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 Table of Contents  
LETTER TO EDITOR
Year : 2013  |  Volume : 21  |  Issue : 1  |  Page : 79-80

Effect of chronic tension on burn scar


1 Department of Surgery, S.V.B. Patel Hospital, New Delhi, India
2 Department of Surgery, M.A.M.C. and L.N. Hospital, New Delhi, India
3 Department of Pathology, Gandhi Medical College, Bhopal, Madhya Pradesh, India
4 Department of Pathology, Shyam Shah Medical College, Rewa, Madhya Pradesh, India

Date of Web Publication22-Nov-2013

Correspondence Address:
Jayanta Bain
Village+Post: Betai, Nadia, West Bengal - 741 163
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-653X.121891

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How to cite this article:
Bain J, Singh AK, Sulya M, Baghel VS. Effect of chronic tension on burn scar. Indian J Burns 2013;21:79-80

How to cite this URL:
Bain J, Singh AK, Sulya M, Baghel VS. Effect of chronic tension on burn scar. Indian J Burns [serial online] 2013 [cited 2020 Jan 24];21:79-80. Available from: http://www.ijburns.com/text.asp?2013/21/1/79/121891

Madam,

Formation of burn scar is a complication of deep burn and it may cause some degree of restriction in joint movements. But most deadly complication from burn scars seems to be the "Marjolin's ulcer" - malignancy of the burn scar. Here we report a case of squamous cell carcinoma of a burn scar over the elbow joint, where along with other factors, chronic stress and tension appear to be a predisposing factor.

A 52-year-old male was admitted in our hospital with two ulcerative lesions arising from his right proximal forearm. He had a history of flame burn 45 years ago, and was treated at home. He developed burn scar on the middle part of his left upper limb running over the elbow joint. Though there was no restriction of movement to his left elbow joint, the scar over the joint became maximally starched and tensed during extension and supination. By profession he was a motor car driver since last 30 years.

On examination, two ulcers of size 3 cm × 3 cm, and 1.5 cm × 1.5 cm were seen with everted edges and well-defined margins; the surfaces were covered with necrotic cast [Figure 1]. On palpation the ulcers were nontender and ulcer base was not fixed to underline tissue. Axillary lymph nodes were not palpable and other systemic examinations were within normal limits.
Figure 1: Ulcers near the cubital fossa of left hand

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Wide local excision of the ulcer was done and a split thickness skin graft was placed to cover the wound. The postoperative period was uneventful. On histopathology well-differentiated squamous cell carcinoma, consistent with Marjolin's ulcer, was found with free resection margin [Figure 2].
Figure 2: Well-differentiated squamous cell carcinoma (HandE ×100)

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Burn scar ulcers are also known as Marjolin's ulcer. [1] Integument through its life experiences a number of carcinogens, but mostly resisted, because skin has a number of defense mechanisms, which is completely or partially lost in a burn scar.

Various theories concerning the mechanism of scar malignancy development are proposed. Scar tissue is generally less resistant to injuries and it heals with difficulty, especially in sites such as the joint area. It is postulated that cells forming the scar tissues release toxins by autolysis and heterolysis. The healing phase is therefore prolonged and groups of rapidly dividing cells susceptible to mutagens form. [2] Burn scars are also frequently depigmented because they have no or very few melanin producing neuro-endocrine cells melanocytes. Melanin plays a major photo-protective role by absorbing, scattering, photo-oxidizing, and scavenging free radicals and prevents damage to DNA, proteins, and cell membranes, to resists the carcinogenic effect of ultraviolet (UV) rays; [3] thus, hypo-pigmented tissue becomes more vulnerable to UV radiations. These scar tissues are relatively avascular, thus become an immunologically crippled site where tumor cells can escape the immunological elimination processes [4] and this is why Marjolin's ulcers are more aggressive in patients with HIV where body immunity decreases. [5]

In our case, along with the above factors, the epithelium of the burn scar over the cubital fossa was maximally and repeatedly stressed over years, as the patient was a car driver. From the experience of tissue expansion we know that when skin is stressed, the tissue surface area increases (mechanical creep) which causes disruption of gap junctions between the epithelial cells, resulting in cell proliferation (biological creep). [6],[7] On molecular level a number of growth factors - cytokines, hormones, adhesion molecules, cytoskeletal elements, and signal transduction proteins - are induced in response to expansion; [8] all this molecules are known factors affecting tumor development. [9] This repeated stress causes may have caused a number of mechanical and biological creep thus inducing breakdown and micro-tear with increased turnover of the epithelial calls. Thus repeated trauma also becomes an etiological factor. [10]

Due to lack of infrastructure in India and other low income countries, primary skin grafting of the burn sites is not always possible, so burn patients are treated conservatively. Thus, burn scar formation and restriction of joint movement are frequent complications. In these situations, early skin grafting and/or Z-plasty to release tensions over the scars, particularly over the joints areas, should be done. This will decrease tension over the burn scar and will subsequently reduce the chances of occurrence of burn scar malignancy.

 
  References Top

1.Da Costa JC. Carcanomatous changes in an area of chronic, ulceration, or Marjolin's ulcer. Ann Surg 1903;37:496-502.  Back to cited text no. 1
[PUBMED]    
2.Turegun M, Nisanci M, Guler M. Burn scar carcinoma with longer lag period arising in previously grafted area. Burns 1997;23:496-7.  Back to cited text no. 2
    
3.Costin GE, Hearing NJ. Human skin pigmentation: Melanocytes modulate skin colour in response to stress. FASEB J 2007;21:976-94.  Back to cited text no. 3
    
4.Castillo JL, Goldsmith HS. Burn scar malignancy in a possible depressed immune setting. Surg Forum 1968;19:511-3.  Back to cited text no. 4
[PUBMED]    
5.Rahimizadeh A, Shelton R, Weinberg H, Sadick N. The development of a Marjolin's cancer in a human immunodeficiency virus-positive hemophilic man and review of the literature. Dermatol Surg 1997;23:560-3.  Back to cited text no. 5
[PUBMED]    
6.Bauer BS. Tissue Expansion. In: Thorne CH, Beasley RW, Aston SJ, Bartlett SP, Gurtner GC, Spear SL, editors. Grabb and Smith's Plastic Surgery. Philadelphia: Wolters Kluwer Lippincott Williams and Wilkins; 2006. p. 84.  Back to cited text no. 6
    
7.DeFilipo RE, Atala A. Stretch and growth: The molecular and physiologic influences of tissue expansion. Plast Reconstr Surg 2001;109:2450-62.  Back to cited text no. 7
    
8.Takei T, Mills I, Aria K, Sumpio BE. Molecular basis for tissue expansion: Clinical implications for the surgeons. Plast Reconstr Surg 1998;102:247-58.  Back to cited text no. 8
    
9.Tan MCB, Goedegebuure SP, Eberlein TJ. Sabiston Text Book of Surgery: The Biological Basis of Modern Surgical Practice. In: Townsend Jr CM, Beauchamp RD, Evers BM, Mattox KL, editors. New Delhi: Elsevier India Private Limited; 2012. p. 695-703.   Back to cited text no. 9
    
10.Ochenduszkieewicz U, Matkowski R, Szynglarewicz B, Kornafel J. Marjolin's ulcer: Malignant neoplasm arising in scars. Rep Pract Oncol Radiother 2006;11:135-8.  Back to cited text no. 10
    


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