Eur J Plast Surg (1995) 18:301-304 ~g,gg~a2, l r ~ , _ . lfIStlC

D u r g e r y © Springer-Verlag 1995

The keloid triad hypothesis (KTH): a basis for keloid etiopathogenesis and clues for prevention P.T. Agbenorku 1, H. Kus 2, T. M y c z k o w s k i 1

1 Department of Plastic Surgery, State Railway Hospital, Wroclaw, Poland 2 Department of Surgical Traumatology, Medical Academy, Wroclaw, Poland

Abstrac t . The basis of ke lo id format ion and its subse- quent behavior , the very high inc idence of recurrence af- ter resection, and other forms of t reatment are not ful ly unders tood. Keloids still r emain a d i l emma in plast ic sur- gery. Ana lyz ing the e t iopathogenes is of keloids in a large number of patients in Ghana and in Poland led to a con- cept of ke lo id tr iad hypothes is (KTH). This is def ined as a group of three e t io logic factors which must s imulta- neous ly coexis t and interact for keloids to form. The etio- logica l factors are: genet ic l inks; bacter ial , viral or any type of infect ive agent; type of surgery - sutures, tension of suture lines, locat ion of sutures in re la t ionship to the body skin lines of tension; etc. At least three of these fac- tors must be present , inter-correlate, in order to form a keloid. These factors have been sub-d iv ided into two groups - major (or main) and minor (or auxi l iary) and are ana lyzed in this paper. In each si tuat ion at least one ma- j o r factor must be present in order for a ke lo id to form.

K e y words: Kelo id t r iad hypothes is (KTH) - M a j o r and minor ke lo id e t io logic factors - Ke lo id prevent ion - Re- sect ion

A ke lo id is def ined as a f i rm tumor- l ike benign nonen- capsu la ted overgrowth of scar t issue occurr ing main ly in the skin, it has we l l -de f ined marg ins and tends to invade the no rma l non- t r aumat i zed skin [2-4] . As a rule it forms in pos t t raumat ic , surgical , pos tburn scars or as a resul t of different skin lesions. Thus, it is an abnormal i ty of the wound hea l ing processes charac te r ized by the de- pos i t ion of excess ive amounts of col lagen. Kelo ids can occur wi thout def ini te known causes ( injury or skin dis- ease) - the so ca l led "spontaneous ke lo ids" [2]. Kelo ids occur more in b lacks than in whites , the rat io be ing ap- p rox ima te ly 9:1. In addi t ion, there may be fami l ia l inci-

Present address: Presented at the VII Congress of the European Section of International Confederation of Plastic, Reconstructive, and Aesthetic Surgery, Berlin, Germany, June 2-5, 1993

Correspondence to: RT. Agbenorku, University, RO. Box 448, U.S.T., Kumasi, Ghana

dence which suggests a genet ic basis [2]. Espec ia l ly typ- ical is the very high recurrence after resec t ion or any other fo rm of t rea tment [1].

Cl in i ca l m a t e r i a l

320 keloid patients were analyzed: 270 from Ghana and 50 from Poland. They ranged from 8 to 69 years of age; the mean age was 32.7 years, 102 males and 218 females (Fig. 1). The mean dura- tion of the keloids was 11.5 years (range 1-34 years). The age of the patients at primary keloid formation is shown in Fig. 2, from which it is clear that the optimum age for primary keloid forma- tion is 10 to 30 years.

The anatomical locations of the keloid scars were also ana- lyzed (Table 1). Keloids occur more in the upper parts of the body except in the central triangle of the face bounded by the eyes and the philtrum of the upper lip - the so called "keloid-free zone" [5] equilateral triangle of the face.

Each patient could clearly remember the cause of their primary lesion (Table 2), the three major causes being

• trauma of all types - 25.0% • skin infections - 22.5% • earlobe piercings - 22.5 %

There was no record of spontaneous keloids. It must be noted that post-burn wounds resulted in only 7.5% of the keloids, contrary to the widespread idea that keloids form usually on the basis of post- burn wounds. Most of the scars as a result of burns are ordinary hypertrophic scars and not keloid scars [1].

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Fig. 1. Histogram of sex distribution of patients

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31.9

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t t 81.9

A g e Groups (years)

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Fig. 2. Age of patient at primary keloid formation

Table 1. Anatomic location of the primary keloid

Anatomic location No of patients

1. Face 60 18.8 2. Ear(s) 55 17.2 3. Neck 38 11.9 4. Shoulders 25 7.8 5. Chest (excluding breast & sternum) 23 7.2 6. Breast(s) 20 6.2 7. Sternum 29 9.0 8. Back of trunk 15 4.7 9. Upper extremities 18 5.6

10. Abdomen 4 1.2 11. Suprapubic area 13 4.1 12. Gluteal regions 6 1.9 13. Lower extremities 14 4.4

320 100.0

Table 2. Etiology of primary keloid

Factor Frequency %

Trauma-scratches, abrasions, 80 25.0 lacerations, e t c - Skin infections -acne, pimples, 72 22.5 chicken pox, boils, etc Earlobe piercing 72 22.5 Post-surgery 40 12.5 Post-burns 24 7.5 Post-vaccination 16 5.0 Scarification 16 5.0 Spontaneous 0 0

320 100.0

The keloid triad hypothesis (KTH)

Analyzing the etiopathogenesis in these patients, a concept of Ke- loid Triad Hypothesis (KTH) is proposed. This is defined as a group of three etiological factors which must simultaneously co-

Table 3. Major and minor keloid etiologic/risk factors

Major etiologic factors 1. Race: eg. African: 2. age: 10 to 30 years is the optimum age of patients

in whom primary keloids develop; 3. genetic: keloid-prone family or not; 4. anatomic location of the injury/wound:

keloids have predilection for the upper part of the body.

Minor etiologic factors 5. direction of incisions and sutures in relationship

to the normal skin lines of tension; 6. tension of wounds/suturing under tension; 7. process of wound healing- by primary or secondary intention; 8. type of micro-organic infection.

exist and interact for the possibility of keloid formation [ 1]. These factors are sub-divided into major (or main) and minor (or auxilia- ry) (Table 3). For example, a keloid patient (Fig. 3):

A. 1. of African race; 2. from a keloid-prone family (genetic); 3. of an infected wound on the chest.

B. I. A man at the age of 28 years (Fig. 4); 2. had scratches after beard shaving; 3. the scratches took a long time to heal.

C. 1. A lady of 18 years of age (Fig. 5); 2. had earlobes pierced in childhood which later got injured; 3. primary and secondary keloidectomies carried out with the resulting larger keloid.

From Table 3 the following combinations of the factors are possi- ble:

eg. 1+5+6 --~ keloid 2+3+7 --~ keloid 3+4+8 --~ keloid

but 5+6+7 --~ no keloid (minor factors only) 6+7+8 --~ no keloid (minor factors only) 2+8+0 ~ no keloid (incomplete triad)

In the KTH it is important that at least one major factor is present. The other two may be minor factors. When all three factors are minor no keloid develops, only a hypertrophic scar may form. Likewise, the coexistence of only two factors may most probably not lead to keloid formation; only a hypertrophic scar may form under these conditions. In other words, a chain of three etiological or risk factors must coexist and interact to induce keloid forma- tion. The clue to keloid prevention is thus to break this chain.

D i s c u s s i o n

By critical analysis of these factors - major and minor keloid etiological or risk factors - it should be possible to prevent or at least reduce the rate of keloid formation. It is probably that wound infect ion plays a s ignif icant role in the keloid pathology [1]. On the basis of ques- t ionnaires answered by keloid patients it was of great s ignif icance to note that a high rate of infected wounds vir tual ly all led to keloid formation. It may be necessary to give prophylactic antibiotics to all wounded patients to prevent their wounds from getting infected; a less in- fected wound is less l ikely to form a keloid. This needs further research as to which type of infective agents - s taphylococcus, streptococcus, E. coli, viruses or other

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micro-organisms might most probably lead to keloid for- mation [11.

Similarly, surgical incisions should be carried out (as much as possible) parallel to the skin lines of tension rather than across them. In other words, surgical inter- vention should be considered as a potential cause of ke- loid formation and as such the necessary precautions need to be taken [1].

C o n c l u s i o n

The KTH is a tool for keloid prevention. The latter is in- deed a desirable endeavor and everyone involved in the health service has a part to play, especially in Africans and other dark skinned people, in whom the lesion has been known to be commoner than in Caucasians to the ratio of 9:1 or more.

R e f e r e n c e s

1. Agbenorku PT (1992) Evaluation of preventive methods and treatment of keloids. Ph.D. Dissertation, Medical Faculty of Wroclaw Medical Academy, Wroclaw, Poland, November 1992

2. Crikelair GF, Ju DMC, Cosman B (1977) Scars and keloids. In: Reconstructive plastic surgery. Saunders 1:413-441

3. Datubo-Brown DD (1990) Keloids: a review of the literature. Br J Plast Surg 43:70-77

4. Harvey-Kemble JV (1988) The management of scars, hypertro- phic scars and keloids. Surg Int 54:1286-1289

5. Robinson JK (1986) Scar formation problems. In: Fundamen- tals of skin biopsy. Year Book Medical Publishers, pp 97-100

A world collection of references on keloids may be obtained from the main author.

Fig. 3. Patient A

Fig. 4. Patient B

Fig. 5. Patient C

RT. Agbenorku