the reported effects of anti-inflammatory, antimicrobial, antiproliferative, and regenerative activities of onion extract, its gel modality has been commercially available for treating, preventing, and reducing dermatologic scars and keloids. Several clinical trials found this gel was well tolerated and helpful for preventing pathological scarring. It was recommended for clinical scar management by the International Advisory Panel on Scar Management in 2014. However, large-sized randomized controlled trials and evidence-based data are still lacking.
A 2021 meta-analysis of randomized controlled trials found that onion extract gel not only has no superiority to commonly used topical treatments, but also has the potential to increase the incidence of adverse effects in scar management; onion extract in silicone gel might be the optimal topical choice for scar treatment; however, more evidence is needed to strengthen these conclusions.
One head-to-head randomized controlled trial evaluating the appearance of laparoscopic surgical scars in 60 subjects after 12 weeks of twice-daily application found that there were no differences between silicone gel and onion extract gel groups in Vancouver Scar Scale, Image Panel Scale, Body Image Scale, or Cosmetic Scale scores (all p > 0.6). Subject compliance and safety with the assigned gel were similar between the two groups.
A separate randomized, double-blinded, placebo-controlled trial in 60 patients after median sternotomy reported that pain and itch scores from patients who applied silicone derivative plus onion extract gel were lower than those in the control group (P < 0.05). Pigmentation was significantly different between the two groups (P < 0.05), although reduction of scores on vascularity, pliability, and height in the treated group was not significant. Overall, evidence strength for onion extract as a standalone topical is mixed to weak when compared against active comparators; combination with silicone appears more promising but requires further large trials.
Traditional use: Many natural substances have been traditionally used to reduce pain and accelerate healing. Aloe vera has been used in a host of curative purposes, including treatment of skin disorders and healing of wounds. The colourless gel that comes from the leaf parenchyma has been used to treat burns because, besides being a potent moisturizing agent, it helps in the healing process of skin lesions and alleviates pain. This use spans ancient Egyptian, Greek, Chinese, and Ayurvedic traditions.
Scientific evidence: Clinical evidence overall remains limited; the majority of reviewed articles on plant-based topicals were ranked as limited quality. One case-control study of Aloe vera compared with silver sulfadiazine cream for the treatment of second-degree burns (n = 30) indicated that the rate of re-epithelialization and healing was greater with Aloe vera. However, no assessment of healed burn scar quality was made, and follow-up was only 24 days. Aloe vera has been included in combination silicone gel formulations studied in randomized trials alongside onion extract; previous studies found that silicone gel, onion extract, and aloe vera were each effective in treating scars with different working mechanisms. The evidence specific to scar quality (as opposed to wound closure speed) is limited and mostly derived from short-duration studies.
While not a natural botanical ingredient, silicone gel and sheeting serve as the standard comparator against which natural topical agents are evaluated in clinical scar trials. Although the mechanism of silicone in the improvement of hypertrophic scars remains unclear, it is recommended in the treatment of hypertrophic scarring. Several products have been reviewed for their clinical evidence in preventing excessive scarring and improving scar formation. Results from clinical trials suggest that the efficacy of silicone gel is equivalent to that of traditional silicone gel sheeting but is easier to use.
While minor wounds may not significantly tax the nutritional reserves of the body, larger wounds, particularly extensive thermal burns, can precipitate a considerable nutritional deficit, further compounded by perioperative fasting protocols that may disrupt the timely resumption of diet critical for recovery.
Uncontrolled hyperglycemia is known to impede fibroblast and endothelial cell functions, particularly in patients with diabetes. The historical context of vitamins such as vitamin C and its association with scurvy elucidates their role as co-substrates for hydroxylase enzymes imperative for collagen synthesis.
In diabetic patients, poorly controlled blood glucose levels can significantly impair wound healing. Hyperglycemia disrupts normal cellular functions and inflammatory responses, leading to delayed wound closure, increased risk of infection, and poor aesthetic results. Tight glycemic control is therefore essential to enhance the body's natural healing process and reduce complications.
During remodeling, vitamins C and E, zinc, and water are critical for collagen synthesis and skin cell maturation. Adequate hydration supports the maintenance of tissue perfusion and nutrient delivery to healing wound sites; dehydration is listed among factors associated with impaired wound healing and chronic ulcer formation.
Smoking significantly impedes wound healing and adversely affects cosmetic outcomes due to its impact on tissue oxygenation and cellular function. The healing process, which involves inflammatory, proliferative, and remodeling stages, relies heavily on proper tissue oxygen levels. Cessation of smoking is one of the most clearly evidence-supported lifestyle modifications for improving wound and scar outcomes.
Physical exercise training has been shown to speed healing in both aged and obese mice and in older adults. Exercise is a relatively low-cost intervention strategy which may be able to be used clinically to prevent or treat impairments in the wound-healing process. Mechanisms proposed include improved tissue oxygenation, enhanced immune surveillance, and attenuation of chronic low-grade inflammation associated with obesity and aging.
Omega-3 fatty acids, found in fish oils, have anti-inflammatory properties that can help modulate the inflammatory response, reducing excessive inflammation and promoting healing. A prolonged or dysregulated inflammatory phase is one of the key drivers of pathological scar formation; dietary strategies aimed at moderating systemic inflammation — including higher intake of omega-3-rich foods, polyphenol-rich fruits and vegetables, and reduced intake of ultra-processed foods — are consistent with the mechanistic evidence, though large prospective trials specifically targeting scar outcomes through dietary pattern interventions have not been conducted.
When looking at combined nutritional interventions — specifically vitamin C and zinc for wound healing — many studies and reviews found unclear benefits to vitamin and mineral supplementation unless patients had confirmed or suspected nutritional deficiencies. A 2014 Cochrane review of 23 studies and a meta-analysis found no clear evidence for the use of nutritional supplementation in pressure ulcers (RR 0.86; 95% CI: 0.73–1.00). The evidence therefore suggests that correcting established deficiencies is more clearly beneficial than routine supplementation in nutritionally replete individuals.
Acemannan, a polysaccharide from Aloe vera inner gel, has been studied for wound healing and scar modulation. In vitro and animal studies demonstrate it stimulates fibroblast proliferation, enhances collagen deposition, and reduces inflammatory cytokines. Human clinical trials specifically on scar tissue are limited but early findings are supportive.
Allantoin is a keratolytic and moisturizing compound used extensively in commercial scar formulations, including the well-studied onion extract/allantoin combination (e.g., Contractubex). Clinical studies show it improves scar texture, reduces pruritus, and supports re-epithelialization. Its moisturizing and immune-modulatory properties complement anti-scarring actions.
Aloe vera has been investigated in multiple clinical studies for wound healing and scar modulation. It reduces inflammation, stimulates fibroblast activity, and supports collagen synthesis. Comprehensive reviews cite it alongside onion extract and vitamin E as a recognized topical plant extract for scar management.
Alpha hydroxy acids (AHAs) promote skin cell turnover and exfoliation, aiding in the improvement of scar texture and pigmentation. They are cited in evidence-based reviews of topical scar treatments and widely used clinically for atrophic and pigmented scars.
Asiaticoside is the primary bioactive triterpenoid saponin of Centella asiatica and has been directly studied for scar treatment. It modulates TGF-β/Smad signaling to regulate collagen synthesis, reduces hypertrophic scar formation, and has shown efficacy in RCTs for burn-related and surgical scars.
Bee propolis has documented wound-healing and anti-scar properties supported by clinical studies. Its flavonoids (including caffeic acid phenethyl ester) exhibit anti-inflammatory, antimicrobial, and collagen-modulating effects relevant to scar healing.
Bromelain, a proteolytic enzyme from pineapple, has evidence for reducing post-surgical swelling and fibrin-related scar tissue formation. It is used as an adjunct to scar treatment by breaking down fibrinous proteins and reducing inflammation that drives scarring.
Centella asiatica (Gotu kola) is one of the best-evidenced natural ingredients for scar treatment, with 6 RCTs and multiple systematic reviews supporting it. Its triterpenoids modulate TGF-β/Smad signaling to regulate collagen, reduce hypertrophic scar formation, and improve post-surgical scar outcomes.
Centella triterpenes (the isolated triterpenoid fraction of Centella asiatica including asiaticoside, madecassoside, asiatic acid) have been studied specifically for scar management and are more potent than crude extracts. They regulate fibroblast activity, suppress TGF-β-driven excess collagen, and improve scar texture and height in clinical trials.
Collagen is the primary structural protein of scar tissue and has been studied extensively as a topical and supplemental agent for wound healing and scar modulation. Clinical trials show hydrolyzed collagen peptides accelerate tissue repair, and collagen dressings improve wound quality and scar outcomes.
Curcumin has been identified in systematic reviews and preclinical/clinical studies as an anti-scarring agent. It suppresses TGF-β/Smad and NF-κB signaling, reduces excessive collagen deposition in hypertrophic scars, and showed benefit in one RCT for scar management.
Topical rosehip oil (Rosa canina) has demonstrated clinically significant benefits for post-surgical scar healing in human studies, including reduced scar dyschromia, erythema, and atrophy. A 2024 systematic review in the Journal of Cosmetic Dermatology confirmed accelerated healing, reduced scar pigmentation, and improved texture in post-surgical scar populations.
EGCG, the primary catechin of green tea, has demonstrated anti-scarring effects by inhibiting the Akt/PI3K pathway, suppressing fibroblast proliferation, reducing TGF-β1 expression, and decreasing collagen synthesis in hypertrophic scar and keloid models. One RCT rated 1b supports its clinical use for scar management.
Glycolic acid is an alpha hydroxy acid used clinically for atrophic scar improvement, working by promoting exfoliation and stimulating collagen production. It is cited in evidence-based dermatological reviews as effective for textural improvement of atrophic scars including acne scars.
Glycosaminoglycans (GAGs), including hyaluronic acid and chondroitin sulfate, are key components of the ECM involved in scar formation and remodeling. Evidence from wound healing and scar models supports their role in promoting organized collagen deposition and reducing pathological scarring.
Multiple clinical trials support Gotu Kola's efficacy in scar prevention and treatment. Topical application has been shown to improve pigmentation and scar scores in split-scar RCTs. Asiaticoside inhibits keloid fibroblast proliferation in a dose-dependent manner while stimulating normal skin collagen synthesis. This is one of Gotu Kola's best-documented dermatological applications.
Green tea extracts, primarily through EGCG, have been studied for scar management with one RCT rated 1b supporting efficacy. Green tea inhibits fibroblast proliferation, TGF-β expression, and collagen synthesis in scar tissue. It is cited in multiple authoritative reviews as a plant extract used for wound healing and scar management.
Hyaluronic acid is a key ECM glycosaminoglycan that modulates wound healing and scar formation. It promotes cell activation, migration, and neovascularization during the scar remodeling phase and has been studied in clinical wound healing formulations, showing improved scar organization.
L-Proline is a critical amino acid for collagen biosynthesis and scar tissue formation. As a primary structural component of collagen's triple helix, it is required for the synthesis of organized scar collagen, and supplementation supports wound healing and collagen quality in scar tissue.
Lavender essential oil has been shown in animal studies to accelerate wound contraction, stimulate type I and III collagen synthesis, increase fibroblast number, and upregulate TGF-β—a key mediator of wound healing and tissue remodeling. A 2020 review in the Journal of Alternative and Complementary Medicine synthesized current evidence. Human clinical data for established scar tissue specifically are limited.
NCCIH reports a preliminary clinical study in which a topical lotion containing mugwort and menthol relieved itching associated with hypertrophic scars. The multi-ingredient nature of the product means mugwort's specific contribution is uncertain. Mugwort is also used in cosmetic formulations recognized by the European CosIng database for skin protective effects.
Nattokinase is a fibrinolytic enzyme from fermented soybeans with evidence for breaking down fibrin-based scar tissue. It is included in clinical pilot studies on systemic enzyme therapy for fibrosis and scar tissue reduction, showing improvements in tissue quality and symptom burden.
Onion extract (Allium cepa) is the most-studied natural ingredient for scar management, with 11 RCTs (4 rated 1b) identified in systematic reviews. Its active flavonoids (quercetin, kaempferol) modulate TGF-β/Smad and IGF-1 signaling, suppress ECM overproduction, and are the basis for commercially available anti-scar products worldwide.
Panthenol (provitamin B5) is commonly incorporated into topical scar formulations for its fibroblast-stimulating, moisturizing, and barrier-repair properties. In vitro and animal studies support fibroblast proliferation promotion, and small clinical studies show improvements in scar redness and pruritus.
Papain has been investigated as a topical scar treatment owing to its proteolytic degradation of excess collagen in hypertrophic scars and keloids. A 2023 PubMed study formulated papain-loaded liposomes and transferosomes for delivery across the stratum corneum specifically targeting hypertrophic scars. An earlier ScienceDirect paper on elastic liposome delivery of papain explicitly cited its role in scar management. Evidence is preclinical/formulation-stage; no controlled human RCTs on scars as a primary endpoint were identified.
Quercetin is the primary bioactive flavonoid in onion extract and has been directly studied for anti-scarring effects. It suppresses TGF-β and IGF-1 signaling, inhibits keloid fibroblast proliferation, reduces ECM deposition, and induces MMP-1 to promote ECM remodeling in scar tissue.
Resveratrol has demonstrated anti-scarring effects in vitro and in vivo by arresting fibroblast cell cycle at G1, reducing hypertrophic scar fibroblast proliferation, decreasing collagen types I and III, and downregulating TGF-β1 and alpha-smooth muscle actin. One RCT (rated 2b) supports clinical use for scar management.
Rose hip preparations have documented evidence for reducing scar formation and stretch marks. Rose hip oil repositions collagen, promotes organized extracellular matrix formation, and avoids abnormal scar tissue development. A HerbalGram 2025 review noted rose hip's ability to avoid development of scars and reduce stretch marks through collagen remodeling and anti-inflammatory mechanisms.
Serrapeptase is a proteolytic enzyme with fibrinolytic activity studied for scar tissue reduction by breaking down excess fibrin in scar tissue. Pilot clinical studies on enzyme supplementation for fibrosis-related scar reduction show improvements in symptoms; anti-inflammatory and fibrinolytic mechanisms are well-established.
Serratiopeptidase is the pharmaceutical name for serrapeptase, with clinical trials demonstrating anti-inflammatory, fibrinolytic, and anti-edemic effects relevant to postoperative scar management. It degrades fibrinous proteins in scar tissue without harming surrounding healthy cells.
Silicon (in the form of organosilicon compounds and silicone gel/sheets) is among the most evidence-based treatments for scar management, with clinical guidelines supporting its use for hypertrophic and keloid scars. Silicone gel and sheeting are first-line recommended non-invasive scar treatments in dermatology.
Turmeric (Curcuma longa), primarily through its curcumin content, has demonstrated anti-scarring effects by inhibiting TGF-β/Smad signaling, reducing fibroblast proliferation, and decreasing pathological collagen deposition in hypertrophic scars. It is cited in multiple systematic reviews of natural products for scar management.
Vitamin C is an essential cofactor for collagen synthesis and scar formation, required for hydroxylation of proline and lysine in procollagen. It is cited in multiple authoritative reviews as a recommended topical and systemic ingredient for scar modulation, and evidence supports it for post-inflammatory hyperpigmentation and scar quality improvement.
Vitamin E has been studied in 4 RCTs for scar management, though evidence is inconsistent. Its antioxidant and anti-inflammatory properties theoretically support scar remodeling; however, current evidence does not strongly support topical vitamin E alone, and it may cause contact dermatitis in some patients.
Zinc plays essential roles in wound healing and scar tissue formation through enzymatic cofactor functions in collagen synthesis, DNA repair, and immune regulation. Zinc deficiency impairs wound healing and scar quality; supplementation supports optimal collagen cross-linking and scar outcomes.
Argan oil is traditionally used in Morocco to heal scars, including post-acne and chicken pox scars. It contains triterpenoids proposed to support scar remodelling. No controlled human clinical trials on argan oil and scar tissue have been published.
Calendula has a traditional cicatrizing (scar-healing) reputation across multiple systems, documented in ethnopharmacological literature. Mechanisms involve collagenase inhibition and fibroblast stimulation. Clinical evidence is indirect; no dedicated scar-reduction RCT exists.
Allantoin, the primary active compound in comfrey, stimulates fibroblast proliferation and ECM synthesis, which are mechanisms relevant to scar tissue remodelling. Allantoin is documented in the cosmeceutical literature to reduce scar visibility by promoting balanced collagen deposition. Traditional herbal use of comfrey for scar management is long-standing, though specific clinical trials in scarring are lacking.
Dragon's blood resin (from Croton lechleri and other species) has a long history of traditional use in wound healing and scar reduction across South American, Asian, and Mediterranean traditional medicine. Scientific studies confirm anti-inflammatory, antioxidant, and fibroblast-stimulating properties, with small clinical studies showing improved scar closure.
Emu oil has been traditionally used by Indigenous Australians for wound and scar healing. Animal studies confirm enhanced wound healing and reduced scar formation. Small clinical studies and reports support anti-inflammatory and scar-modulating effects, though large RCTs are lacking.
Geranium EO is used traditionally to reduce scar formation and promote skin regeneration through its cell-renewal and astringent properties. It is documented in herbal medicine for its use in wound recovery and scar management.
H. italicum has a long tradition in Mediterranean folk medicine for reducing scars and hematomas. Its italidione-containing EO is held in aromatherapy to remodel fibrous scar tissue and reduce bruising. Scientific support is indirect, derived from studies on collagen remodeling and anti-inflammatory activity rather than dedicated scar-reduction trials.
Jojoba oil has traditional use as a skin healing and scar-softening agent, and is included in authoritative scar treatment ingredient lists. It provides a liquid wax ester structure similar to skin sebum, supporting skin barrier function and hydration in scar tissue.
Myrrh has a longstanding traditional application for wound healing and scar reduction, documented in Ancient Egyptian prescriptions and Western herbal traditions. Topical myrrh ointments are used for wounds, chronic ulcers, and scar-prone injuries. A clinical RCT found myrrh mouthwash improved post-extraction wound healing.
Shea butter has longstanding traditional use across Sub-Saharan Africa for wound healing and scar reduction. Its triterpene constituents may inhibit fibroblast overproduction and stimulate collagen remodeling. Clinical evidence is limited but the moisturizing and anti-inflammatory properties plausibly support improved healing environments and reduced scar visibility.
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