Biomedical Engineering Reference
In-Depth Information
( A )
( B )
Figure 6.8 ( A ) Before treatment. ( B ) Using elastic tissue stains, a 600% increase in Grenz zone is noted 90 days after resurfacing, indicating new collagen formation.
In addition, layer of solar elastosis is reduced.
Another fi nding from this study is that in using single-pulse
vaporization with a fl uence of 3-7 J/cm 2 and a pulse width of
less than 1 ms, CO 2 laser resurfacing is a self-limiting proce-
dure, plateauing at a depth of 250-300
m in the dermis, too
superfi cial a wound to result in scarring because of depth
alone. Therefore adherence to proper treatment techniques is
critical in avoiding excessive thermal injury.
Previous histologic studies of dermabraded skin revealed a
new, orderly epidermis overlying an upper papillary dermal
band of new collagen or “scar.” Similar results (increased colla-
gen I formation in the papillary dermis) have been reported
after 10 months of treatment with topical tretinoin for photo-
aged skin. Biopsy specimens obtained at baseline and 3 and
12 weeks after dermabrasion were analyzed and correlated with
clinical assessment. Clinical reduction in wrinkling correlated
signifi cantly with an increase in fi broblast procollagen-1 mRNA
and an increase in procollagen-1 protein, suggesting that clini-
cal improvement might be a result of increased collagen syn-
thesis. Similar increases in Grenz zone collagen were reported
after laser resurfacing (81,82,86). This new collagen production
and remodeling may be a signifi cant factor in achieving rejuve-
nation of facial photodamage, as well as in improvement in
atrophic acne scars (Fig. 6.8). Continued improvement in facial
wrinkling has been noted to occur for as long as 6 months
postoperatively and in acne scars for 12 months or more.
Long-term biopsies (up to 4 years postoperatively) have shown
reversal of epidermal dysplasia, maintenance, and continued
thickening of the Grenz zone, and marked improvement in the
layer of solar elastosis underlying the Grenz zone, with reduc-
tion in overall depth and development of a more fi brillar char-
acter (Figs 6.9 and 6.10).
A further consideration is that consecutive passes with the
laser result in the laser encountering desiccated, thermally
denatured collagen with little water to act as a target for the
laser. This results in a progressively decreased depth of vapor-
ization per pulse. When less of the pulse energy goes into
vaporization, progressively more energy is deposited into the
tissue, potentially causing thermal necrosis by diffusion. In
this situation, the pulse width and repetition rate become
critical.
In addition to the vaporization and coagulation effects of
these lasers removing up to 250-300
μ
Figure 6.9 Ultraviolet light damage to skin results in epidermal atrophy and
fl attening of rete ridges with the development of precancerous and cancerous
epidermal cells. Amorphous elastotic material (solar elastosis) replaces nor-
mal collagen and elastin. Capillaries become reduced in number with thin
fragile walls.
dermis, with decreasing tissue ablation with each sequential
pass, a second mechanism of laser-tissue interaction appears
to be important in achieving the desired clinical results. A dis-
cernible shrinkage of the skin is visible as the laser reacts with
the dermis, tightening the loose folds of skin. This is thought
to be a result of heat-induced collagen shrinkage (101).
When the CO 2 laser interacts with tissue, three distinct zones
of tissue alteration correlate to the degree of tissue heating.
The zone of direct impact results in vaporization of intracel-
lular water and tissue ablation. Underlying this is a zone of
irreversible thermal damage and denaturation resulting in tis-
sue necrosis. Below this layer is a zone of reversible, nonlethal
thermal damage (Fig. 6.11), in which collagen shrinkage is
thought to occur, accounting for the visible tissue tightening
observable as the CO 2 laser interacts with the dermis.
Skin Rejuvenation
Clinical observations have confi rmed the value of collagen
shrinkage in the rejuvenation of photodamaged skin. This is a
signifi cant component of the clinical improvement seen in
laser resurfacing. Its exact mechanism and relative importance
have been debated. We have hypothesized that the shortened
μ
m of tissue in the
 
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