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Wound Healing and Scar Biology

Overview

Hypertrophic scar development and eventual spontaneous resolution lack a single known mechanism [1]. The balance between scar formation and tissue regeneration is determined by specific TGFβ isoforms and downstream mediators, where inhibition of the canonical TGFβ signalling pathway blocks regeneration [2]. Myofibroblast apoptotic cell death is pivotal in distinguishing normal scars from hypertrophic scars, with a lack or late induction of this process implicated in hypertrophic outcomes [7]. Macrophages are critical in the early repair response; their depletion significantly reduces vascularized granulation tissue formation, impairs epithelialization, and minimizes scar formation [4].

Moist wound treatment remains the standard therapy for wound management, though definitive research trials on the success of different dressings are still needed [19]. The wound-healing community is currently formulating consolidated guidelines for common types of ulcers to lead to standardized, evidence-based clinical protocols [6]. For negative pressure wound therapy, a clear wound healing goal must be determined, and discontinuation should be considered if no improvement is observed between two consecutive dressing changes or after 1 week of treatment [9].

Surgical incisions that initially healed with good scar quality generally heal well following subsequent incision through the previous scar [5]. However, research in support of some techniques utilized within scar management programmes is limited, and anecdotal evidence and clinical experience continue to prevail in the choice of treatment for scar management [8]. The clinical effects of new antineoplastic agents on wound healing are complex and uncertain, with recommendations regarding these agents and wound healing based on database opinions and case reports [10].

How It Works

The precise mechanisms driving the development [1] and eventual spontaneous resolution [1] of hypertrophic scars remain undefined. These pathological outcomes stem from a dysregulated wound healing process characterized by altered extracellular matrix composition and profibrotic cytokine signaling, typically resulting from deep burns with prolonged healing times [13]. Specific TGFβ isoforms and downstream mediators determine the balance between scar formation and tissue regeneration [2], while inhibition of the canonical TGFβ signaling pathway blocks regeneration [2]. Understanding these biologic mechanisms, including the roles of cytokines like TGF-beta and CTGF, is essential for addressing scar and contracture issues [12].

Macrophages are critical in the early repair response; their depletion significantly reduces vascularized granulation tissue formation [4], impairs epithelialization [4], and minimizes scar formation [4]. A pivotal distinction between normal and hypertrophic scars may be a lack or late induction of myofibroblast apoptotic cell death [7]. The immune system supports healing by recognizing antigens [21], participating in debridement [21], and contributing to tissue repair via innate and adaptive responses [21]. However, altered immune responses following burn and thoracic trauma are associated with a reduced capacity for wound healing [11].

Systemic and local factors significantly modulate healing. Optimal wound healing requires adequate nutrition, as deficiencies impede progression through normal healing stages [14]. Smoking exerts transient effects on the tissue microenvironment [22] but causes prolonged impairment of inflammatory and reparative cell functions, leading to delayed healing and complications [22]. In diabetic wounds, molecular cascades of cytokines and erstwhile factors are responsible for delayed healing [20]. While platelets secrete growth factors that positively influence rapid healing and tissue regeneration [16], the administration of basic fibroblast growth factor failed to improve mechanical or functional properties of intrasynovial flexor tendon repair despite a substantial biologic response [15].

What the Evidence Shows

Pathophysiology and Cellular Mechanisms The specific mechanisms driving the development and eventual spontaneous resolution of hypertrophic scars remain unknown [1]. Hypertrophic scarring and contractures result from deep burns with prolonged healing times, involving a dysregulated wound healing process characterized by altered extracellular matrix composition and profibrotic cytokine signaling [13]. A pivotal difference between normal and hypertrophic scars may be a lack or late induction of myofibroblast apoptotic cell death [7]. Specific TGFβ isoforms and downstream mediators determine the balance between scar formation and tissue regeneration, while inhibition of the canonical TGFβ signalling pathway blocks regeneration [2]. Macrophages are critical in the early repair stage; their depletion significantly reduces vascularized granulation tissue formation, impairs epithelialization, and minimizes scar formation [4].

Growth Factors and Biological Modulators Platelets secrete growth factors and active metabolites that positively influence clinical situations requiring rapid healing and tissue regeneration [16]. FGF gene expression is associated with improved patient-reported outcomes after Achilles tendon repair and may predict healing success [18]. However, the administration of basic fibroblast growth factor failed to improve mechanical or functional properties of intrasynovial flexor tendon repair in a canine model [15]. The clinical relevance of various growth factors identified in basic science for flexor tendon wound healing remains unclear for the practicing hand surgeon [34]. Current data does not show consistent improvement in healing or clinical outcomes with bone marrow stimulation or leukocyte-rich PRP for rotator cuff repair [27].

Pharmacologic and Systemic Influences Methotrexate is effective in suppressing keloid formation after syndactyly release and controlling recurrence after keloid surgery [29]. Acute, high-dose systemic corticosteroid use likely has no clinically significant effect on wound healing, whereas chronic systemic steroids may impair healing in susceptible individuals [17]. The review highlights complex and uncertain clinical effects of new antineoplastic agents on wound healing; available recommendations are based on database opinions and case reports [10]. An altered immune response following burn and thoracic trauma is associated with reduced wound healing capacity in a rat model of polytrauma [11].

Clinical Management and Outcomes Surgical incisions that initially healed with good scar quality generally healed well following subsequent incision through the previous scar in children with cerebral palsy undergoing surgical implant removal [5]. Early controlled motion of stable or surgically stabilized joints appears to improve ligament scar behavior, though no treatment identified to date stimulates true ligament regeneration [28]. Moist wound treatment is standard therapy, but definitive research trials on the success of different dressings are still needed [19]. The clinical importance of running subcuticular closure enabling robust perfusion after TKA remains uncertain as patients lacked risk factors for wound healing complications [3].

Future Directions and Guidelines Research supporting techniques within scar management programmes is limited, with anecdotal evidence and clinical experience prevailing in treatment choice [8]. Future directions for anti-adhesive agents in tendon repair include implementing randomized controlled trials and developing multifunctional biomaterials to improve patient outcomes [26]. The wound-healing community is currently formulating consolidated guidelines for common types of ulcers to lead to standardized, evidence-based clinical protocols [6]. For negative pressure wound therapy in orthopaedic surgery, a clear wound healing goal must be determined, and discontinuation should be considered if no improvement is observed between two consecutive dressing changes or after 1 week of treatment [9].

Practical Considerations

Scar Biology and Management

The specific mechanisms driving the development or eventual spontaneous resolution of hypertrophic scar remain unknown [1]. Current understanding emphasizes that specific TGFβ isoforms and downstream mediators determine the balance between scar formation and tissue regeneration, while inhibition of the canonical TGFβ signalling pathway blocks regeneration [2]. Macrophage depletion restricted to the early stage of repair significantly reduces vascularized granulation tissue formation, impairs epithelialization, and minimizes scar formation [4]. Understanding these biologic mechanisms, including the roles of cytokines like TGF-beta and CTGF, allows hand surgeons to better address scar and contracture issues [12]. Research supporting many scar management techniques remains limited, with anecdotal evidence and clinical experience prevailing in treatment choices [8]. Surgical incisions that initially healed with good scar quality generally heal well following subsequent incision through the previous scar in children with cerebral palsy undergoing surgical implant removal [5].

Wound Healing Modifiers

Optimal wound healing requires adequate nutrition, as deficiencies impede the normal processes allowing progression through healing stages [14]. Acute, high-dose systemic corticosteroid use likely has no clinically significant effect on wound healing, whereas chronic systemic steroids may impair healing in susceptible individuals [17]. The clinical effects of new antineoplastic agents on wound healing are complex and uncertain, with recommendations based on database opinions and case reports [10]. In Achilles tendon repair, FGF gene expression is associated with improved patient-reported outcomes and may serve as a predictor for healing [18].

Closure Techniques and Devices

Staples: In total knee arthroplasty, primary skin incision closure with staples demonstrates lower wound complications, decreased wound closure times, and an overall reduction in resource utilization compared to other methods [23]. Medizip: The non-invasive skin closure system Medizip offers comparable scar results and complication rates to intracutaneous sutures, while significantly reducing closure time and costs [25].

Negative Pressure Wound Therapy

Indications and Goals: A clear wound healing goal must be determined for negative pressure wound therapy in orthopaedic surgery [9]. Closed incision negative-pressure wound therapy (ciNPWT) is clinically effective for incisions at high risk for perioperative complications, though specific indications continue to be defined [30]. Discontinuation Criteria: If no improvement is observed between two consecutive dressing changes or after 1 week of treatment, discontinuation should be considered [9].

General Principles

Wound management represents a significant healthcare and financial burden requiring a multidisciplinary approach [24]. Orthopaedic surgeons must be familiar with fundamental principles and evidence-based concepts for managing acute and chronic wounds to optimize outcomes [24].

Key Evidence

  • [L5] Although no single mechanism is yet known to account for the development of hypertrophic scar, nor for its eventual spontaneous resolution, insights obtained during the past 5 to 10 years hold out hope that rational, drug-based, treatments may one day replace the invasive surgery and other physical treatments. (10.1016/s0749-0712(21)00203-1)
  • [L5] Specific TGFβ isoforms and downstream mediators play different roles in determining the balance between scar formation and tissue regeneration, and inhibition of the canonical signalling pathway blocks regeneration. (10.3390/jdb4020021)
  • [L1] However, the clinical importance remains uncertain as patients lacked risk factors for wound healing complications. (10.1007/s11999-015-4209-x)
  • [L5] Depletion of macrophages restricted to the early stage of the repair response significantly reduced the formation of vascularized granulation tissue, impaired epithelialization, and resulted in minimized scar formation. (10.4049/jimmunol.0903356)
  • [L2] Surgical incisions that initially healed with good scar quality generally healed well following subsequent incision through the previous scar. (10.2106/jbjs.15.01418)
  • [L5] The wound-healing community is currently in the process of formulating consolidated guidelines for each of the common types of ulcers to lead to standardized, evidence-based clinical protocols. (10.1016/j.ad.2014.03.008)
  • [L5] A pivotal difference between normal scars and hypertrophic scars may be a lack or late induction of myofibroblast apoptotic cell death. (10.1016/s0749-0712(21)00204-3)
  • [L5] Research in support of some of the techniques utilised within scar management programmes is limited, with anecdotal evidence and clinical experience continuing to prevail in the choice of treatment. (10.1177/175899830501000201)
  • [L4] A clear wound healing goal must be determined, and if no improvement is observed between two consecutive dressing changes or after 1 week of treatment, discontinuation should be considered. (10.1016/j.otsr.2016.04.018)
  • [L5] The review highlights the complex and uncertain clinical effects of new antineoplastic agents on wound healing, noting that available recommendations are based on database opinions and case reports. (10.5435/jaaos-d-24-00097)
  • [L5] This altered immune response that follows was associated with a reduced capacity for wound healing. (10.1186/s13018-019-1082-4)
  • [L5] Understanding the underlying biologic mechanisms of scar and contracture, including the roles of cytokines like TGF-beta and CTGF, allows hand surgeons to better address these issues and suggests new avenues of research to improve patient outcomes. (10.1016/j.hcl.2009.06.007)
  • [L5] Hypertrophic scarring and contractures result from deep burns that take longer to heal, involving a dysregulated wound healing process with altered extracellular matrix composition and profibrotic cytokine signaling. (10.1016/j.hcl.2016.12.004)
  • [L5] Optimal wound healing requires adequate nutrition, as nutrition deficiencies impede the normal processes that allow progression through stages of wound healing. (10.1177/0884533609358997)
  • [L5] Despite a substantial biologic response, the administration of basic fibroblast growth factor failed to produce improvements in either the mechanical or functional properties of the repair. (10.2106/jbjs.i.01601)
  • [L4] Platelets secrete growth factors and active metabolites that have a positive influence in clinical situations requiring rapid healing and tissue regeneration. (10.1160/th03-07-0440)
  • [L4] Acute, high-dose systemic corticosteroid use likely has no clinically significant effect on wound healing, whereas chronic systemic steroids may impair wound healing in susceptible individuals. (10.1016/j.amjsurg.2012.11.018)
  • [L2] FGF gene expression is associated with improved patient-reported outcome and may be used as a predictor for healing. (10.1186/s40634-021-00335-0)
  • [L5] Moist wound treatment is standard therapy, but definitive research trials on the success of different dressings are still needed. (10.1007/s00120-007-1593-1)
  • [L5] This review focuses on the molecular cascades of cytokines and erstwhile factors responsible for delayed wound healing, molecular targets and recent advancements in complete healing and its cure. (10.1016/j.biopha.2019.108615)
  • [L5] Wound healing is a complex biological process where the immune system recognizes and combats antigens, participates in debridement, and contributes to tissue repair through innate and adaptive responses. (10.1016/j.injury.2006.02.035)
  • [L2] Smoking has a transient effect on the tissue microenvironment and a prolonged effect on inflammatory and reparative cell functions leading to delayed healing and complications. (10.1097/sla.0b013e31824f632d)
  • [L1] Primary skin incision closure with staples demonstrated lower wound complications, decreased wound closure times, and an overall reduction in resource utilization. (10.1016/j.arth.2017.04.004)
  • [L5] Wound management is a significant healthcare and financial burden requiring a multidisciplinary approach; orthopaedic surgeons must be familiar with fundamental principles and evidenced-based concepts for managing acute and chronic wounds to optimize outcomes. (10.5435/jaaos-d-17-00024)
  • [L1] The non-invasive skin closure system Medizip represents a safe option in the spectrum of surgical wound treatment, offering comparable scar results and complication rates to intracutaneous sutures while significantly reducing closure time and costs. (10.1007/s004020100308)
  • [L5] Future directions include implementing randomized controlled trials and developing multifunctional biomaterials to improve patient outcomes. (10.1186/s13018-025-06436-1)
  • [L5] Current data does not show consistent improvement in healing or clinical outcomes with bone marrow stimulation or leukocyte-rich PRP. (10.5435/jaaos-d-25-00069)
  • [L5] Early controlled motion of stable or surgically stabilized joints appears to improve ligament scar behavior, but no treatment identified to date stimulates true ligament regeneration. (10.5435/00124635-199603000-00002)
  • [L4] The use of methotrexate to suppress keloid formation after release of syndactyly and for control of recurrence after surgery for keloid is effective. (10.1177/1753193411402146)
  • [L4] ciNPWT has been shown to be clinically effective for incisions at high risk for perioperative complications, although specific indications continue to be defined. (10.5435/jaaos-d-17-00054)
  • [L5] The article reviews the molecular basis of flexor tendon wound healing and the role of growth factors, noting that while basic science reports have identified various factors, their clinical relevance for the practicing hand surgeon remains unclear. (10.1016/j.jhsa.2004.04.020)

References

[1] MOLECULAR AND CELLULAR ASPECTS OF FIBROSIS FOLLOWING THERMAL INJURY. Hand Clinics. 2000. DOI: 10.1016/s0749-0712(21)00203-1

[2] Signalling by Transforming Growth Factor Beta Isoforms in Wound Healing and Tissue Regeneration. Journal of Developmental Biology. 2016. DOI: 10.3390/jdb4020021

[3] The Chitranjan Ranawat Award: Running Subcuticular Closure Enables the Most Robust Perfusion After TKA: A Randomized Clinical Trial. Clinical Orthopaedics & Related Research. 2016. DOI: 10.1007/s11999-015-4209-x

[4] Differential Roles of Macrophages in Diverse Phases of Skin Repair. The Journal of Immunology. 2010. DOI: 10.4049/jimmunol.0903356

[5] Outcomes of Cutaneous Scar Revision During Surgical Implant Removal in Children with Cerebral Palsy. Journal of Bone and Joint Surgery. 2016. DOI: 10.2106/jbjs.15.01418

[6] Nuevos modelos experimentales para el estudio de la homeostasis y la enfermedad cutánea. Actas Dermo-Sifiliográficas. 2015. DOI: 10.1016/j.ad.2014.03.008

[7] CONTROL OF WOUND CONTRACTION. Hand Clinics. 2000. DOI: 10.1016/s0749-0712(21)00204-3

[8] Scar Management in Hand Therapy – is our Practice Evidence Based?. The British Journal of Hand Therapy. 2005. DOI: 10.1177/175899830501000201

[9] Negative pressure wound therapy in orthopaedic surgery. Orthopaedics & Traumatology: Surgery & Research. 2017. DOI: 10.1016/j.otsr.2016.04.018

[10] Wound-Healing Effects of Common Antineoplastic Agents and Perioperative Considerations for the Orthopaedic Surgeon. Journal of the American Academy of Orthopaedic Surgeons. 2024. DOI: 10.5435/jaaos-d-24-00097

[11] Burn and thoracic trauma alters fracture healing, systemic inflammation, and leukocyte kinetics in a rat model of polytrauma. Journal of Orthopaedic Surgery and Research. 2019. DOI: 10.1186/s13018-019-1082-4

[12] Scar and Contracture: Biological Principles. Hand Clinics. 2009. DOI: 10.1016/j.hcl.2009.06.007

[13] Biological Principles of Scar and Contracture. Hand Clinics. 2017. DOI: 10.1016/j.hcl.2016.12.004

[14] Understanding the Role of Nutrition and Wound Healing. Nutrition in Clinical Practice. 2010. DOI: 10.1177/0884533609358997

[15] The Effects of Exogenous Basic Fibroblast Growth Factor on Intrasynovial Flexor Tendon Healing in a Canine Model. Journal of Bone and Joint Surgery. 2010. DOI: 10.2106/jbjs.i.01601

[16] Autologous platelets as a source of proteins for healing and tissue regeneration. Thrombosis and Haemostasis. 2004. DOI: 10.1160/th03-07-0440

[17] Corticosteroids and wound healing: clinical considerations in the perioperative period. The American Journal of Surgery. 2013. DOI: 10.1016/j.amjsurg.2012.11.018

[18] FGF gene expression in injured tendons as a prognostic biomarker of 1‐year patient outcome after Achilles tendon repair. Journal of Experimental Orthopaedics. 2021. DOI: 10.1186/s40634-021-00335-0

[19] Pathophysiologie der Wundheilung und modernes Wundmanagement im urologischen Kontext. Der Urologe. 2007. DOI: 10.1007/s00120-007-1593-1

[20] Mechanistic insight into diabetic wounds: Pathogenesis, molecular targets and treatment strategies to pace wound healing. Biomedicine & Pharmacotherapy. 2019. DOI: 10.1016/j.biopha.2019.108615

[21] Wound healing: Immunological aspects. Injury. 2006. DOI: 10.1016/j.injury.2006.02.035

[22] Wound Healing and Infection in Surgery. Annals of Surgery. 2012. DOI: 10.1097/sla.0b013e31824f632d

[23] A Meta-Analysis and Systematic Review Evaluating Skin Closure After Total Knee Arthroplasty—What Is the Best Method?. The Journal of Arthroplasty. 2017. DOI: 10.1016/j.arth.2017.04.004

[24] Advances in Wound Management. Journal of the American Academy of Orthopaedic Surgeons. 2018. DOI: 10.5435/jaaos-d-17-00024

[25] Results of a prospective randomised study comparing a non-invasive surgical zipper versus intracutaneous sutures for wound closure. Archives of Orthopaedic and Trauma Surgery. 2002. DOI: 10.1007/s004020100308

[26] Anti-adhesive agents in tendon repair: mechanisms, preclinical evidence, clinical challenges, and future perspectives—a narrative review. Journal of Orthopaedic Surgery and Research. 2025. DOI: 10.1186/s13018-025-06436-1

[27] Orthobiologic Augmentation to Improve Rotator Cuff Repair Outcomes: Current and Future Strategies. Journal of the American Academy of Orthopaedic Surgeons. 2025. DOI: 10.5435/jaaos-d-25-00069

[28] Ligament Healing: Current Knowledge and Clinical Applications. Journal of the American Academy of Orthopaedic Surgeons. 1996. DOI: 10.5435/00124635-199603000-00002

[29] Keloid formation after syndactyly release in patients with associated macrodactyly: management with methotrexate therapy. Journal of Hand Surgery (European Volume). 2011. DOI: 10.1177/1753193411402146

[30] The Use of Closed Incision Negative-Pressure Wound Therapy in Orthopaedic Surgery. Journal of the American Academy of Orthopaedic Surgeons. 2018. DOI: 10.5435/jaaos-d-17-00054

[34] Clinical implications of growth factors in flexor tendon wound healing. The Journal of Hand Surgery. 2004. DOI: 10.1016/j.jhsa.2004.04.020

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b. Where Your right to use the Licensed Material has terminated under Section 6(a), it reinstates:

1. automatically as of the date the violation is cured, provided it is cured within 30 days of Your discovery of the violation; or

2. upon express reinstatement by the Licensor.

For the avoidance of doubt, this Section 6(b) does not affect any right the Licensor may have to seek remedies for Your violations of this Public License.

c. For the avoidance of doubt, the Licensor may also offer the Licensed Material under separate terms or conditions or stop distributing the Licensed Material at any time; however, doing so will not terminate this Public License.

d. Sections 1, 5, 6, 7, and 8 survive termination of this Public License.

Section 7 -- Other Terms and Conditions.

a. The Licensor shall not be bound by any additional or different terms or conditions communicated by You unless expressly agreed.

b. Any arrangements, understandings, or agreements regarding the Licensed Material not stated herein are separate from and independent of the terms and conditions of this Public License.

Section 8 -- Interpretation.

a. For the avoidance of doubt, this Public License does not, and shall not be interpreted to, reduce, limit, restrict, or impose conditions on any use of the Licensed Material that could lawfully be made without permission under this Public License.

b. To the extent possible, if any provision of this Public License is deemed unenforceable, it shall be automatically reformed to the minimum extent necessary to make it enforceable. If the provision cannot be reformed, it shall be severed from this Public License without affecting the enforceability of the remaining terms and conditions.

c. No term or condition of this Public License will be waived and no failure to comply consented to unless expressly agreed to by the Licensor.

d. Nothing in this Public License constitutes or may be interpreted as a limitation upon, or waiver of, any privileges and immunities that apply to the Licensor or You, including from the legal processes of any jurisdiction or authority.

Creative Commons is not a party to its public licenses. Notwithstanding, Creative Commons may elect to apply one of its public licenses to material it publishes and in those instances will be considered the “Licensor.” The text of the Creative Commons public licenses is dedicated to the public domain under the CC0 Public Domain Dedication. Except for the limited purpose of indicating that material is shared under a Creative Commons public license or as otherwise permitted by the Creative Commons policies published at creativecommons.org/policies, Creative Commons does not authorize the use of the trademark "Creative Commons" or any other trademark or logo of Creative Commons without its prior written consent including, without limitation, in connection with any unauthorized modifications to any of its public licenses or any other arrangements, understandings, or agreements concerning use of licensed material. For the avoidance of doubt, this paragraph does not form part of the public licenses.

Creative Commons may be contacted at creativecommons.org.