Therapy of pathological scars

Authors

  • Justinus A. Wagner

    Corresponding author
    1. Department of Dermatology, Venereology and Allergology, Leipzig University Hospital, Germany
    • Correspondence to

      Dr. med. Justinus A. Wagner

      Klinik für Dermatologie, Venerologie und Allergologie

      Universitätsklinikum Leipzig A.ö.R.

      Philipp-Rosenthal-Straße 23

      04103 Leipzig, Germany

      E-mail: justinus.wagner@medizin.uni-leipzig.de

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  • Section Editor Prof. Dr. Jan C. Simon, Leipzig

  • 58.6 million Germans have scars – 10.6 million wish they did not have them.

  • It is impossible, after the fetal stage, to restore the skin to its original condition.

  • Wound healing depends on many endogenous and exogenous factors.

  • Keloids are lesions in which the scar tissue grows beyond the wound bed.

  • Unlike keloids, hypertrophic scars can also resolve spontaneously.

  • Distinguishing them clinically is sometimes difficult.

  • Scars with contour problems are often perceived as cosmetically disturbing by patients.

  • Before treating any scar, the scar type should be diagnosed.

  • In addition to subjective parameters and systems, scars may also be measured objectively.

  • Given that each individual scar is different, it is impossible to make recommendations for a standard therapy.

  • In most instances, combination therapy is advisable.

  • Surgical planning with diverse surgical techniques is paramount for good healing of the scar.

  • Along with reducing symptoms, the goal of scar treatment is to minimize volume and color.

  • In surgical correction of pathological scars as monotherapy, depending on the type of scar, a higher rate of recurrence may be expected.

Summary

The various clinical manifestations of scarring are an important topic for physicians in many disciplines. The prevention of excessive scarring is more successful than the treatment afterwards. Multiple options exist for prevention, wound repair modulation, and treatment of scars. This publication includes an overview of the pathogenesis, clinical classification, documentation, prevention, and invasive and non-invasive therapy options.

Introduction

A scar (Latin: cicatrix) is the final condition resulting from a complex repair mechanism of the human body. Despite its importance, people who have scars often would rather their experiences were not visible on their body, as every scar tells a story. While some patients would like to erase their scars, thereby eliminating usually painful memories, in certain cultures or sub-cultures people intentionally bring about a scar healing process which is proudly displayed. Scarification (Latin: scarification, or scoring) refers to intentionally producing cutaneous scars. This technique is rooted deeply in the traditions of various peoples in which scarring is considered body decoration, or an initiation rite or symbol of belonging to a particular clan. Scarring is thought to represent courage and masculinity. This ritual is not limited to African tribes; in the Brazilian rain forest there are crocodile people, who modify their skin to conform to nature. In the Western world as well, there is what is known as a “scarification culture.” Bodily modifications in terms of scarification are experiencing a renaissance. Depending on the technique used, the trend is known as cutting or branding and may be compared with tattooing. This is distinguished from psychological/pathological causes of scarring due to self-harm. There is also the issue of the attractiveness or stigmatization of people with scars. One study showed that men with facial scars were found attractive mainly by women who would consider having a short-term relationship. The authors suggested that there was an association between facial scarring and increased testosterone levels, reflecting attributes such as masculinity, courage, and strength [1].

Yet, on the whole – regardless of scar morphology – most people do not find scars desirable. A representative survey found that 58.6 million Germans have scars. Of these, 10.6 million wish they did not have a scar, and of these one in four women (7.6 million) and one in ten men (3.0 million) (Source: Innofact on behalf of Bi-Oil®).

Healing of skin wounds

Wound healing is a vital, complex repair mechanism that occurs after damage to the integrity of the skin. The resulting fibrous tissue is inferior (Latin: reparatio), representing the final condition after wound healing and restoration of integrity. Restoration of integrity (reparative regeneration), or complete healing with restoration of the skin without a permanent defect, is impossible in after the fetal stage of development. Fetal wound healing is characterized by lower transforming growth factor (TGF)-β expression, which is connected with the absence of scar formation. The complex mechanism of wound healing must be fast and efficient, as it can be essential for an individual's survival. This mechanism developed over the course of evolution; it mainly restores the function of the surface integrity without any relation to aesthetic components. Proper wound healing is completed in one to two weeks. In histological sections, the structure of this inferior fibrous replacement tissue is seen in the loss of the appendages of the skin. Normal wound healing is a complex process which may be divided into the following phases [2]:

  • Exudative phase: the defect is filled with coagulated blood, fibrin, and fibronectin.
  • Resorptive phase: migration of neutrophilic granulocytes (IL-1, tumor necrosis factor alpha [TNFα]) and monocytes/macrophages.
  • Reparative phase: granulation tissue formation, angiogenesis.
  • Re-epithelization
  • Wound contraction

Granulation tissue development occurs with resorption of the exudates and increased collagen synthesis. There is formation primarily of type III collagen, which is transformed gradually into type I collagen. In the final scar, the ratio of these two types of collagen is about 8.5 : 1.5 (type I : type III). In keloids, the ratio between collagen types I and III is about 17 : 1 [3].

Another functional division of wound healing consists of the following (after Krupp):

  • Inflammatory phase (days 1–8),
  • Proliferative phase (days 8–14),
  • Reconstructive phase (day 14–6/24 months).

Pathogenesis and definition of pathological scars

Pathological wound healing depends on many endogenous and exogenous factors. Basically, there is an imbalance between production and breakdown of collagen. The mechanism is only partly understood. There is a well-balanced interplay between fibroblasts, myofibroblasts, inflammatory cells, and their mediators (cytokines).

Wound healing may be influenced by diverse factors such as defect size, stability/instability, wound tension, contraction, infection, location, pathogenesis, healing period, surgical technique, cytokines (transforming growth factor [TGF], platelet derived growth factor [PDGF], platelet activated factor [PAF]), genetic predisposition, neuronal factors, vitamins, hormones, immune system, pO2, perfusion, and accompanying diseases such as diabetes mellitus, etc. [4]. Table 1 provides an overview of the expression of various extracellular matrix molecules.

Table 1. Extracellular matrix molecules; *missing data, 1 = normal skin, —– significantly under expressed, +++++ significantly over expressed; Sidgwick [3]
Extracellular matrixFetal tissueImmature scarMature scarHypertrophic scarKeloid
Collagen I+++++++++++
Collagen II++++1+++++
Fibrillin--1
Elastin—--1++
Fibronectin++++1++++++
Hyaluronic acid++++++1
Laminin+**11
Dermatopontin***
Periostin***++++
Tenascin+++++1++++++
Decorin***

Histology

Hypertrophic scars and keloids can only be partly distinguished from one another histologically, given that there is considerable overlap. The changes also depend on the age of the scars, their location, and various other accompanying factors.

Hypertrophic scars generally have cell-rich connective tissue and usually parallel collagen fibers at the surface. There may also be focal nodular areas. In the latter, in particular, there are numerous alpha-actin-positive myofibroblasts.

In keloids, a more cell-poor connective tissue dominates, and the collagen fibers are organized randomly and in larger nodules (Figure 1a). The fibers are hypereosinophilic, hyaline, and thicker (Figure 1b). In addition – often in the center of the scar – there are cell-poor areas. Alpha-actin-positive myofibroblasts (Figure 1c) are either absent of found only focally. Between the fibers there are abundant small vessels in both hypertrophic scars as well as in keloid.

Figure 1.

Keloid with abnormally dense, broad, hypereosinophilic, focal fragmented collagen fibers in random order (hematoxylin eosin) (a). The collagen fibers appear hypereosinophilic and thickened (higher resolution of Figure 1a, hematoxylin eosin) (b). Absence of myofibroblasts in the keloid (immunohistochemistry, smooth muscle actin staining – alpha-SMA) (c).

Keloid

Keloids represent an overgrowth of scar tissue, which is not limited to the original borders of the wound. This type of scar has only a low tendency toward regression; most keloid patients have a genetic predisposition. Pathological fibroblast activity, in particular, may be seen as a trigger. After TGF-β-stimulation, they form up to twelve times more collagen than would normal fibroblasts [5]. The pathomechanism is not entirely understood, but there is often an association with injuries and inflammations. In addition, some patients are clearly predisposed (positive family history and own medical history as well as skin type). Fibroblasts in keloids produced increased type I procollagen, vascular endothelial growth factor (VEGF), transforming growth factor (TGF) β1/β2, platelet derived growth factor (PDGF-)alpha receptors. Keloid fibroblasts have lower rates of apoptosis and a down-regulation of apoptosis genes. Yet, no “keloid gene” has been identified as yet [6].

The term keloid was first coined in 1800 as “cheloid”, which is related to the ancient Greek word “chele” (water soldier) [6]. A keloid is a benign hyperproliferation of scar tissue and the result of abnormal, excessive wound healing following skin trauma. This pathological type of scar is defined, in contrast to hypertrophic scarring, by overgrowth of the original boundaries of the scar. It is often accompanied by itching and pain. A progressive growth pattern is characteristic. Unlike hypertrophic scars, keloids do not regress spontaneously. Typical locations include the shoulders, chest, cleavage area, neck, and ears. It has been postulated that there is increased wound tension at these sites. Keloids rarely occur on the palms of the hands or soles of the feet. A relationship with infections and burns has been reported. Following trauma, keloids usually resolve after one to three months, or occasionally after a year [6] (Figure 2a, b).

Figure 2.

Sternal keloid (a). Ear keloid (b).

Hypertrophic scar

By definition, hypertrophic scars do not extend beyond the original wound bed. In rare instances, itching occurs. Unlike keloids, they have the potential for spontaneous regression after a period of months. This should be taken into consideration when assessing the indications for treatment and selecting the appropriate method. In clinical practice, differentiating keloids from hypertrophic scars is occasionally challenging. Similar to keloids, fibroblasts also form higher levels of TGF-β and PDGF [7]. In general, these types of scars are characterized by a lacking decrease in fibroblast activity. Clinically, hypertrophic scars appear to have greater tension (Figure 3). Table 2 gives an overview of clinical differences between keloids and hypertrophic scars.

Table 2. Distinguishing characteristics for hypertrophic scars and keloids, modified from the German S2k guidelines for the therapy of pathological scars (hypertrophic scars and keloids) [8]
 Hypertrophic scarKeloid
IncidenceOftenRare, correlates with skin type
ExtentDoes not go beyond original woundGoes beyond original wound
Occurrence< 6 months after injury> 6 months after injury
RegressionFrequentNo regression
Prior injuryYesYes, also minimal trauma
LocalizationEntire skin surfaceEntire skin surface, often ear, sternum, shoulder girdle
Genetic predispositionNot knownYes
Figure 3.

Postoperative hypertrophic scar.

Pathogenesis and definition of scars with contour problems

Most scars with contour problems result from surgery; their pathogenesis is well understood. Contour problems include increased tension, pocket formation (related to diagonal contractures in oblique incisions), step-offs (with adaptation of differing tissue thicknesses), and trapdoor phenomena (e.g., parallel/semicircular scars) [9] (Figures 4, 5).

Figure 4.

Trapdoor phenomenon after flap plasty (bilobed flap) of rhinophyma.

Figure 5.

Dehiscent scar.

Classification of scars

Before treating any scar, the scar type should be diagnosed. The diagnosis of the type of scar is a crucial factor in further invasive or non-invasive treatment. Distinguishing scar types may also be difficult clinically. Table 3 provides an overview.

Table 3. Classification of scars [9, 10]
Old, mature scarLight, flat scar
Immature scarRed, sometimes itching/painful, slightly raised scar in a transitional stage. Matures with age of scar and gets flatter. Pigmentation may be lighter, darker or same (Figure 6).
Linear hypertrophic scarRed, elevated scar on original incision. Enlargement in 3–6 months, then tendency to regress. Maturation phase up to 2 years.
Large hypertrophic scarFor instance with burn injuries
Dehiscent (hypertrophic) scarExpanded (hypertrophic) scar, wider than original scar borders
Small keloidFocal, itching, red, scar bed, extending beyond original scar. Scar formation up to one year after trauma; does not resolve spontaneously. Frequent recurrence after surgical monotherapy. Individual and depending on site.
Large keloidLarge exophytic scar larger than 0.5 cm, usually painful and itching, can also arise from small scars. Possible scar growth for several years.
Normotrophic scar with contour problemsWith increased tension, pocket formation, diagonal contracture due to oblique incision, step-offs with adaption of different tissue thicknesses, or trapdoor phenomena.
Atrophic scarIndented scars

Documentation

The documentation of pathological scars to compare scarring status at baseline with the results of treatment is important and should be done for every patient. In general, documentation should be reproducible, easy to use, precise, and non–invasive. Important parameters that may be objectified in the documentation of the scar include the size, thickness, color, perfusion, flexibility, and stability. Subjective parameters include pain, itching, impaired function, and aesthetic appearance. Various systems and schemes are available with which one can distinguish subjective from objective documentation. The Vancouver Scar Scale (VSS) (Table 4) is used primarily in clinical studies. In addition, the POSAS (patient and observer scar assessment scale), the VAS (visual analogue scale), the Stony Brook Scar Evaluation Scale (SBSES), and the Manchester Scar Scale (MSS) may be used. The subjective character and thus limited reproducibility and comparability between observers or even centers should also be taken into account. Objective approaches such as obtaining a mold of the exophytic scar with volume measurement, are optimal (Figure 7). This method is simple. quickly done and has proven to be feasible in everyday clinical practice. Along with the intensity of vascularization, volume and redness are important clinical factors. Redness may be measured using diverse color measurement devices in various color modes. Yet, given the complexity of the technique, and the high cost of the devices, it is not feasible for everyday use in clinical practice. Measuring the size of the scar, as well as the use of standardized photo documentation (i.e., same light source [temperature differences yield different color measurements] and same distance) are advised. Three-dimensional photo systems are optimal. In addition to virtually standardized image quality, they have software-supported options for volume measurement and depiction of redness (Figures 8, 9).

Table 4. VSS (Vancouver Scar Scale) [11]
 Scar characteristicsScore
VascularityNormal0
 Pink1
 Red2
 Violet3
Pigmentationnormal0
 Hypopigmented1
 Hyperpigmented2
Flexibilitynormal0
 Soft1
 Yielding2
 Firm3
 Hard4
 Contraction5
SizeFlat0
 < 2 mm1
 2–5 mm2
 > 5 mm3
 Total13
Figure 6.

Immature scar, postoperative, two months.

Figure 7.

Modeling of two silicon components (a). Taking an imprint (b). After short-term hardening, for example, a filling with H2O is made (c). Subsequent aspiration: 1 ml = 1 cm3 (d).

Figure 8.

3D photography of acne keloids on the right shoulder with measurement of the volume (Vectra, Canfield, USA).

Figure 9.

3D image with red value depiction of sternal keloids (Vectra, Canfield, USA).

Scar treatment

From a patient standpoint, the result of surgery is usually measured by the quality of the scar, since it is the only visible parameter: “A beautiful scar usually comes from a good surgeon.” Given this perception, it is essential to thoroughly inform and educate the patient. Along with pathological scars, such as keloids and hypertrophic scars, dehiscent, atrophic, and normotrophic scars with contour problems are possible. The pathogenesis of scars with contour problems is well understood, making them easier to treat. Keloids and hypertrophic scars are more difficult to treat, given that the pathomechanism is only partly understood. The indication is assessed on an individual basis and is based on the patient's complaints. Treatment of pathological scars should be based on the current S2K guidelines [8]. The success of treatment depends on the individual situation at the time of the initial visit as well as the experience of the treating physician. One should try to put the patient's expectations into perspective by thoroughly educating him or her, discussing the potential for recurrence or treatment failure. The treatment method of choice cannot be standardized for scars; combination treatment is often needed [8].

Differentiating between individual scar types may be clinically difficult in some patients, but it is important in terms of treatment. In addition to clinical morphology, scar types differ in regard to histopathology and immunohistochemistry [9].

The best scar treatment is scar prevention. Scar formation is a result of any operation or trauma. Predisposing factors must be taken into account before every operative (initial) intervention: these include scar history, skin type (from Fitzpatrick III onward), patient age, skin tension, lines of tension, location (ear, shoulder girdle, chest, near joints, etc.), and size. Finally, surgical technique also has an influence (atraumatic, multi-layer closure, suture material, suture technique, placement of dressing, dressing changes, wound care, removal of sutures, etc.) on the resulting scar.

Surgical planning is paramount for the final result for almost all scar types in any operation. Especially in patients with pre-disposing factors, as well as for scar correction, the following should be taken into account:

  • Plan the lines of incision along the skin cleavage lines (Figure 10),
  • Vertical incisions,
  • Atraumatic treatment of wound margins (without crushing, selection of suitable surgical instruments),
  • Minimization of centrifugal tension during surgery,
    • Minimization of centripetal tension (adaption) by: sufficient undermining or tension-free grafting, subcutaneous/dermal-suture to relieve tension,
    • Dressings (strips, bandages on extremities),
  • Suitable suture material,
  • Suture technique,
  • Dressing changes/wound care,
  • Avoid postoperative infections,
  • Time of suture removal,
  • Adjuvant conservative therapy.
  • Preventive measures in patients with elevated risk include [10]:
  • Hypoallergenic micropore bandages with elastic properties,
  • Silicone gel dressings/ointments (after re-epithelization, they should be promptly applied and used for at least 12 hours a day for a few weeks),
  • For severe scarring, intralesional triamcinolone injections should be used.
Figure 10.

Langer lines dorsal (a), ventral (b), face (c), head lateral (d) (modified according to Arco et al.).

Scar correction

Indication

Hypertrophic scars and keloids are benign skin changes. Very rarely, carcinomas may develop at the site of the scar many years later. Issues include the aesthetic appearance, itching, pain, and possible functional impairment (joint mobility). The indication for scar treatment must be made on an individual basis, taking into account the scar type, the patient history, the age of the scar, potential complications, as well as the possibility of recurrence. Especially with hypertrophic scars, an expectant approach may be taken, given that this type of scar may resolve completely within one year, or up to two years. The individual history of prior scars is useful. In addition, it is difficult to distinguish them from immature scars in early stages.

The first step is to diagnose the type of scar (Tables 2 and 3). This is essential for further treatment. While normotrophic scars with contour problems are clinically obvious, differentiating between hypertrophic and immature scars and keloids may be difficult. In keloid scars, the clinical feature of overgrowth beyond the former wound margins is a useful feature. To differentiate between immature scars, it is useful to know when the trauma and intervention occurred, as well as the subsequent growth behavior (improvement?).

Scars with contour problems, dehiscent scars: depending on the cause of the contour problem, and given appropriate indications/patient's wishes, revision is usually adequate. The revision comprises simple scar excision, thinning of the flap, correction of the adaptation level, and relief or distribution of tension. Ablative options with laser may also be used, depending on the clinical appearance. Postoperative application of silicone gel may also aid healing of the scar.

Immature scars: An expectant approach should be taken. Depending on the patient history and progress, to prevent the potential development of a pathological scar, silicone gel dressings, compression dressings, or laser treatment (e.g., pulsed-dye laser) may be used.

Therapy options

An enormous range of treatments are now available for scarring. These vary in terms of invasiveness and the possibility for combining them. They should be selected on the basis of scar type, location, size of the scar, symptoms, clinical appearance, how long the patient has had it, and history of prior “scar behavior.” Optimal scar therapy requires close/intense involvement of the patient. Scar treatment is generally more than once-quarterly therapy, but rather is performed in short intervals.

Before any treatment, thorough education (including discussing the potential for recurrence) is needed, and documentation (see above) should be obtained.

Non-invasive therapy options

Corticosteroids

Corticosteroids are among the most important agents used to treat scars. Their effect is in the inhibition of iNOS transcription (inducible NO synthase) and a decrease in collagen production as well as inhibition of synthesis of the collagenase inhibitor alpha-2-macoglobulin. Attention should be paid to strict intralesional injection of triamcinolone acetonide; this is identifiable as a blanching effect (Figure 11). Triamcinolone acetonide may be administered, for instance, in a crystal suspension with 10–40 mg/ml (max. 5 mg/cm2) as a pure agent, or in dilution every four weeks [12]. Potential adverse effects may occur if administration is too deep and include lipoatrophy or generalized pain, crystal deposition, telangiectasias, infections, or pigmentation changes. The success rate is 50–100 %; recurrences occur in 9–50 % [13]. In corrective surgery, in our own experience, direct intraoperative/postoperative administration is a proven method.

Figure 11.

“Blanching effect” during intralesional triamcinolone injection.

Cryotherapy

Freezing the tissue with liquid nitrogen is an established method. It causes tissue damage due to exposure to cold with vasoconstriction and subsequent ischemia [14]. The scar is sprayed in two freeze-thaw cycles for 10–20 seconds with liquid nitrogen (Figure 12). In addition to the spray technique, contact and intralesional application of cold are possible. Based on recent studies, intralesional cryotherapy methods are effective and have led to a reduction in itching, pain, and keloid volume of 50–70 % with low rates of recurrence [15]. Undesirable effects include depigmentation, pain, and blistering with subsequent wound healing disorders or superficial infections. Studies have reported a high overall response rate of up to 82 % [8]. A combination of triamcinolone and cryotherapy has proven beneficial [12].

Figure 12.

Cryotherapy.

Pressure

Compression bandages cause a build-up of continuous pressure of 15–40 mmHg, triggering vascular hypoperfusion. The pressure should be maintained for the whole day for a period of months or even years. Good patient compliance is essential. This method is especially appropriate for large surface-area involvement (except for ear keloids: ear clips), such as burn injuries. Medical supply stores can provide individually-tailored bandages [8, 12].

Silicone

The use of silicone, whether as dressing, gel, or cream, is a popular and widespread treatment option, given that it is easily used and is widely recommended. Silicone may be used for 12–24 weeks for 12–24 hours per day. The mechanism of action is not entirely understood, but is believed to be due to increased tissue hydration. This is thought to lead to a reduction in angiogenesis and thus diminished capillary circulation in the scar tissue. There are a number of studies on this topic showing the benefit of silicone. A recent study has published contradictory results, however, showing that there are no clear subjective or significant, objective differences [16].

Radiotherapy

Ionizing rays have anti-proliferative and anti-inflammatory effects. Postoperative irradiation should be done within 24 hours with a total dosage of about 12 Gy in six to ten fractions up to 2 Gy (daily or every other day) each. The exact dosage, as well as the type of radiation and quality, should be determined by a radiologist. Side effects include erythema, hyperpigmentation, loss of pigmentation, xerosis, and telangiectases [8].

Botulinum toxin A

Botulinum toxin A may also be used to relieve tension about the wound. A prospective, placebo-controlled, randomized study has reported significantly improved clinical appearance of the scar in terms of frontal findings [17]. Possible complications, costs, and benefits should thus be carefully considered.

Interferon (INF)

Interferon α-2b is injected intralesionally twice at intervals of four to seven days as an off-label treatment. To prevent recurrence, it may be injected immediately postoperatively. Interferon-alpha and -gamma reduce collagen I/III synthesis as well as glycosaminoglycan formation. In addition to flu-like symptoms, pain and inflammatory reactions may occur at the injection site [8].

5-fluorouracil (5-FU)

In the United States, intralesional administration of 5-FU (50 mg/ml with a total dosage of a maximum of 50–150 mg per session and a maximum of 16 injections) once weekly for up to 16 weeks, is used as a therapy option. 5-FU acts by inhibiting the fibroblast proliferation. Current guidelines in Germany do not recommend it for treatment of hypertrophic scars. It may be an alternative, however, for the treatment of refractory keloids. Contraindications include anemia, leukopenia, thrombocytopenia, pregnancy, infections, and bone marrow suppression. A blood count should be taken at the beginning of treatment and after four sessions. Treatment is off-label [8].

Imiquimod

Imiquimod is an immunomodulator which induces the formation of cytokines such as TNFα and INFα. It thus has an inhibitory effect on collagen production. Topical application for scar treatment is done off-label; treatment of postoperative patients has yielded some good results [12]. Yet, on the whole, the results are contradictory. Due to lacking and controversial data, no recommendations may be made at present [8].

Onion extract (Extractum cepae)

It is believed that onion extract has anti-inflammatory, bactericidal properties, as well as acting against fibroblast- proliferation. It is given several times daily and treatment may continue for several weeks of months. Treatment may begin after wound epithelization. In the current guidelines on scar therapy, onion extract may be used for hypertrophic scars or as an adjuvant therapy; it may also be used for prophylaxis/prevention of recurrence in hypertrophic scars and keloids [8].

Laser therapy

Ablative lasers such as Er:YAG and CO2 lasers have maximum absorption in H2O, causing vaporization of cell layers by delivery of short pulses. Laser treatment is an alternative to the customary method of shave excision. Depending on the scar characteristics and individual preferences, doctors may select either laser type. The advantage of laser removal is the fine adjustments possible in scar removal and virtually bloodless treatment. Many centers use Er:YAG lasers (2,940 nm), either as combination (ablative and thermal) therapy, or as a purely thermal (non-ablative) method for scar treatment. The delivery of heat in long-pulsed (sub-ablative) modes affects collagen connective tissue. The warmth induces a heat shock response (HSR), which is due to a temporary change in cellular metabolism. The result is formation of heat shock proteins (HSP). HSP70 is thought be essential to the production of the growth factor TGFβ. This plays an important role in general inflammatory cascade as well as in fibroblast processes [18]. The development of fractional methods now allows for the use of ablative-fractional (AFXL) and non-ablative fractional (NAFXL) systems. Based on evidence-based recommendations for fractional laser treatment, the NAFXL method is considered the method of choice, while AFXL comes in second for scar therapy [19]. In the future, transepidermal drug delivery may be a new treatment option, after fractional treatment [20].

Other non-ablative laser systems include lasers with the target chromophore oxyhemoglobin. Via coagulation, treatment produces vascular occlusion with subsequent hypoperfusion or tissue hypoxia. A few studies have reported good results with the 585 nm flashlamp-pumped pulsed dye laser for scar treatment. Goldmann and Fitzpatrick reported a significant improvement in erythematous hypertrophic scars after treatment with a 585 nm flashlamp-pumped pulsed dye laser. The result may be improved by combining treatment with intralesional administration of triamcinolone [21] [18]. One study found no significant relationship between the clinical result and fluence (3, 5, and 7 J/cm2). There was a better clinical response with lower fluence and multiple treatments (6 treatments in 4-week intervals) [22].

In general, before laser treatment, precise photo documentation should be done and the patient thoroughly informed. The patient should understand what may be realistically expected and, depending on the system used, he or she should be aware of the potential for recurrence, and in rare instances even worsening of the condition.

Operative therapy

Surgical correction of pathological scars should only be performed once the scar type has been determined. Caution is advised for immature scars and active -hypertrophic scars. Only if there is a manifest clinical problem, or if cosmetically indicated, and/or if there is tension, may surgical intervention be indicated. In keloids, surgical indications are stricter, given that excision alone is associated with high rates of recurrence. Surgery is thus the last option, after using and exhausting non-invasive methods. Most operations may be done under local anesthesia or tumescent anesthesia [23]. Only in combination with other accompanying treatment options such as cryotherapy, triamcinolone injections, compression dressings, radiotherapy, or imiquimod may this treatment be used (Table 5).

Table 5. Overview of the actually S2k guideline “Therapy of pathological scars” [8]
 Therapy of hypertrophic scars and keloidsPostoperative therapyPostoperative prophylaxis in high-risk patients/predisposition
CorticosteroidsRecommended; combination with cryotherapy advised.Keloids: advised.May be considered.
CryotherapyRecommended.Keloids: may be advisable individual patients.Not advised.
Surgical intervention

Depending on scar type, duration, and disfigurement.

Hypertrophic scar: treatment < 1 year is not advised, except with tension (relaxation of tension, e.g., with grafts) or cosmetic disfigurement.

Keloids: after exhausting conservative methods, except for keloids with a narrow base, or small, cosmetically disturbing keloids due to wound healing disturbances, primary operative therapy may be advised.

Keloids: intralesional triamcinolone, compression therapy, radiation therapy, cryotherapy. 
Ablative laser treatment

May be advised in scars that are not active and which have contour problems.

CO2 keloid removal as monotherapy is not advised.

For keloids with a narrow base, CO2 removal in combination with adjuvant therapies may be advised.

  
Non-ablative laser treatmentMay be advised for erythema reduction, e.g., for recent vascularized scars.  
Radiation therapyNot advised for hypertrophic scars; occasionally for keloids.Not used for hypertrophic scars, may be advised for keloids.Not advised.
Silicone gelMay be considered as adjuvant therapy.May be advised.May be advised.
Extractum cepaeHypertrophic scars: may be considered as adjuvant therapy.May be considered.May be considered.
Compression therapyMay be advised for large scars and keloids or for certain sites (e.g., ear).If location suitable, may be advised. 
FluorouracilNot advised for hypertrophic scars, may be advised for treatment-refractory keloids. Not advised.
InterferonNot recommended as monotherapy, may occasionally be considered in combination with triamcinolone.  

Excision

Surgical excision is the last resort in scar treatment. Depending on the scar type, age, and findings, this radical approach may be effective and perhaps the only possibility for significantly reducing large scars or tension.

Operative therapy of manifest hypertrophic scars and keloids is usually first done by excision and primary wound closure. This should not be done as monotherapy, but should be augmented by complementary options, as high recurrence rates are otherwise to be expected. Excision only, with a healthy margin, is no longer performed for keloids, due to the high recurrence rate. Rather, it should be performed in combination with administration of intralesional steroids, etc. For excisions without any accompanying therapy, the risk of recurrence is between 45 and 100 % [9]. In combination with triamcinolone, the recurrence rate may be reduced to 50 % [24]. Some studies suggest that excision of the scar while leaving a narrow margin of scar tissue lowers the recurrence rates for keloids and hypertrophic scars. Yet, others have reported the opposite [8]. Thus, the old discussion of incisions is still open, and either approach may be used. Due to the tendency of hypertrophic scars to regress spontaneously, surgical scar correction should be done at the earliest one year after the scar has formed.

A simple spindle-shaped excision is advisable if the scar is already following the corresponding lines of tension, with no contractures or tension, and is of a limited size given the site. The goal is not only excision, but also to minimize tension using suitable techniques (extensive undermining, multi-layered closure, suture technique) and minimize the contours.

Cosmetically, an S-shaped excision (lazy S) is very challenging. This causes a small improvement in the distribution of tension in regard to the lines of tension.

A Z-graft is a method for distributing tension by around 90 degrees. It is used primarily for relaxation of scar contractures. After the actual scar excision, a 60° incision is made at either end to make the letter “Z.” The two flaps are then switched. In addition to distributing tension, there is also diminished tension on the future scar. In longer scars, and/or with a small surrounding surface, serial Z-grafts may be used.

A W-graft is a further alternative. The scar is further cut in a zigzag fashion and adapted accordingly. This technique may be used, for instance, if the site is very narrow or if there is a risk of the scar going beyond an aesthetic unit. The distribution of tension is very low [9].

If the results of treatment are still not satisfactory after 3–6 sessions or 3–6 months, the treatment regime should be modified [8].

Table 5 provides a modified overview of current German guidelines on the treatment of pathological scars [8].

Summary

Scars of all types are an interesting topic in clinical practice; they are a concern for doctors as well as patients. The pathomechanism continues to be only partly understood. This is reflected in the lacking treatment options. Still, innovative options continue to be added to the treatment portfolio. At present, the goal is (unfortunately) not yet complete restoration, but rather merely a reduction of symptoms such as itching, pain, and contractures, as well as an improvement in aesthetic appearance. The “secret” of successful scar treatment is multimodal combination therapy at the right time and of appropriate duration. Additional studies and the development of treatment options are needed.

Acknowledgements

We thank Dr. M. Ziemer for her contribution to the histology section and for providing the histological images. For his critical reading of the manuscript, we thank Dr. M. Kendler. The high quality of the clinical photographs are thanks to Mr. M. Karsten.

Fragen zur Zertifizierung durch die DDA

  1. Eine reparative Regeneration (Restitutio ad integrum) ist …
    1. immer möglich.
    2. von der Pathogenese abhängig.
    3. vom Narbentyp abhängig.
    4. nur postfetal möglich.
    5. nur fetal möglich.
  2. Welches Kriterium ist für das Keloid untypisch?
    1. wächst über die Wundgrenzen hinweg
    2. verbleibt innerhalb der ursprünglichen Wundgrenze
    3. oft mit Juckreiz / Schmerz
    4. lokalisationsabhängig
    5. genetische Prädisposition
  3. Welche Faktoren haben keinen Einfluss auf die Entstehung von pathologischen Narben?
    1. Infektion
    2. Wundspannung
    3. Apoplex
    4. Traumata
    5. OP-Technik
  4. Welche Aussage über Keloide stimmt?
    1. Keloide bilden sich nach einem Jahr immer spontan zurück.
    2. Keloide wachsen invasiv und destruierend.
    3. Keloide korrelieren mit dem Hauttyp.
    4. Keloide sollen sofort hochdosiert bestrahlt werden.
    5. Keloide betreffen nur ältere Patienten.
  5. Unreife Narben …
    1. können mit hypertrophen Narben verwechselt werden.
    2. gehen immer in ein Keloid über.
    3. müssen exzidiert werden.
    4. weisen auf eine pathologische Wundheilung hin.
    5. sind unbedingt mit UVB zu behandeln.
  6. Welche Aussage über OP-Techniken und Narbenprophylaxe stimmt nicht?
    1. Beachtung der Hautspaltlinien
    2. Beachtung atraumatischer OP-Techniken
    3. Beachtung der Zugspannung
    4. zur Patientenmobilitätsprophylaxe OPs nur in ITN möglich
    5. Beachtung der Nahttechnik
  7. Welche Aussage zur Narbenbehandlung trifft zu?
    1. Keloide sollten nur operativ entfernt werden.
    2. Hypertrophe Narben sollten nur bestrahlt werden.
    3. Dehiszente Narben sollten mit einer PDT behandelt werden.
    4. Die Prävention wird überschätzt.
    5. Die Prävention ist wichtig.
  8. Glukokortikosteroide …
    1. sind für die Narbentherapie ungeeignet.
    2. sollen streng intraläsional injiziert werden.
    3. sollen streng subkutan injiziert werden.
    4. zeigen bei richtiger Applikation einen „Redness“-Effekt.
    5. können für dehiszente Narben verwendet werden.
  9. Welche Aussage zur postoperativen Prophylaxe bei Prädisposition/ Risikopatienten stimmt nicht?
    1. Glukokortikosteroide können erwogen werden.
    2. Silikongel kann empfohlen werden.
    3. Zwiebelextrakt kann erwogen werden.
    4. Radiatio kann nicht empfohlen werden.
    5. Radiatio kann empfohlen werden.
  10. Postoperativ sollten Patienten …
    1. in die Sauna.
    2. ein Lichthardening durchführen.
    3. proteinreiche Ernährung einhalten.
    4. Sonnenschutz einhalten.
    5. frische Narbe belasten.

Liebe Leserinnen und Leser,

der Einsendeschluss an die DDA für diese Ausgabe ist der 17. Januar 2014. Die richtige Lösung zum Thema „Lupus erythematodes. Teil I: Epidemiologie, Genetik und Immunologie“ in Heft 8 (August 2013) ist: 1c, 2d, 3c, 4d, 5a, 6b, 7c, 8b, 9a, 10b.

Bitte verwenden Sie für Ihre Einsendung das aktuelle Formblatt auf der folgenden Seite oder aber geben Sie Ihre Lösung online unter http://jddg.akademie-dda. de ein.

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