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Mony, M.P.; Harmon, K.A.; Hess, R.; Dorafshar, A.H.; Shafikhani, S.H. Conventional and Emerging Treatments for Hypertrophic Scarring. Encyclopedia. Available online: https://encyclopedia.pub/entry/41784 (accessed on 27 July 2024).
Mony MP, Harmon KA, Hess R, Dorafshar AH, Shafikhani SH. Conventional and Emerging Treatments for Hypertrophic Scarring. Encyclopedia. Available at: https://encyclopedia.pub/entry/41784. Accessed July 27, 2024.
Mony, Manjula P., Kelly A. Harmon, Ryan Hess, Amir H. Dorafshar, Sasha H. Shafikhani. "Conventional and Emerging Treatments for Hypertrophic Scarring" Encyclopedia, https://encyclopedia.pub/entry/41784 (accessed July 27, 2024).
Mony, M.P., Harmon, K.A., Hess, R., Dorafshar, A.H., & Shafikhani, S.H. (2023, March 01). Conventional and Emerging Treatments for Hypertrophic Scarring. In Encyclopedia. https://encyclopedia.pub/entry/41784
Mony, Manjula P., et al. "Conventional and Emerging Treatments for Hypertrophic Scarring." Encyclopedia. Web. 01 March, 2023.
Conventional and Emerging Treatments for Hypertrophic Scarring
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This entry is adapted from the peer-reviewed paper 10.3390/cells12050678

Hypertrophic scarring (HTS) is an aberrant form of wound healing that is associated with excessive deposition of extracellular matrix and connective tissue at the site of injury. Scarring is a major clinical problem, affecting some 100 million patients in the developed world alone. According to the current and emerging therapies, which  demonstrate the inadequacy of therapies to address HTS. A better understanding of the impaired mechanisms underlying HTS would surely lead to the development of more effective targeted therapies to treat this debilitating and costly pathological condition.

hypertrophic scar keloids wound healing

1. Conventional Therapies

Treatments of hypertrophic scars often focus on correction of factors that are associated with pathological scar development. These include wound stabilization, minimizing mechanical irritation, balancing wound healing phases, attenuating pro-fibrotic mechanisms, inducing anti-fibrotic mechanisms, and promoting the remodeling of collagenous scar components. Published guidelines on the treatment of hypertrophic scars and keloids include many different modalities without one single, widely accepted protocol[1][2]. Several treatments and techniques have been shown to prevent the development of hypertrophic scar development. (These conventional treatments have been summarized in Table 1). Reduction in tension on the dermal layer when closing wounds is effective and can be achieved with fascial and subcutaneous tensile reduction sutures in wounds of adequate depth [3]. Additionally, dermal closure using sutures arranged in a zig-zag pattern or using z-plasties should be performed whenever possible[3][4]. Closure with 3–0 VLoc 90 barbed suture (VLoc, Covidien, North Haven, CT, USA) compared to interrupted suture with 4–0 nylon produced significant improvements in the Vancouver scar scale (VSS) and patient and observer scar assessment scale (POSAS) scores in patients undergoing anterolateral thigh flap procedures with identical methods of deep closure between groups[5].
Table 1. Conventional treatments for hypertrophic scarring.
Treatment Mechanism
Tensile reduction suture closure[3] Reduces tension on the dermal layer when closing wound
Paper tape, silicone sheets[6][9] Hydration, increased temperature, prevent dermal inflammation
Wound compression[7] Reduces capillary perfusion, accelerated collagen maturation
Laser[30][31][32][33][34][35] Destroys microvascularization, resulting in hypoperfusion and hypoxia
Silicone cream[11][12] Hydration of the stratum corneum and cytokine-mediated signaling from keratinocytes to dermal fibroblasts
Flavonoids[11] Anti-inflammatory, antioxidant, anti-bacterial
Botulinum toxin-A[13][14][15][16][17] Decreases proliferation, migration, and secretion of pro-fibrotic factors from fibroblasts
Scar excision[18] Removal of affected tissue
Microneedle[20][21][22] Disruption of existing collagen, stimulation of MMP-9 * release
Corticosteroids[6][24] Anti-inflammatory, local vasoconstriction
Botulinum toxin-A[24][26][27] Decreases proliferation, migration, and secretion of pro-fibrotic factors from fibroblasts
* Abbreviations: MMP-9 (metalloproteinase 9).
Following the closure of initial wounds, several therapies can also be applied early in the healing process. Similarly to the aforementioned suturing techniques, wound stabilization using paper tape or silicone sheets can also prevent the dermal inflammation that contributes to hypertrophic scar and keloid formation[6]. Wound compression using pressure garment therapy at 15–40 mmHg has been shown to improve outcomes[8]. Regarding ideal pressure, one review of pressure garment therapy for the treatment of burn wounds found that the application of pressure at 17–24 mmHg resulted in improved scar height, softness, and cosmetic appearance compared to a pressure below 5 mmHg[9]. Cohesive silicone sheets that added pressure to the wound also outperformed silicone gel sheets in improving scar assessment scale scores[7]. Intermittent application of pressure through regular massage therapy has not been shown to improve outcomes, suggesting that constant pressure must be applied[10].
Topical agents applied to heal wounds have also been shown to reduce hypertrophic scar formation, including flavonoids and silicone cream[11][12]. The local injection of Botulinum toxin-A postoperatively has also been shown to significantly improve scar assessment scale scores compared to controls[13][14][15]. In a recent study of optimal dosing of Botulinum toxin-A, postoperative injections of 8 units showed significantly improved Stony Brook Scar Evaluation Scale (SBSES) scores compared to the injections of 4 units[16]. The culture of human fibroblasts with Botulinum toxin-A resulted in decreased proliferation, migration, and secretion of pro-fibrotic factors, while JNK phosphorylation levels were increased, providing evidence for possible mechanisms of this benefit[17].
Scar revision is the simplest method of treating pre-existing HTS and encompasses procedures aimed at excisional debulking of hypertrophic scar tissue[18](Table 2). Closure during these procedures is specifically directed at providing favorable cosmetic results and should employ the methods described above for prophylaxis against scar recurrence. To be effective, scar revisions should be performed over 1 year from the original injury to give adequate time for the scar to mature[11], as immature scars are prone to hypertrophic healing and give poor results after scar revision[19].
However, excision may not be necessary, as more conservative measures have proven to be effective. For example, in one study, mechanical disruption of existing hypertrophic scars using microneedle roller therapy improved scar pigmentation to resemble surrounding tissue more closely, and significantly improved both the mean patient satisfaction scale (PSS) and observer satisfaction scale (OSS) between preoperative and postoperative sampling[20]. Another study found that microneedle therapy improved modified Vancouver scar scale (mVSS) scores significantly more than carbon dioxide (CO2) laser therapy for hypertrophic scars [21]. This benefit may be explained by microneedle therapy disrupting existing collagen and stimulating the release of MMP-9[22].
Pharmacologic agents have also been used frequently in the treatment of hypertrophic scars, with common agents including corticosteroids, chemotherapeutic agents, and Botulinum toxin-A. Corticosteroids provide benefits through their potent anti-inflammatory effects and are believed to induce local vasoconstriction when applied to hypertrophic scars and keloids. Tapes and plasters containing corticosteroids effectively treat hypertrophic scars and keloids when applied to these lesions and should be positioned to avoid contact with surrounding tissue [6]. The most common use of corticosteroids in the treatment of hypertrophic scars and keloids by far is the intralesional injection of triamcinolone (TAC). A recent literature review and meta-analysis of this therapy found that compared to 5-FU and verapamil, TAC alone improved scar vascularity[23]. However, TAC therapy also had higher rates of skin atrophy and telangiectasias, especially at the commonly used dose of 40 mg/mL[23]. Significant differences in favor of other agents were found for scar height (5-FU, TAC + 5-FU), scar pliability (TAC + 5-FU, Botulinum toxin-A), scar pigmentation (TAC + 5-FU), VSS score (TAC + 5-FU, TAC + platelet rich plasma), and POSAS score (bleomycin) when compared against TAC alone [24]. A study of TAC vs. TAC + 5-FU found significant differences favoring TAC + 5-FU in mean reduction in scar height, overall POSAS score, and the overall rate of efficacy. Rates of telangiectasias (commonly known as “spider veins”), skin atrophy, hypopigmentation, and recurrence were significantly higher in the group receiving TAC, while the rates of ulceration were significantly higher in the group receiving TAC + 5-FU[25]. A literature review and meta-analysis of intralesional Botulinum toxin-A injection found significantly improved visual analog scale (VAS) scores compared to intralesional corticosteroid and placebo injection[26]. In a split-scar study of patients with existing hypertrophic scars, injection of Botulinum toxin-A was found to significantly improve mean VSS score pre- and post-treatment as compared to the placebo control [27].
The energy-based therapy is well established as a treatment modality for hypertrophic scars and keloids, with its use dating back to the 1980s[28]. Lasers are the mainstay of energy-based treatments, with a multitude of different laser devices utilizing different wavelengths for specific targets[29]. Laser therapy is often used in the treatment of formed hypertrophic scars but can also be used preventatively in the early postoperative period. In a split-scar study of patients undergoing total knee arthroplasties, scar treatment with a 595 nm pulsed-dye laser was associated with significantly improved overall VSS scores compared to an untreated scar[30][31][32][33][34][35].
The guidelines for the use of energy-based treatment for acne scars have included specific recommendations for use with hypertrophic acne scars and keloids. In patients with active acne, a 1064 nm ND:YAG laser is preferred, and pulsed-dye vascular lasers are the laser treatment of choice for hypertrophic acne scars. Pulsed-dye lasers (PDL) may also be used to assist with the delivery of 5-FU and/or TAC. Non-laser devices, including Tixel (Novoxel, Ltd., Berlin, Germany) and EnerJet (PerfAction Technologies Ltd., Rehovot, Israel), were also recommended for the treatment of hypertrophic acne scars[36]. Similar guidelines for traumatic scars recommend non-ablative fractional laser (NAFL) for hypertrophic scars, except in the presence of significant thickness and textural irregularity, where ablative fractional laser (AFL) therapy is preferred[30]. In a study comparing no laser treatment, CO2 laser treatment alone, and intense pulsed light (IPL) + CO2 laser, both treatment groups had statistically significant improvements in POSAS score and Manchester scar scale (MSS) score compared to the placebo, without significant difference between the treatment groups. The only significant difference between treatment groups was in favor of the combination therapy for scar color and texture, indicating that CO2 alone is sufficient and IPL can be used for an additional benefit for these specific factors[37]. Regarding protocols for CO2 laser, a study of varying densities for fractional CO2 laser treatment found that high (25.6%) density significantly improved VAS and POSAS scores compared to low (7.4%) and medium (12.6%) densities in treating mature hypertrophic burn scars[31]. A split-scar study of low-energy CO2 fractional laser treatment showed significantly improved POSAS scores for all elements except for patient-scored irregularity compared to the control for pediatric patients with early-stage hypertrophic burn scars[32]. A study of CO2, PDL, and CO2 + PDL for the treatment of hypertrophic burn scars found significant improvements in posttreatment POSAS for all treatment groups. Focused analyses found that scar height was improved by PDL or CO2 + PDL for scars <0.3 cm, and a significant reduction in scar height was achieved by CO2 + PDL only for scars older than 9 months. Although the guidelines for hypertrophic acne scars include the use of laser-assisted delivery of corticosteroids, a study of fractional ER:YAG laser alone or in combination with topical clobetasol found no significant benefit from the addition of steroids, with both treatment groups achieving significant posttreatment improvements in scar thickness and POSAS scores[33][36]. Recently, studies have compared IPL to non-laser therapies. Significant differences in scar pliability, hyperpigmentation, and median VAS favored IPL vs. silicone sheet, but significant differences in VAS and histopathological characteristics favored cryotherapy vs. IPL[34][35].

2. Emerging Treatments

Given the prevalence of hypertrophic scarring, new treatments are continually developed. Intralesional TAC, for example, was found to improve scar height, pliability, and pigmentation when combined with 5-FU and reduced the number of treatment sessions and remission time when combined with 1550 nm erbium glass fractional laser treatment (Table 2)[24][25][38][39]. While Botox A with TAC showed no difference in scar appearance, it significantly reduced pain and pruritis[40]. Scars treated with RFA plus verapamil and 5-FU experienced the fastest scar volume reduction with relief of symptoms and hyperemia compared to either agent alone [41]. Additionally, the combination of intense pulse light (IPL) and CO2 laser significantly improved scar color and texture[37]. The combination of lasers with 5-FU and/or TAC delivered intralesionally or via laser assistance has thus been recommended for the treatment of hypertrophic acne scars[30][36].
Table 2. Emerging therapeutics for hypertrophic scarring.
Treatment Proposed Mechanism
Corticosteroids + 5-Fluorouracil[24][25][38][39] Anti-inflammatory, local vasoconstriction, inhibit fibroblasts proliferation, decrease collagen synthesis
Laser + Verapamil + 5-Fluorouracil or corticosteroids[41] Destroy microvascularization resulting in hypoperfusion and hypoxia, inhibit fibroblast proliferation, decrease collagen synthesis, anti-inflammatory
CO2 * Laser + Intense Pulse Light [37] Destroy microvascularization resulting in hypoperfusion and hypoxia, promote new dermal collagen formation and rapid differentiation of keratinocytes
Losartan[42] Fibroblasts with decreased contractile activity, migration, and adhesion
Oxandolone + hyaluronic acid gel[43] Decrease inflammation, collagen and fibroblast cellularity, vascularization, and myofibroblast activity
Dipeptidyl peptidase-4 inhibitors[44] Attenuate collagen synthesis and deposition
1,4-Diaminobutane[45] Inhibits collagen cross-linking
Autologous fat grafting[46] Decreases the expression of the myofibroblast marker α-SMA * and ECM * components
Stem cells[47][48] Reduce inflammation, cellularity, and collagen filaments
Platelet-rich plasma[49][50][51] Reduces expression of TGF-β1 * and CTGF mRNA
CD206 * + Macrophages and Fibroblasts[52] Increase MMP-1 * and decrease expression of pro-fibrotic factors, COL1A1 *, COL2A1 *, α-SMA *, CTGF *, and TGF-β1 *
IL-6 *[52] Increases expression of anti-fibrotic genes
IFN-γ *[53] Increases expression of COL1A1 * and COL3A1 * mRNA and decreases expression of MMP-2 * (gelatinase)
* Abbreviations: CO2 (carbon dioxide); CD206 (cluster of differentiation 206); IL-6 (interleukin 6); IFN-γ (Interferon gamma); α-SMA (alpha smooth muscle actin); ECM (extracellular matrix); TGF-β1 (transforming growth factor beta-1); COL1A1 (collagen type I alpha 1 chain); COL2A1 (collagen type II alpha 1 chain); COL3A1 (collagen type III alpha 1 chain), CTGF (connective tissue growth factor); TGF-β1 (transforming growth factor beta 1); MMP-2 (matrix metalloproteinase 2).
The role of angiotensin II in scar activity has recently been examined[42]. Human dermal fibroblasts treated with losartan, an angiotensin II type 1 receptor antagonist, displayed decreased contractile activity, fibroblast migration, gene expression of TGF-β1, type 1 collagen, and MCP-1, while reducing monocyte migration and adhesion [42]. In rat models, the consumption of losartan showed decreased cross-sectional area and elevation index in scars, with decreased α-SMA+ and CD68+ during immunostaining [42]. Another in vivo model demonstrated a reduced incidence of hypertrophic scarring with decreased inflammation, collagen and fibroblast cellularity, vascularization, and myofibroblast activity with the topical administration of oxandrolone and hyaluronic acid gel[43]. Clinically, the administration of dipeptidyl peptidase-4 inhibitors was shown to reduce the risk of hypertrophic scarring and keloid onset by less than half in patients who underwent sternotomy, while 1,4-diaminobutane (1,4 DAB) in breast reduction patients resulted in significantly greater scar satisfaction and less scar hardness measured by Rex Durometer[44][45].
Autologous fat grafting also presents as a novel therapy to improve the function and appearance of scars. While the underlying mechanism is unknown, exposure to adipocytes decreased the expression of the myofibroblast marker α-SMA and ECM components[46]. The reprogramming of myofibroblasts was found to be triggered by BMP-4 (bone morphogenetic protein 4) and activation of PPARγ (peroxisome proliferator-activated receptor gamma) signaling, which initiated tissue remodeling[46].
As is the case in many other fields of medicine, stem cells are also a promising therapeutic target for HTS. Mesenchymal stem cells (MSC) isolated from the mouse whisker hair follicle outer root sheath were applied to an in vivo full-thickness wound model[47]. A quantitative evaluation revealed reduced inflammation, cellularity, and collagen filaments, as well as thinner dermal and epidermal layers in the MSC-treated wounds, indicating a reduction in hypertrophic scars. Another study examined the effect of combined treatment with a non-ablative laser and human stem cell-conditioned medium on burn-induced hypertrophic scar formation[48]. The treatment group was found to have reduced erythema, trans-epidermal water loss, and scar thickness.
Platelet-rich plasma (PRP) has also been identified as a promising therapy for scarring. In one study, primary dermal fibroblasts isolated from hypertrophic scars were cultured in a medium supplemented with 5% PRP or platelet-poor plasma (PPP)[49]. The PRP group was found to have reduced expression of TGF-β1 and connective tissue growth factor (CTGF) mRNA. Other studies have examined combination treatments with both PRP and ablative fractional CO2 lasers and have found the combination to be more beneficial than either treatment alone[50][51].
In addition, identifying the molecular targets for potential treatments is an ongoing source of investigation. Co-cultures of anti-inflammatory cluster of differentiation 206 (CD206)+ macrophages and fibroblasts showed decreased expression of fibrotic factors, such as type 1 and 2 collagen, alpha-smooth muscle actin, connective tissue growth factor, and TGF-β, with upregulation of MMP-1. IL-6 was also found to be increased in the medium, with an increase in anti-fibrotic gene expression when IL-6 was added to fibroblasts. Cytotherapy with cultured CD206+ macrophages or a direct administration of recombinant human IL-6 has been shown to dampen the expression of pro-fibrotic mediators (e.g., COL1A1 *, COL2A1 *, α-SMA *, CTGF *, and TGF-β1) in fibroblast in cell culture studies[52].
In vitro studies of fibroblasts have revealed that IFN-γ inhibits collagen synthesis[53]. IFN-γ knockout mice were found to have reduced wound closure, lower wound breaking strength, and dampened expression of collagen type 1A (COL1A1) and collagen type 3 A1 (COL3A1) mRNA, but a greater expression of MMP-2 (gelatinase) mRNA[53]. The study concluded IFN-γ may be involved in both the proliferation and maturation stages of wound healing and, therefore, may be a target for potential treatments.

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Manjula P. Mony
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Kelly A. Harmon
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Ryan Hess
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Amir H. Dorafshar
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Sasha H. Shafikhani
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