gms | German Medical Science

GMS Verbrennungsmedizin

Deutsche Gesellschaft für Verbrennungsmedizin (DGV)

ISSN 1869-1412

Medical needling: improving the appearance of hyperthrophic burn-scars

Review Article

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  • author Matthias C. Aust - Department of Plastic, Hand and Reconstructive Surgery, Hannover Medical School, Hannover, Germany
  • Kerstin Reimers - Department of Plastic, Hand and Reconstructive Surgery, Hannover Medical School, Hannover, Germany
  • corresponding author Peter M. Vogt - Department of Plastic, Hand and Reconstructive Surgery, Hannover Medical School, Hannover, Germany

GMS Verbrennungsmedizin 2009;3:Doc03

doi: 10.3205/vmed000007, urn:nbn:de:0183-vmed0000076

Published: October 6, 2009

© 2009 Aust et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Abstract

Patients with postburn scarring frequently request help in improving their aesthetic appearance. A variety of operative and non operative procedures are performed to improve post burn scar quality. Most of these procedures have in common that they injure or destroy the epidermis, its basal membrane or violate the papillary dermis and thus lead to fibrosis in the residual dermis and may cause potential adverse effects such as dyspigmentation or scarring. The ideal treatment would be to preserve the epidermis and promote normal collagen and elastin formation in the dermis. It was recently shown in clinical trials that medical needling is an alternative for safely treating postburn scarring, wrinkles, stretch marks and for smoothening the skin without the risk of dyspigmentation or scarring. In contrast to ablative laser treatments, the epidermis remains intact. Thus, the procedure can be repeated safely and is also applicable in regions where laser treatments and deep peels are of limited use.


Introduction

Patients with postburn scarring frequently request help in improving the aesthetic appearance of their residual cicatricial deformity. It is their hope to eradicate the physical evidence of a scar and to re-establish a normal appearance and texture to the site of injury. The quality-of-life is an important issue in this regard.

This quest has led to the application of many different topical therapies which have included carbon dioxide (CO2) laser resurfacing, dermabrasion and deep chemical peels. These treatments all follow the same principle: the level of the offending scar is taken down closer to the level of the surrounding normal skin [1], [2], [3], [4]. The ideal treatment would be to do exactly the opposite: improving the scar quality and building up the scarred tissue to the level of the normal skin. In addition it is important to recognize that ablating the epidermis of scarred skin with subsequent protracted reepithelialization may render the skin more sensitive to photodamage and dyschromia [5], [6], [7]. In order to rejuvenate scarred skin and re-establish a more normal appearance the maintenance or establishment of a perfect epidermis with natural dermal papillae, good hydration, normal colour, and normal resilience is required.

Percutaneous collagen induction (PCI) therapy was introduced in 1997 as an indication for the treatment of scars and wrinkles [8]. Recently it could be shown that PCI is a safe alternative method for the treatment of postburn injury, wrinkles, stretch marks and for smoothening the skin without the risk of dyspigmentation or scarring [9].


Technique

Orentreich and Fernandes independently described “subcision” or dermal needling [8], [10]. This involves pricking the skin and then scarifying the dermis with a needle to build up connective tissue under scars. However, this technique could not be used over large surface areas. Camirand and Doucet used a tattoo gun to treat scars with “needle abrasion” [11]. The fundamental similarity of these different techniques is that the needles disrupt the old collagen structures that connect the scar with the upper dermis. The associated trauma induces inflammatory cascade of a regular wound-healing. The scar collagen is broken down and replaced with new collagen under the epidermis.

Based on these principles, Fernandes developed a new technology, percutaneous collagen induction, to initiate the natural posttraumatic inflammatory cascade by rolling needles vertically, horizontally, and diagonally with pressure over the treated area ([8], Figure 1 [Fig. 1]). The needles penetrate 2.5 to 3 mm into the dermis leading to thousands of dermal microwounds that result in a confluent zone of very superficial inflammation, triggering the release of growth factors that ultimately result in increasing the patient’s own normal woven collagen (Figure 2 [Fig. 2]). For percutaneous collagen induction, the skin should be anesthetized with regional nerve blocks and/or infiltration of local anesthetic and conscious sedation (where large or sensitive areas are being treated), or general anesthesia.

Preoperative care

The patients’ skin should be prepared preoperatively for at least 1 month with vitamin A and vitamin C cream applied topically twice daily to maximize dermal collagen formation.

The necessity for using vitamins A and C for percutaneous collagen induction has been well described by Aust [9], [12]. Vitamin A, a retinoic acid, is an essential vitamin (actually a hormone) for skin. It expresses its influence on 400 to 1000 genes that control proliferation and differentiation of all the major cells in the epidermis and dermis [13], [14], [15], [16].

Retinyl esters are the main form of vitamin A in the skin and for these reasons, we have elected to apply vitamin A in its ester forms (retinyl palmitate and retinyl acetate), with little use of retinal or retinoic acid directly.

In recent years we learned that transforming growth factor (TGF)-β plays an enormous role in the first 48 hours of scar formation. Whereas TGF-β1 and TGF-β2 promote scar collagen, TGF-β3 seems to promote regeneration and scarless wound healing with a normal collagen lattice [17], [18]. Vitamin A may control the release of TGF-β3 in preference to TGF-β1 and TGF-β2 because, in general, retinoic acid seems to favour the development of a regenerative lattice-patterned collagen network rather than the parallel deposition of scar collagen found with cicatrization.

Vitamin C is also essential for the production of normal collagen [13], [14], [15], [16]. Percutaneous collagen induction and vitamin A switch on the fibroblasts to produce collagen and therefore increases the need for vitamin C.

Post-operative care

The patients have no open wound and consequently require only a short healing phase. Immediately after medical needling, the area is swollen and superficially bruised (Figure 3 [Fig. 3]). After the initial bleeding stops within a few minutes, there is a serous ooze, which stops within the first few hours after the operation. To absorb the bleeding and serous ooze, the treated area should be covered with cool, damp swabs that are periodically replaced for the first 2 hours after the operation. The skin is finally washed with a tea tree oil-based cleanser and the vitamin A and C regimen immediately starts again. Patients usually do not require post-operative analgesia if the procedure has been performed under local anaesthesia. When the procedure has been performed under general anaesthesia without any local/topical anaesthetic, the patient may complain of burning for the first hour post-operatively, so it is wise to administer an analgesic at the end. The edema can be quite significant when needling has been performed but starts resolving from the second day post-operatively, and by the fourth or fifth day there is usually only mild erythema remaining. Patients are usually able to return to normal daily life by the seventh day. Discolouration disappears usually within five days.


Pathophysiology of percutaneous collagen induction

Percutaneous collagen induction via medical needling aims to stimulate collagen production by producing microwounds and initiating the normal postinflammatory chemical cascade on this way. There are three phases in the body’s wound-healing process, which follow each other in a predictable fashion. This has been well described in The Biology of the Skin by Falabella and Falanga [19]. Platelets and eventually neutrophils release growth factors such as TGF-α, TGF-β, platelet-derived growth factor, connective tissue activating protein III, connective tissue growth factor, and others that work in concert to increase the production of intercellular matrix. Monocytes then also produce growth factors to increase the production of collagen III, elastin, glycosaminoglycans, and so forth. Approximately 5 days after skin injury, a fibronectin matrix forms with an alignement of the fibroblasts that determines the deposition of collagen. Eventually, collagen III is converted into collagen I, which remains for 5 to 7 years. With this conversion, the collagen tightens naturally over a few months. Percutaneous collagen induction causes even further smoothening of scars several weeks or even months after the injury [9], [12].

During the usual conditions of wound healing, scar tissue is formed with minimal regeneration of normal tissue. It seems that the controlled wound milieu created during percutaneous collagen induction, by minimizing the usual stresses such as exposure to air, infection, mechanical tension, and so forth, may take us closer to regenerative healing.

Scarless healing induced by transforming growth factor-beta3

We have learned in recent years that transforming growth factor beta (TGF-β) plays an enormous role in scar formation. While TGF-β1 and TGF-β2 promote scar collagen, TGF-β3 appears to promote scarless wound healing with a normal collagen lattice [18], [20]. Embryonic wounds that heal without a scar are characterized by low levels of TGF-β1 and TGF-β2, as well as high levels of TGF-β3, a skin morphogenetic factor predominantly synthesized by keratinocytes and fibroblasts. By contrast, adult wounds contain predominantly TGF-β1 and TGF-β2 [17]. Ferguson's research has focused on the TGF family of molecules where TGF-β3 elicits a scar-free or regenerative healing response, whereas TGF-β1 and TGF-β2 elicit a fibrotic scarring response.

It could be shown that percutaneous collagen induction leads to an initial upregulation of TGF-β1 and -β2 two and four weeks after treatment followed by a strong downregulation at eight weeks post needling for TGF-β1 and -β2. Furthermore there is a strong upregulation of TGF-β3 two weeks post needling without any downregulation at level four and eight weeks post-operatively (own data, submitted). On the basis of this research we can postulate that PCI offers a novel modality to rejuvenate and improve both skin appearance and quality by lessening or preventing scarring.

Skin regeneration and remodeling of extracellular matrix

Another study could show that PCI modulates gene expression in skin of those genes that are relevant for extracellular matrix remodeling (own data, submitted). It was demonstrated that PCI with topical vitamins resulted in a 140% increase in epidermal thickness; an increase in gene and protein expression of collagen I, glycosaminoglycans (GAGs) and growth factors such as vascular endothelial growth factor (VEGF), epidermal growth factor (EGF) and fibroblast growth factor (FGF7) which are all relevant for skin regeneration. The collagen fiber bundles were found to be qualitatively increased, thickened, and more loosely woven in both the papillary and reticular dermis after medical needling. The epidermal-dermal interface showed regular dermal papillae; cellular polarity and normal epidermal differentiation appeared to be maintained; and the connective tissue network within the reticular dermis was regularly thickened and organized what is shown in a healthy collagen matrix. In this study the regeneration processes after percutaneous collagen induction have been observed to qualify and quantify the changes in type I collagen. PCI might bring us closer to the idea in regenerating healthy skin in vivo.


Clinical outcome of percutaneous collagen induction

Recently, the safety and efficiency of percutaneous collagen induction could be shown for the treatment of wrinkles, scars and stretch marks [9]. 480 patients were treated by medical needling and evaluated for the result one year postoperatively. There was a significant increase in patient satisfaction after 12 months. Additionally, the histological analysis show a thickened epidermis without any evidence for inury or damage. In opposite to ablative treatments the epidermis remains intact. For this reason, the procedure can be repeated safely and is also suited to regions where laser treatments and deep peels cannot be performed. Most patients will begin to see results after the very first appointment. Depending on the degree of improvement that is required a series of needling sessions can be necessary.

In another study 16 patients were treated with medical needling for postburn scarring due to deep 2nd degree burn injury (own data, submitted). As the study mentioned above, the patients were evaluated or their satisfaction and histological analysis were performed 12 months postoperatively. The improvement was rated by the patients as mean of 80 percent better than before the treatment (Figure 4 [Fig. 4]). Histological examination demonstrated a considerable normalisation of the extracellular collagen-elastin matrix in the reticular dermis and an increase in collagen deposition at 12 months post-operatively. The collagen also appears to have been laid down in a normal lattice pattern, rather than in parallel bundles as seen in scar tissue (Figure 5 [Fig. 5]). Hematoxylin and eosin staining demonstrated a normal Stratum corneum, thickened epidermis (45 percent thickening of the Stratum granulosum), and normal rete ridges at 1 year post-operatively (Figure 6 [Fig. 6]). However, the original structure of normal and healthy skin could not be restored. This is shown especially by a decreased cell density in the dermis and epidermis and a partial irregular fiber structure in the dermis compared to normal skin.

Percutaneous collagen induction and postinflammatory dyspigmentation

An often adverse effect of ablative procedures are pigmentation problems caused by the destruction or injury of the epidermis and basal membrane which can lead to fibrosis of the papillary dermis [21], [22], [23]. These damages can result in hypo- or hyperpigmentations. There was no evidence for dyspigmentation in any of the clinical trials of percutaneous collagen induction [9].

The effects of percutaneous collagen induction on melanocytes and the mediators of postinflammatory dyspigmentation were examined in another trial [12]. No signs of dermabrasive reduction of epidermal thickness or damage of the epidermis or basement membrane were evident. The number of melanocytes was unchanged after medical needling. Additionally, DNA microarray experiments demonstrated that Interleukin-10 was increased after percutaneous collagen induction therapy, while the expression of the MC1R gene (Melanocortin 1 receptor), coding for a melanocyte-stimulating hormone, indicated a faint down-regulation both up to 2 weeks post-operatively. Therefore, in opposite to dermabrasive procedures, percutaneous collagen induction therapy appears to have a lower risk of dyspigmentation.


Advantages and disadvantages

Percutaneous collagen induction has proven to be very effective in minimizing burn scars, by promoting the replacement of scar collagen with normal collagen and the reduction of depressed and contracted scars. As opposed to ablative laser treatments, the epidermis remains intact and is not damaged. For this reason, the procedure can be repeated safely and is also suited to regions where laser treatments and deep peels cannot be performed. Additionally, the patients have no open wound and consequently require only a short healing phase. Because the epidermis and Stratum corneum are only clefted and are never removed, there is no exposure to air and no risk of photosensitivity or any postinflammatory dyspigmentation.

Disadvantages of the procedure are potential blood exposure of the surgeon, the need for complete anaesthesia of the treated area, unsightly swelling and bruising for the first 4 to 7 days. Also the result will have to be expected after a longer interval than with laser resurfacing [9], [10].


Notes

Conflicts of interest

Dr. Matthias Aust is the Medical Consultant for Care Concept, Distributors for Environ Skin Care Products and Roll-CitR in Germany.

Prof. Vogt has no sources of funds supporting the work and no financial interest.


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