The effects of ultraviolet irradiation on wound contraction in the hairless guinea pig S. F. Davidson.
S. K. Brantley,
Dir~isiorl of’ Plustk Mississippi, USA
S. G. Johnson.
Surger~~, Depcrrtr~wt~t
H. S. H. Hsu and S. K. Das
of Swgw~~,Urliwr.sit>,
of’ Mississippi
A4rcliccrl Center. Jutkwm.
.SUMM,d RI’. Ultraviolet radiation has been shown to alter wound tensile strength and evoke a number of intracellular changes in fibroblasts. We examined the effects of relatively high doses of ultraviolet radiation on subsequent wound contraction of circular wounds in the hairless guinea pig model. Female hairless guinea pigs were divided into two experimental groups receiving 80 J/cm* or 480 J/cm’ every other day for 16 weeks. Age-matched unirradiated animals were used as controls. After exposure, all animals had either a 4 mm punch biopsy (80 J/cm’) or a 2.4 cm diameter ((480 J/cm’) Groups 3 and 4) circular area excised from the dorsum. The extent of wound enlargement immediately following wounding of the irradiated animals was decreased as compared to the controls. The rate of wound contraction was significantly lower during early stages of wound contraction in each group of irradiated animals, and wound contraction was significantly slower overall in both groups of irradiated animals compared to controls.
The mechanism of wound contraction has long been a point of controversy (Gabbiani et ~1.. 1973: McGrath and Hundahl. 1982; Peacock, 1984: Pen-Dogterom et rd., 1987). At present. the mechanical force for wound contraction is thought to be provided by modified fibroblasts. the myofibroblasts. which share many of the morphologic and biochemical properties found in smooth muscle cells (Zahir, 1964; Montandon rt (11.. 1973; Guber and Rudolph. 1978: Rudolph. 1979). Whether the force of contraction is derived from myofibroblasts beneath the wound margin (picture frame theory) or within the wound contents (pull theory) is debatable; however. recent evidence suggests that myofibroblasts are present throughout the granulation tissue and are not concentrated at the periphery of the wound (Rudolph. 1979; Peacock. 1984: Das. 1988). Despite this controversy. any factor affecting the function of myofibroblasts influences the rate of wound contraction. Numerous traumatic injuries and some surgical wounds are allowed to close by secondary intention. Often these wounds are in sun-exposed areas. such as the face and upper extremities. To our knowledge. no one has investigated the effects of predominantly UVA radiation on wound contraction. Although UVA radiation was initially considered innocuous. it penetrates into the dermis in fair-skinned Caucasians (Bicker 4t ~1.. I985 ; Whitman tt cd.. 1985 : Strickland. 1986: Tyrrell and Pidoux. 1987). Previous work in our laboratory indicated that wound tensile strength was significantly reduced in UVA/B and UVA-exposed guinea pigs compared to controls (Davidson et d.. 1989. I99 I : Brantley rt d.. 199 I : Das c’t t/l.. 199 I ). itz ritrn fibroblasts exposed to predominantly UVA light had a reversible inhibition of “H-thymidine uptake (Williams et rrl.. 1993). and irradiated fibroblasts had 508
diminished capabilities to contract collagen lattices (unpublished data). UVA radiation may. therefore, affect the contractile function of fibroblasts. These results provided the impetus for the present study. which assesses the effects of a relatively high dose of predominantly UVA radiation on subsequent wound contraction in circular wounds of different size in the hairless guinea pig model.
Materials and methods Thirty-six female hairless guinea pigs (strain IAF: HA/HO) were obtained from the Charles River breeding stock. The animals were kept in accordance with NIH guidelines. provided a diet of Purina guinea pig food and daily supplementation with green spinach. and allowed water l/d lihitum. The animals were divided into four groups: Group I animals (n = 10) were irradiated with 80 J/cm’ of ultraviolet irradiation predominantly of the UVA wavelength (98.3 “/6 UVA. I .7% UVB) every other day for I6 weeks for a cumulative dose of 4,560 J/cm’. Group 2.animals (n = IO) served as age-matched controls and were not irradiated. Group 3 (n = 8) animals received 480 J/cm’ ultraviolet irradiation (9X.3 9/b UVA, I .7 “,L UVB) over a 9-hour period every other day for a total of 21 weeks (cumulative dose = 35.510 J/cm”: 34,916 J/cm” UVA, 604 J/cm” UVB). Group 4 animals (n = 8) served as controls and received no irradiation. The ultraviolet source was a Psoralite Model 2001 with a bank of six voltarc fluorescent bulbs (ERE-HO. F7D) at a distance of 6 inches. Spectral analysis was accomplished with an Optica Model 742 spectrometer at a distance of 6 inches. with the representative spectrum displayed in Figure I,
The M.ound contraction rate was ahaehsed by magnifhing the photographs three times and calculating the surface area of the defect using a Kurta IS/Three digitising board and a Zeiss videoplan II p.lanimetric computer program. The multivariate profile analgia was used on data measured repeatedly at the L,arious time points to assess the effects of ultra\iolt:t light on the rate of wound contraction. Wilks’ lamhcl~t statibtic was used to compute the corresp m,lrked areas were excised. inclusive of 1‘1111 thickness skin and panniculus carnosus. Meticu1~1~1s haernc~~ta~1\ M;IS obtained with a bipolar cautery. and the V.C~LII~~ were irrigated with normal saline. Each \voun~I LIIK~ ;I rcfcrcncc scale were photographed \sith ;I stationarv camera while the animal\ were rcstraincd. Ben/o-in solution was then applied to the \I\in surrounding the bounds and an occlusive Op-site dressing applied to cxh wound. The wounds were i~lspected .)II ;I daily basis with the dressings removed. and each 14c>unci was n-photographed using the same ~\stem. F#.-,r (iroups I and 2. the photograph5 were tlthcn L~II post-wounding days 2. 5. 8. and I I. For (rroups i and -k. the photographs were taken w postu ounding da! ‘r I 7. 3. 4. 7. I 1. 15. 18. 7.1. 32 ;lnd 47.
. ..
30 25 20
C‘~~~tro/.~. Histological control
9
35
g 5 2
Hisrolo,yr
10
40
5
The irradiated animals showed ;I dramatic decrease in weight gain. with the average weight attained being approximately 150 g less than control4 ihfi~ g). ‘The irradiated animals had pigmentation ot‘ the ears and dorsum of the feet and numerous superficial \cratches and scars from aggressive animal interaction during the irradiation period. These animal> were mot-c sensitive to touch and were frequentI\ noted to iick their backs and scratch them with the;,- teeth. .4t the time of the surgical excision of the tbn ;Ire;t\. the skin of the irradiated guinea pigs itas noted IO ha\e ;! different testure and to cut more easily. Some hypervascularit? wa> also noted bctwecn the skin xnd panniculus carnosus at the time cjf excision. In general. the edges of the wounds of the irradiated animals did not appear to recede to the same extent ah did those of the controls. This wab borne out b! the initial wound surface area calculation. We also noted iI M;IS more difficult to keep the occlusive dressings on I.hc irradiated guinea pigs for the first 3 days. a\ the\ \bere more attentive to their backs. As ;t cnnwq~~crtcc. tlleir wounds became slightly more desiccated than those ot the controls. Following the discontlnu~ltion of irradiation, the small scratches on the tlorsum of the irradiated guinea pigs disappeared within -I tia! S. The guinea pigs also experienced weight gain.
l .-.-----
f.., -..
0
A.-.-.-.-A
UVA (Group Control
1)
(Group
findings in the det-m~\ of the pigs were those of normal $kin. in-
guinea
n
w -----
Expenmental
O--------o
Control
(Group
(Group
3)
4)
a 2)
15 10 p=O.35 5
for
intervals
I
0 0
‘A._ **. .-. -... -*,_
simultaneous
Iconfidence
-....,
1 2
4
2 1
‘0
,._ “A
6
0
TIME
(days)
Fig. 2
10
0 12
14
L_ I.___--_d
0
_
1
2
3
4
7
11
Post-operative Fig.
_
15 Day
.1
_.._
_ _
16
23
I__
32
a7
British Journal of Plastic Surgery
5I0
eluding the usual contiguration of stratum corneum, stratum granulosum. and the spinous and basal layers. The dermis had fairly well-defined papillary and reticular layers. The papillary collagen was arranged in thin, loose, pale-staining bands while the collagen of the reticular dermis was disposed in thicker, broader bundles. The pilosebaceous units showed orderly arrangement, and elastic fibres in the papillary dermis were mostly parallel to the free epidermal surface. There was no evidence of inflammatory response. E.\-/“~i/,lc~llttr/. In weeks I and 2, some inflammatory response was evident in the dermis, with the presence of an eosinophilic infiltrate. Dermal elastosis was noted as early as 8 weeks. By week 16, there was fragmentation of the collagen fibres with a plump feathery appearance. and increased elastosis. Additionally. there was a layer of scar formation at the dermal-epidermal junction secondary to the continuing repair process.
Wound contraction lagged significantly in the irradiated animals compared to the controls (Wilks’ p < 0.05 for comparisons of experimental groups to their respective controls; Figs _3 and 3). This difference was significant when one compares the mean values for all groups (Figs 2 and 3). The initial wound size was significantly smaller in both irradiated groups and there was a prolonged lag phase in the irradiated animals.
Discussion In this study. exposure of guinea pigs to UVA/B resulted in decreased initial wound size. a prolonged lag phase in early inflammatory process, and an overall decrease in the rate of wound contraction. A possible explanation for the smaller initial wound size in irradiated animals is that disruption of both elastin and collagen tibres decreased contraction of those fibres surrounding the incision. This phenomenon has received scant attention. The prolonged lag phase seen in irradiated animals suggests that UVA/B inhibits some step(s) in early wound healing. Normal wound repair is dependent on a series of rate-limiting interlinked steps, including chemotaxis and adhesion of various cells such as fibroblasts, keratinocytes. and endothelial cells. to the supporting matrix components (Sank et c/l., 1989). These cells proliferate at the wound site before contraction occurs. If ultraviolet radiation influences the adhesion or chernotaxis of fibroblasts to the wound site. a prolonged lag phase may occur. Our study indicates that UVA radiation can inhibit the overall rate of wound contraction. Investigation into the area of ultraviolet irradiation and wound contraction has been rather limited. Marks et al. (1990) found that fibroblasts from sun-exposed skin contracted collagen-fibroblast lattices significantly more than fibroblasts from sun-protected skin.
although sun-exposed fibroblasts seem to lose their ability to contract as aging skin is exposed to more actinic radiation. These results seem to contradict our findings of decreased wound contraction in irradiated animals. However. i/l c>it~ studies simplify the process and the finding that older sun-exposed tibroblasts lose their ability to contract is consistent with our findings. Degradation of irl .riru collagen fibres may result from enzymatic degradation caused by disruption of lysosomal membranes in the papillary dermis. Even if the amount of collagen is not influenced by UVAjB radiation, the histologic finding that UVA/B causes disruption ofcollagen fibres suggests that the ability of fibroblasts to contract may be compromised. The ultraviolet source provided a relatively constant spectrum over a wide surface area for up to 600 hours without significant changes. The UVA/B source closely resembles the spectrum emitted by representative tanning beds and sunbathing using UVB sunscreens. Although we attempted to minimise the amount of UVB irradiation to which the animals were exposed, the light source did provide 1.7 Y/o UVB (cumulative dose = 604 J/cm’ over the irradiation period). perhaps a significant contributor to our findings. The exact mechanism by which ultraviolet light inhibits wound healing is only speculative, but ultraviolet light has the capability of aKecting a wide range of cellular functions and structures. Depending upon the wavelength. UV has been shown to promote DNA synthesis. influence membrane structure. and to decrease collagen synthesis (Carter and Balin, 1983 ; Pospilova and Tykva. 1983; Bicker et I//.. 1985). Possibly a combination of these factors results in the delayed wound contraction observed in the experimental group. Our studies on the effects of ultraviolet light on wound tensile strength and the rate of wound contraction have demonstrated that both the strength and contraction of a wound can be negatively affected by ultraviolet radiation and, furthermore. that UV radiation may exacerbate the already challenging clinical problem of delayed wound healing. Prolonged periods of elective suntanning should be avoided.
References Bicker, D. R.. Epstein, J. H.. Fitzpatrick, T. B., Harber, L. C., Patbak, M. and Urbach, F. (1985). Risk and benefits from high-
intensity ultraviolrt
A sources uwd for cosmetic purpose. .Iow~r~l .ictrc/en~~ ,I/ Drw~~rr/o/qy~~. 12. 3X0. Brantley, S. K.. Davidson, S. F. and Das, S. K. ( I99 I j. A dose related q/ rk
rlr,wkun
curve of wound tensile strength following ultraviolet irradiation in the halrless gunea pig. .-lrw~i~~~ J~wwtrl o/ .\l&c~/ ,S~~i~wc~c~.\. 302. 15.
Carter. D. .%I.and Balin. A. K. (19X3). Dermatnloglcal
aspects of aging. Mc&trl C‘/ink.r o/‘:Vort/~ .4nwrktr. 67. 53 I Das, S. K. (198X). Wound healing, operatl\r Incxions. and skin grafts. In : Hardy. J. D. (Ed.) Harc/~.‘.v %J.\-rhooX o/ Sr~,yw~~. 2nd Edition. Philadelphia. J. B. Lippincott Company. p. 11)6. Das, S. Ii., Brantley, S. K. and Davidson, S. F. (I991). Wound tcnsilc strength in the hairless guinea pig following irradiation nith pure ultraviolet-A light. Brlri.cl~ Jow~~~r/ o/‘/%l.rrrc~ Swgcy~~. 44. 509. Davidson. S. E‘., Talbot, P. J. and Das, S. K. ( 1989). Etfects of longterm lrradlation on wound healing. .S~r,yrc~~/F~wuw. 40. 643. Davidson, S. F., Brantley, S. K. and Das, S. K. ( 1991). The elTecr\ 01 ultraviolet radiation on wound healing. Bvitislz Jcww~/ of f/~.cfi~~ Suryw1~. 44. 1 IO.
S. K. Brantley,
Dir~isiorl of’ Plustk Mississippi, USA
S. G. Johnson.
Surger~~, Depcrrtr~wt~t
H. S. H. Hsu and S. K. Das
of Swgw~~,Urliwr.sit>,
of’ Mississippi
A4rcliccrl Center. Jutkwm.
.SUMM,d RI’. Ultraviolet radiation has been shown to alter wound tensile strength and evoke a number of intracellular changes in fibroblasts. We examined the effects of relatively high doses of ultraviolet radiation on subsequent wound contraction of circular wounds in the hairless guinea pig model. Female hairless guinea pigs were divided into two experimental groups receiving 80 J/cm* or 480 J/cm’ every other day for 16 weeks. Age-matched unirradiated animals were used as controls. After exposure, all animals had either a 4 mm punch biopsy (80 J/cm’) or a 2.4 cm diameter ((480 J/cm’) Groups 3 and 4) circular area excised from the dorsum. The extent of wound enlargement immediately following wounding of the irradiated animals was decreased as compared to the controls. The rate of wound contraction was significantly lower during early stages of wound contraction in each group of irradiated animals, and wound contraction was significantly slower overall in both groups of irradiated animals compared to controls.
The mechanism of wound contraction has long been a point of controversy (Gabbiani et ~1.. 1973: McGrath and Hundahl. 1982; Peacock, 1984: Pen-Dogterom et rd., 1987). At present. the mechanical force for wound contraction is thought to be provided by modified fibroblasts. the myofibroblasts. which share many of the morphologic and biochemical properties found in smooth muscle cells (Zahir, 1964; Montandon rt (11.. 1973; Guber and Rudolph. 1978: Rudolph. 1979). Whether the force of contraction is derived from myofibroblasts beneath the wound margin (picture frame theory) or within the wound contents (pull theory) is debatable; however. recent evidence suggests that myofibroblasts are present throughout the granulation tissue and are not concentrated at the periphery of the wound (Rudolph. 1979; Peacock. 1984: Das. 1988). Despite this controversy. any factor affecting the function of myofibroblasts influences the rate of wound contraction. Numerous traumatic injuries and some surgical wounds are allowed to close by secondary intention. Often these wounds are in sun-exposed areas. such as the face and upper extremities. To our knowledge. no one has investigated the effects of predominantly UVA radiation on wound contraction. Although UVA radiation was initially considered innocuous. it penetrates into the dermis in fair-skinned Caucasians (Bicker 4t ~1.. I985 ; Whitman tt cd.. 1985 : Strickland. 1986: Tyrrell and Pidoux. 1987). Previous work in our laboratory indicated that wound tensile strength was significantly reduced in UVA/B and UVA-exposed guinea pigs compared to controls (Davidson et d.. 1989. I99 I : Brantley rt d.. 199 I : Das c’t t/l.. 199 I ). itz ritrn fibroblasts exposed to predominantly UVA light had a reversible inhibition of “H-thymidine uptake (Williams et rrl.. 1993). and irradiated fibroblasts had 508
diminished capabilities to contract collagen lattices (unpublished data). UVA radiation may. therefore, affect the contractile function of fibroblasts. These results provided the impetus for the present study. which assesses the effects of a relatively high dose of predominantly UVA radiation on subsequent wound contraction in circular wounds of different size in the hairless guinea pig model.
Materials and methods Thirty-six female hairless guinea pigs (strain IAF: HA/HO) were obtained from the Charles River breeding stock. The animals were kept in accordance with NIH guidelines. provided a diet of Purina guinea pig food and daily supplementation with green spinach. and allowed water l/d lihitum. The animals were divided into four groups: Group I animals (n = 10) were irradiated with 80 J/cm’ of ultraviolet irradiation predominantly of the UVA wavelength (98.3 “/6 UVA. I .7% UVB) every other day for I6 weeks for a cumulative dose of 4,560 J/cm’. Group 2.animals (n = IO) served as age-matched controls and were not irradiated. Group 3 (n = 8) animals received 480 J/cm’ ultraviolet irradiation (9X.3 9/b UVA, I .7 “,L UVB) over a 9-hour period every other day for a total of 21 weeks (cumulative dose = 35.510 J/cm”: 34,916 J/cm” UVA, 604 J/cm” UVB). Group 4 animals (n = 8) served as controls and received no irradiation. The ultraviolet source was a Psoralite Model 2001 with a bank of six voltarc fluorescent bulbs (ERE-HO. F7D) at a distance of 6 inches. Spectral analysis was accomplished with an Optica Model 742 spectrometer at a distance of 6 inches. with the representative spectrum displayed in Figure I,
The M.ound contraction rate was ahaehsed by magnifhing the photographs three times and calculating the surface area of the defect using a Kurta IS/Three digitising board and a Zeiss videoplan II p.lanimetric computer program. The multivariate profile analgia was used on data measured repeatedly at the L,arious time points to assess the effects of ultra\iolt:t light on the rate of wound contraction. Wilks’ lamhcl~t statibtic was used to compute the corresp m,lrked areas were excised. inclusive of 1‘1111 thickness skin and panniculus carnosus. Meticu1~1~1s haernc~~ta~1\ M;IS obtained with a bipolar cautery. and the V.C~LII~~ were irrigated with normal saline. Each \voun~I LIIK~ ;I rcfcrcncc scale were photographed \sith ;I stationarv camera while the animal\ were rcstraincd. Ben/o-in solution was then applied to the \I\in surrounding the bounds and an occlusive Op-site dressing applied to cxh wound. The wounds were i~lspected .)II ;I daily basis with the dressings removed. and each 14c>unci was n-photographed using the same ~\stem. F#.-,r (iroups I and 2. the photograph5 were tlthcn L~II post-wounding days 2. 5. 8. and I I. For (rroups i and -k. the photographs were taken w postu ounding da! ‘r I 7. 3. 4. 7. I 1. 15. 18. 7.1. 32 ;lnd 47.
. ..
30 25 20
C‘~~~tro/.~. Histological control
9
35
g 5 2
Hisrolo,yr
10
40
5
The irradiated animals showed ;I dramatic decrease in weight gain. with the average weight attained being approximately 150 g less than control4 ihfi~ g). ‘The irradiated animals had pigmentation ot‘ the ears and dorsum of the feet and numerous superficial \cratches and scars from aggressive animal interaction during the irradiation period. These animal> were mot-c sensitive to touch and were frequentI\ noted to iick their backs and scratch them with the;,- teeth. .4t the time of the surgical excision of the tbn ;Ire;t\. the skin of the irradiated guinea pigs itas noted IO ha\e ;! different testure and to cut more easily. Some hypervascularit? wa> also noted bctwecn the skin xnd panniculus carnosus at the time cjf excision. In general. the edges of the wounds of the irradiated animals did not appear to recede to the same extent ah did those of the controls. This wab borne out b! the initial wound surface area calculation. We also noted iI M;IS more difficult to keep the occlusive dressings on I.hc irradiated guinea pigs for the first 3 days. a\ the\ \bere more attentive to their backs. As ;t cnnwq~~crtcc. tlleir wounds became slightly more desiccated than those ot the controls. Following the discontlnu~ltion of irradiation, the small scratches on the tlorsum of the irradiated guinea pigs disappeared within -I tia! S. The guinea pigs also experienced weight gain.
l .-.-----
f.., -..
0
A.-.-.-.-A
UVA (Group Control
1)
(Group
findings in the det-m~\ of the pigs were those of normal $kin. in-
guinea
n
w -----
Expenmental
O--------o
Control
(Group
(Group
3)
4)
a 2)
15 10 p=O.35 5
for
intervals
I
0 0
‘A._ **. .-. -... -*,_
simultaneous
Iconfidence
-....,
1 2
4
2 1
‘0
,._ “A
6
0
TIME
(days)
Fig. 2
10
0 12
14
L_ I.___--_d
0
_
1
2
3
4
7
11
Post-operative Fig.
_
15 Day
.1
_.._
_ _
16
23
I__
32
a7
British Journal of Plastic Surgery
5I0
eluding the usual contiguration of stratum corneum, stratum granulosum. and the spinous and basal layers. The dermis had fairly well-defined papillary and reticular layers. The papillary collagen was arranged in thin, loose, pale-staining bands while the collagen of the reticular dermis was disposed in thicker, broader bundles. The pilosebaceous units showed orderly arrangement, and elastic fibres in the papillary dermis were mostly parallel to the free epidermal surface. There was no evidence of inflammatory response. E.\-/“~i/,lc~llttr/. In weeks I and 2, some inflammatory response was evident in the dermis, with the presence of an eosinophilic infiltrate. Dermal elastosis was noted as early as 8 weeks. By week 16, there was fragmentation of the collagen fibres with a plump feathery appearance. and increased elastosis. Additionally. there was a layer of scar formation at the dermal-epidermal junction secondary to the continuing repair process.
Wound contraction lagged significantly in the irradiated animals compared to the controls (Wilks’ p < 0.05 for comparisons of experimental groups to their respective controls; Figs _3 and 3). This difference was significant when one compares the mean values for all groups (Figs 2 and 3). The initial wound size was significantly smaller in both irradiated groups and there was a prolonged lag phase in the irradiated animals.
Discussion In this study. exposure of guinea pigs to UVA/B resulted in decreased initial wound size. a prolonged lag phase in early inflammatory process, and an overall decrease in the rate of wound contraction. A possible explanation for the smaller initial wound size in irradiated animals is that disruption of both elastin and collagen tibres decreased contraction of those fibres surrounding the incision. This phenomenon has received scant attention. The prolonged lag phase seen in irradiated animals suggests that UVA/B inhibits some step(s) in early wound healing. Normal wound repair is dependent on a series of rate-limiting interlinked steps, including chemotaxis and adhesion of various cells such as fibroblasts, keratinocytes. and endothelial cells. to the supporting matrix components (Sank et c/l., 1989). These cells proliferate at the wound site before contraction occurs. If ultraviolet radiation influences the adhesion or chernotaxis of fibroblasts to the wound site. a prolonged lag phase may occur. Our study indicates that UVA radiation can inhibit the overall rate of wound contraction. Investigation into the area of ultraviolet irradiation and wound contraction has been rather limited. Marks et al. (1990) found that fibroblasts from sun-exposed skin contracted collagen-fibroblast lattices significantly more than fibroblasts from sun-protected skin.
although sun-exposed fibroblasts seem to lose their ability to contract as aging skin is exposed to more actinic radiation. These results seem to contradict our findings of decreased wound contraction in irradiated animals. However. i/l c>it~ studies simplify the process and the finding that older sun-exposed tibroblasts lose their ability to contract is consistent with our findings. Degradation of irl .riru collagen fibres may result from enzymatic degradation caused by disruption of lysosomal membranes in the papillary dermis. Even if the amount of collagen is not influenced by UVAjB radiation, the histologic finding that UVA/B causes disruption ofcollagen fibres suggests that the ability of fibroblasts to contract may be compromised. The ultraviolet source provided a relatively constant spectrum over a wide surface area for up to 600 hours without significant changes. The UVA/B source closely resembles the spectrum emitted by representative tanning beds and sunbathing using UVB sunscreens. Although we attempted to minimise the amount of UVB irradiation to which the animals were exposed, the light source did provide 1.7 Y/o UVB (cumulative dose = 604 J/cm’ over the irradiation period). perhaps a significant contributor to our findings. The exact mechanism by which ultraviolet light inhibits wound healing is only speculative, but ultraviolet light has the capability of aKecting a wide range of cellular functions and structures. Depending upon the wavelength. UV has been shown to promote DNA synthesis. influence membrane structure. and to decrease collagen synthesis (Carter and Balin, 1983 ; Pospilova and Tykva. 1983; Bicker et I//.. 1985). Possibly a combination of these factors results in the delayed wound contraction observed in the experimental group. Our studies on the effects of ultraviolet light on wound tensile strength and the rate of wound contraction have demonstrated that both the strength and contraction of a wound can be negatively affected by ultraviolet radiation and, furthermore. that UV radiation may exacerbate the already challenging clinical problem of delayed wound healing. Prolonged periods of elective suntanning should be avoided.
References Bicker, D. R.. Epstein, J. H.. Fitzpatrick, T. B., Harber, L. C., Patbak, M. and Urbach, F. (1985). Risk and benefits from high-
intensity ultraviolrt
A sources uwd for cosmetic purpose. .Iow~r~l .ictrc/en~~ ,I/ Drw~~rr/o/qy~~. 12. 3X0. Brantley, S. K.. Davidson, S. F. and Das, S. K. ( I99 I j. A dose related q/ rk
rlr,wkun
curve of wound tensile strength following ultraviolet irradiation in the halrless gunea pig. .-lrw~i~~~ J~wwtrl o/ .\l&c~/ ,S~~i~wc~c~.\. 302. 15.
Carter. D. .%I.and Balin. A. K. (19X3). Dermatnloglcal
aspects of aging. Mc&trl C‘/ink.r o/‘:Vort/~ .4nwrktr. 67. 53 I Das, S. K. (198X). Wound healing, operatl\r Incxions. and skin grafts. In : Hardy. J. D. (Ed.) Harc/~.‘.v %J.\-rhooX o/ Sr~,yw~~. 2nd Edition. Philadelphia. J. B. Lippincott Company. p. 11)6. Das, S. Ii., Brantley, S. K. and Davidson, S. F. (I991). Wound tcnsilc strength in the hairless guinea pig following irradiation nith pure ultraviolet-A light. Brlri.cl~ Jow~~~r/ o/‘/%l.rrrc~ Swgcy~~. 44. 509. Davidson. S. E‘., Talbot, P. J. and Das, S. K. ( 1989). Etfects of longterm lrradlation on wound healing. .S~r,yrc~~/F~wuw. 40. 643. Davidson, S. F., Brantley, S. K. and Das, S. K. ( 1991). The elTecr\ 01 ultraviolet radiation on wound healing. Bvitislz Jcww~/ of f/~.cfi~~ Suryw1~. 44. 1 IO.
