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12.3 Pathologic Responses toWound Healing
159
Fig. 12.2 (a, b)
Hyperpigmented neck
scars in a male patient
with pigmented skin
who suffered burns to
the upper body, neck,
and lower face. The
widespread hypertrophic
scarring is noticeable
Fig. 12.3 (a, b)
Hypopigmentation and
hyperpigmentation of
the neck scars in a
female patient who
suffered burns to the
upper body and neck
ab
ab
signicantly between published studies
(Maghfour et al. 2022). Medical tattooing to
match the surrounding skin color has offered
improvement in selected cases. Surgical excision
of the scar and resuturing are effective; however,
there is no guarantee that the new scar will be
free of the problem. Finally, application of cultured or non-cultured melanocytes has offered
improvement in selected cases (Chadwick etal.
2012). Future research of treating inactive mela-
nocytes present in the burn scar regions with a
pigment stimulator towards re-pigmentation
might offer a more effective clinical solution to
hypopigmentation (Carney etal. 2021).
12.3.2 Hypertrophic Scars, Keloids,
andContractures
There is a wide spectrum of cutaneous scarring
ranging from mature linear scars to hypertrophic
scars and keloids. Hypertrophic scars are conned to the boundaries of the original lesion,
whereas keloids project beyond the margins of
the original wound. Both types of excessive scarring, whose incidence is estimated at 15% of all
acquired scars worldwide (Monstrey etal. 2014),
have physical, aesthetic, psychological, and
social consequences. Physical symptoms include
itching, stiffness, tenderness, and pain (Van Loey
et al. 2008; Isoardo etal. 2012). Psychological
consequences include diminished self-esteem,
stigmatization, disruption of daily activities, anxiety, and depression (Robert etal. 1999). Risk
factors that promote hypertrophic scar and keloid
growth include local factors (tension on the
wound/scar), systemic factors (e.g., hypertension), genetic factors (e.g., single nucleotide
polymorphisms), and lifestyle factors (Ogawa
2022).
Hypertrophic scars are classied as either lin-
ear or widespread. The former usually result
from trauma (Fig.12.4), whereas the latter result
mainly from burn injuries and eventually from
extensive soft-tissue trauma (Figs. 12.2 and
12.5). Hypertrophic scars usually show a rapid
growth phase (up to 6months) and then gradually
regress (over the next few years); keloids result
mainly from burn injuries and eventually from
extensive soft-tissue trauma and typically persist
for a long period of time; they do not regress
spontaneously. All individuals can form hyper-
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trophic scars and keloids; however, the incidence
of the latter is much higher in black-skinned individuals than in whites. The most common H&N
site for hypertrophic scars is the neck, whereas
keloids are most frequently seen on the earlobes
and cheeks (Verhaegen etal. 2009) (Fig.12.6).
12 Wound Healing Disturbances: TheUnfavorable Result
Fig. 12.4 Linear hypertrophic scar at the base of the right
nose
Fig. 12.5 (a, b)
Widespread
hypertrophic scarring
after trauma to the right
cheek and nose
ab
Fig. 12.6 Ear keloid in a colored female patient
12.3 Pathologic Responses toWound Healing
161
Histopathologically, both hypertrophic scars
and keloids contain an excess of dermal collagen.
Hypertrophic scars primarily contain well- organized
type III collagen, whereas keloids contain disorganized type I and type III collagen bundles (Gauglitz
et al. 2011). Collagen bundle distance was found
to be signicantly larger in keloidal scars, which
suggests that thicker collagen bundles are present
in keloids (Verhaegen etal. 2009). Twenty to 30%
of hypertrophic scars showed mast cells, whereas a
moderate degree of perivascular chronic inammatory inltrate was seen in keloids showing 73% of
mast cells in reticular dermis (Moshref and Mufti
2010). Myobroblasts, seen in 33.3% of keloidal
scars, are considered to play an important role in the
pathogenesis of keloids. They are absent in hypertrophic scars. A high amount of activated immune cell
inltrate consisting of CD3+, CD4+, and CD45RO
has been detected in keloids. Furthermore, the signicantly higher CD4(+)-to-CD8(+) ratio suggests
an imbalance in these inammatory cell populations, which along with the high percentage of mast
cells may contribute to keloid formation (Moshref
and Mufti 2010). Other cytokines which have been
implicated in the pathophysiology of keloids are
IL-6, IL-8, and IL-10 (Berman etal. 2017). Keloid
broblasts show increased numbers of growth factor receptors and respond more briskly to growth
factors like TGF-β, which may upregulate these
abnormal cells from the beginning of the wound
healing (Gauglitz etal. 2011). Other growth factors
(PDGF, IGF-1) are also known to regulate cell proliferation, differentiation, and growth. TGF-β seems
to upregulate the expression of PDGF receptors
and IGF-1 receptors in unusually high numbers in
keloid broblasts (Messadi etal. 1998). Inhibition
of TGF-β1 by the receptor for activated C-kinase
1 (RACK1) inhibits collagen synthesis in keloid
broblasts, as was shown by Zhou et al. (2015).
RACK1 is a potential target for the treatment of
keloids. Controlled, double- blind, randomized
phase I/II clinical studies have shown that avotermin, human recombinant transforming growth factor beta-3 (TGF-β3), administered as an intradermal
injection at the time of surgery, leads to short- as
well as long-term (>1 year) improvement in scar
appearance compared with placebo and standard
wound care (Durani etal. 2008). Another substance
which has been shown to improve postoperative
scar appearance by decreasing tensile forces is botulinum toxin A (BTX-A). A recent meta-analysis of
randomized controlled trials evaluating the effect of
BTX-A on maxillofacial and neck scars reported
that a statistically signicant difference in scar
width was identied between the BTX-A group
and control group. A statistically signicant difference in patient satisfaction as well as visual analysis
scores was observed between the BTX-A group and
the control group (Zhang etal. 2016).
Excessive scar formation can be prevented by
a wide range of measures that reduce inammation and promote rapid wound healing. Early
debridement, reduction of the infection risk
through rinsing and disinfection, tension-free
closure, and optimal dressings providing moist
wound healing are essential steps in the management of every wound.
Studies have shown that after wound healing
water still evaporates more rapidly through scar
tissue. The elevated transepidermal water loss
normalized after 200–400 days (Suetake et al.
1996). Maintaining a moist wound environment
facilitates and accelerates the wound healing process (Field and Kerstein 1994; Vogt etal. 1995).
Concerns that moisture in wounds would increase
the risk of clinical infection over traditional therapies are unfounded (Field and Kerstein 1994).
Delivery of antimicrobials, analgesics, other bioactive molecules such as growth factors, as well
as cells and micrografts is possible, when treating
wounds in a controlled wet environment. The liquid in the chamber becomes a reservoir and acts
as a sustained-release system. The tissue absorption is deducted from the remaining concentration of the agent in the chamber after a certain
time (Junker etal. 2013). Treatment of hypertrophic scars depends on scar contracture severity:
In less severe cases, conservative therapies are
indicated. In severe cases, surgery is the rst
choice (Ogawa 2022). Keloid treatment depends
on the number and size of the lesions. Small and
single keloids can be treated by surgery with
adjuvant therapy (e.g., radiotherapy) or multimodal conservative therapy. For large and
multiple keloids, volume- and number-reducing
surgery is a choice (Ogawa 2022).
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12 Wound Healing Disturbances: TheUnfavorable Result
Pressure garments can be used prophylactically in burn patients with widespread scars. A
meta-analysis (six trials involving 316 patients)
for burn scar height showed a small but statistically signicant decrease in height for the pressure garment therapy-treated group (standarized
mean differences: –0.31; 95% CI: –0.63, 0.00)
(Anzarut et al. 2009). Engrav et al. (2010)
observed an improvement of hardness, color, and
thickness of scars after pressure garment therapy;
however, the clinical benet was restricted to
those patients with moderate or severe scarring
(Engrav etal. 2010). Steinstraesser etal. (2011)
added silicone spray or silicone sheeting to compression. The combined therapy produced results
equivalent to those achieved with pressure garment therapy alone in the prevention of hypertrophic scars.
Silicone gel sheeting has been used since the
early 1980s for the treatment of widespread
hypertrophic burn scars. The precise mechanism
of action of silicone sheeting has not been
dened, but clinical trials have reported that it is
safe and effective if worn over the scar for
12–24h per day for at least 2–3months (Berman
etal. 2007). O’Brien and Jones (2013) conducted
a literature search regarding randomized controlled studies comparing silicone gel sheeting
for prevention or treatment of hypertrophic or
keloid scars with any other nonsurgical treatment, no treatment or placebo. In the prevention
studies, when compared with a no-treatment
option, silicone gel sheeting reduced the incidence of hypertrophic scarring in people prone
to scarring (RR: 0.46, 95% CI 0.21–0.98).
However, these studies were highly susceptible
to bias. In treatment studies, silicone gel sheeting produced a statistically signicant reduction
in scar thickness (mean difference 2.00, 95% CI
2.14–1.85) and color amelioration (RR: 3.49,
95% CI 1.97–6.15), but again these studies were
highly susceptible to bias (O’Brien and Jones
2013). In a more recent report, Bleasdale etal.
(2015) stated: “The clinical support of topical
silicone gel products, relative to all alternative
scar therapies, is considered the internationally
recommended rst line form of scar management, and favored by consensus among health
care professionals. However, there still remains
the need for further clinical evidence and a better
understanding of the mechanism behind the benet of silicone gel for use in the prevention of
abnormal scarring.”
Silicone gel sheets, compression garments,
and occlusive/adhesive skin taping are all applied
to form an occlusion on the scar surface, reduce
tension, and/or increase pressure on the scar
itself. Part of the effect of pressure could be
attributed to the occlusion of small blood vessels
resulting in the reduction of oxygen tension and
thus decrease of (myo-) broblast proliferation
and collagen synthesis (Macintyre and Baird
2006).
A recent study from Washington, DC, reported
that less collagen was built after pressure application compared with sham and untreated scars.
Collagen 1A2 and 3A1 transcript decreased by
41.9-fold and 42.3-fold, respectively, compared
with uninjured skin after pressure treatment,
whereas a 2.3- and 1.3-fold increase was seen in
untreated scars. Pressure-treated scars also had
lower levels of collagen I and III compared with
sham and untreated scars (Tejiram et al. 2016).
Sharp etal. (2016) conducted a literature search
(1950–2014) regarding pressure therapy for the
management of hypertrophic scarring. Based on
the best available evidence, the authors recommend pressure therapy in order to decrease scar
height and erythema. It should be used for grafts
and wounds requiring 14–21 days to heal, for
23 h/day for 12 months, t to achieve
20–30mmHg of pressure, t by a skilled technician, and replaced every 2–3 months. Pressure
therapy should not be used to treat abnormal pigmentation, nor used to hasten scar maturation
(Sharp etal. 2016). Pressure therapy can be used
as an adjuvant therapy to surgery in keloid treatment (e.g., ear keloids). Treatment of patients
after surgical excision of ear keloids for 12h a
day for 6–18 months with custom-molded ear
clips resulted in a success rate of 70.5% of treated
patients (Tanaydin et al. 2016). Devices/clips
have been designed, which monitor pressure in
order to provide optimal pressure therapy for
better outcome after ear keloid excision
(Sasidharan etal. 2015).
12.3 Pathologic Responses toWound Healing
163
Other recent studies relate the action of compression therapy with mechanoreceptor (nociceptor and cellular mechanoreceptor) responses
(Yagmur et al. 2010). Mechanical forces can be
perceived by the above two types of skin receptors. The mechanosensitive nociceptors receive
mechanical stimuli, and signals are then transmitted to the dorsal root ganglia that contain
neuronal cell bodies in the afferent spinal nerves.
Neuropeptides which are released from the afferent sensory neurons in the skin modulate scarring through skin and immune cell functions
(Ogawa 2011). Clinical application of this basic
research has shown the importance of reducing
skin tension in order to prevent recurrence after
hypertrophic scars or keloids have been surgically removed. Subcutaneous/fascial tensile
reduction sutures and skin aps (perforator aps,
propeller aps), which release tension on the
wound, in combination with postoperative radiotherapy can successfully treat huge keloids
(Ogawa etal. 2011).
Postoperative follow-up of post-traumatic
H&N scars is essential in order to assess the
progress of wound healing and normal scar formation. If preventive therapy has been initiated,
its continuation or termination is decided.
Furthermore, one should determine whether
additional interventions are required in order to
improve the aesthetic appearance of the scar.
Patients who develop early hypertrophy in their
linear scar (6 weeks to 3 months post-trauma)
should undergo treatment (including silicone
based products and pressure therapy) or if this
has already been initiated, it should be intensied
(Monstrey etal. 2014). In patients with ongoing
hypertrophy, more invasive measures are indicated. The only invasive management option
which currently has enough evidence to be recommended in evidence-based guidelines is intralesional injection of corticosteroids (Monstrey
etal. 2014; Del Toro etal. 2016). The most commonly used corticosteroid is triamcinolone acetonide (10–40mg/mL), which should be injected
into the papillary dermis every 2–4weeks until
the scar is attened. Side effects include pain,
skin atrophy, hypopigmentation, and telangiectasias (Sproat et al. 1992). Objective response in
terms of no recurrence was noted in 91.9% of
patients with keloids and 95.24% of patients with
hypertrophic scars at a mean follow-up of
30.5months after intralesional injection of triamcinolone acetonide (Chowdri et al. 1999). In
cases of keloids, surgical excision of the lesion
precedes triamcinolone injection. The latter
increases basic broblast growth factor (FGF)
production while decreasing transforming growth
factor-beta 1 (TGF-β1) production by human dermal broblasts, endogenous endothelial growth
factor (EGF), and insulin-like growth factor-1
(IGF-1). Surgical excision and subsequent intradermal corticotherapy injection are considered to
be the most effective and safe regimen for keloid
management (Roques and Téot 2008).
Additional injectable treatment options
include intralesional 5-uorouracil (5-FU), a
chemotherapeutic agent. 5-FU was introduced as
a treatment for keloids in the 1990s. Bijlard etal.
(2015) conducted a systematic review of the clinical evidence on the effectiveness of 5-FU in
keloid treatment. 5-FU treatment was effective in
45–96% of patients; triamcinolone acetonide
plus 5-FU may perform better than triamcinolone
alone. However, the poor level of evidence did
not allow denitive conclusions and the authors
stressed the need for further research in order to
establish the superiority of repeated intralesional
triamcinolone/5-FU injections over triamcinolone alone (Bijlard et al. 2015). A number of
other chemotherapeutic agents have been proposed for the treatment of keloids, and occasionally for hypertrophic scars. Jones et al. (2015)
reviewed 27 non-randomized trials evaluating the
inuence of different chemotherapeutics (5-FU,
mitomycin C, bleomycin, and steroid injection)
either alone or in combination with other chemotherapeutic agents or alternative treatment
modalities. Scar improvement ≥50% was found
in the majority of cases treated with 5-FU, with
similar results found for mitomycin C, bleomycin, and steroid injection. Combined intralesional
5-FU and steroid injection produced statistically
signicant improvement when compared to
monotherapy. Monotherapy recurrence rates
ranged from 0% to 47% for 5-FU, 0–15% for
bleomycin, and 0–50% for steroid injection.
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12 Wound Healing Disturbances: TheUnfavorable Result
However, combined therapy demonstrated lower
recurrence rates (surgical excision and adjuvant
5-FU 19%, surgical excision, and steroids 6%).
The use of a combination therapy (usually surgery and chemotherapy) is currently supported
by most of the literature (Jones etal. 2015; Choi
etal. 2022).
Verapamil is a calcium channel antagonist,
which both decreases collagen synthesis and
increases collagen breakdown. The effectiveness
of verapamil in preventing and treating keloid
was assessed in a recent literature review (Wang
et al. 2016). The results showed that verapamil
could improve keloid and hypertrophic scars but
was not signicantly different from conventional
corticosteroid injections. Few adverse effects
were observed. However, the result of the review
should be considered skeptically, as most of the
included studies had a high risk of bias due to
methodological errors (Wang etal. 2016). Future,
well-designed high-quality studies will probably
elucidate the true value of verapamil in the treatment of hypertrophic scars and keloids.
Laser therapy is another invasive option which
has been widely used for the treatment of hypertrophic scars and keloids since its introduction by
Castro etal. in 1983. Several laser systems have
been used, most of which achieve their effect of
scar remodeling through photothermolysis.
Pulsed-dye laser achieves selective photothermolysis, whereby wavelengths are absorbed preferentially by hemoglobin; this makes it ideal for
the treatment of vascular tissues such as hypertrophic scars (Ogawa 2010). New laser systems
(810/830nm and 532nm) have also been effective, especially on pigmented hypertrophic scars
(Capon etal. 2010). Symptoms such as pain and
pruritus have also been relieved by laser therapy
(Capon etal. 2010). A recent meta-analysis of 28
well-designed clinical trials (919 patients) on
laser therapy (Jin etal. 2013) reported that gross
response rate for laser therapy is 71% (95% Cl,
63–78%), with rates of 68%, 72%, and 69%
being observed for scar prevention, hypertrophic
scars, and keloid treatment, respectively. Most
effective laser systems proved to be the
585/595 nm pulsed-dye laser and 532 nm
potassium- titanyl-phosphate laser systems. Mean
laser uence was 6.6J/cm2 (range, 3–10.4J/cm2)
received in four (range, 2–6) sessions. Scar height
and erythema were signicantly reduced, whereas
the results for scar pliability were not signicant.
The gross complication rates reported ranged
from 0% to 20%. Transient erythema/purpura,
pain, and edema were observed most often and
resolved in 7–10days posttreatment. More severe
adverse events included crusting, hyper/hypopigmentation, blister, and supercial burns, which
resolved in 1–3 months posttreatment. Average
follow-up was 6.96months (range, 1–39months)
with no recurrence or progression observed during the follow-up period (Jin et al. 2013). The
authors concluded that laser therapy is safe and
efcacious for the treatment of hypertrophic
scars; however, the level of evidence for keloids
is still low. Randomized controlled trials with
larger sample sizes and longer follow-up duration
are needed (Jin etal. 2013).
More aggressive modes of treatment have also
been utilized for the treatment of keloids.
Radiotherapy after surgical excision is a widely
applied method. External beam radiotherapy and
brachytherapy have followed surgery in order to
prevent recurrence of keloids. A literature review
showed that a relatively high dose must be
applied in a short overall treatment time for effectively treating keloids. A biologically effective
dose of 30Gy seems to be the optimal treatment
and should be administered within 2 days after
surgery (Kal and Veen 2005). Postoperative
brachytherapy is also effective in the treatment of
keloids. De Cicco et al. (2014) retrospectively
compared low-dose-rate (LDR) (median delivered dose 16 Gy) with high-dose-rate (HDR)
(median dose 12 Gy) interstitial brachytherapy.
Recurrence rate was similar for both LDR and
HDR. Better symptomatic relief, however, was
reported in case of HDR treatment compared
with the LDR regimen. Recurrence rate was signicantly higher in males, in patients younger
than 44years, for arms, neck, and chest wall anatomical sites and for symptomatic keloids (De
Cicco etal. 2014). The results of a retrospective
comparative study between external beam
radiotherapy (EBRT) and interstitial high-doserate brachytherapy (HDR) were recently pub-
12.3 Pathologic Responses toWound Healing
165
lished by Hoang et al. (2017). The authors
retrospectively reviewed 128 patients with 264
keloid lesions treated by post-excision EBRT or
post-excision HDR brachytherapy. Nineteen percent of keloids recurred with post-excision EBRT
(42-month follow-up) and 23% recurred with
post-excision brachytherapy (12-month followup). While the recurrence rates were not statistically different, keloids treated with EBRT
recurred signicantly later than those treated by
HDR brachytherapy by a mean of 2.5years. The
authors concluded that a randomized controlled
study will help dene optimal adjuvant radiotherapeutic treatment (Hoang etal. 2017). The most
commonly reported side effect of radiotherapy
was changes in skin pigmentation (Mankowski
et al. 2017). Radiation therapy to the head and
neck as an adjunctive treatment for recurrent
keloids carries the potential for the late development of carcinoma (Fortson et al. 2012). The
risks, however, are small as suggested by the
existing evidence especially in older patients. In
younger adults and especially if radiotherapy is
being considered in adolescents or children, the
balance of risk vs. benet needs to be seriously
considered (McKeown etal. 2015).
Numerous emerging therapies (tacrolimus,
sirolimus, doxorubicin, transforming growth
factor- beta, epidermal growth factor, verapamil,
retinoic acid, tamoxifen, onion extract, hydrogel
scaffold, and skin tension off-loading device)
have also been studied for keloid and hypertrophic scars (Berman et al. 2017). However, the
most commonly used evidence-based methods
for the treatment of existing hypertrophic scars
are silicone, pulsed-dye laser, corticosteroids,
5-uorouracil, bleomycin, and scar massage. For
keloid scars, effective adjuncts to excision
include corticosteroids, mitomycin B, bleomycin, and radiation therapy (Khansa etal. 2016).
A scar contracture is an abnormal shrinkage or
shortening of a non-matured scar that can result
in functional impairment and distort facial features and is often seen in combination with scar
hypertrophy especially after extensive burns. In a
population of 1865 study patients, 33% developed at least one contracture at hospital discharge
(Goverman etal. 2017). Most contractures were
moderate or mild (ca. 80%). Statistically signicant predictors of contracture development were
male sex, black race, Hispanic ethnicity, medical
problems, neuropathy, TBSA grafted, and TBSA
burned. Predictors of the severity of contracture
included male sex, black race, medical problems,
ash burn, neuropathy, TBSA burned, and TBSA
grafted (Goverman etal. 2017). In another, prospective, multicenter study, patients who successfully avoided developing burn scar contracture
were adult males with an educated background
and few associated physical, medical, or social
problems (Richard et al. 2017). Patients were
judged to have a high pain tolerance and were
compliant with rehabilitation (Richard et al.
2017).
It is likely that scar contractures develop
despite early therapeutic interventions such as
positioning and splinting; new and better prevention strategies should therefore be identied in
order to prevent them (Goverman et al. 2017).
When present, however, they should be surgically
corrected at an early stage to release tension in
the scar, which will eventually restore function
and reduce scar hypertrophy. Common methods
of correction are Z-plasties, skin grafts, or various aps. The new healthy tissue brought in by
the latter is free of the inammatory cells found
in the base of the burn wound and, therefore, is
resistant to further contraction.
12.3.3 Other Scar Problems
The Stretched Scar
Skin tension after wound closure does not always
result in a hypertrophic scar or a keloid.
Occasionally, stretched scars are the result of
wound closure under tension (Fig. 12.7). An
experimental (cadaver) study by Meyer and
McGrouther (1991) demonstrated that hypertrophic scarring occurs in areas of high tension with
“pull” in many directions, whereas a stretched
scar results from increased tension in one axis
only. Tension relief, as mentioned earlier, is crucial for the nal outcome. Tissue undermining
and/or prolonged dermis support, preferably by a
subcuticular nonabsorbable suture (Elliot and
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12 Wound Healing Disturbances: TheUnfavorable Result
Fig. 12.7 (a) Stretched
scar of the forehead in a
6-year-old girl. The
suture marks
(crosshatching) are
clearly visible. (b) Four
years later, the suture
marks are still visible.
The scar has become
hypopigmented. (c)
Stretched scar at the
posterior scalp. The
suture marks are clearly
visible
a
c
Mahaffey 1989), usually lead to formation of a
narrow and aesthetically pleasing scar.
Suture Marks
Suture marks or crosshatching (Fig.12.7) is due
to a number of factors: heavy sutures, tight
sutures, large bites, sutures left in place for a long
time, and use of staples especially in black
patients. Suture marks range from light, punctuate indentations to heavy, unsightly scars.
Epidermis may grow into the suture tracts, if
suture material is left in place too long, causing
small sinuses and cysts (Furnas and Farzadmehr
2001). Choosing the appropriate suture material,
avoiding tight sutures, and removing sutures
early are the main steps one should take in order
to avoid crosshatching.
Concavities andConvexities
Scars which cross concavities (medial canthal
hollow, alar groove, neck, etc.) tend to form bowstrings, webs, or bridal bands (Fig.12.8). On the
other hand, scars that cross convexities have the
tendency to spread (Furnas and Farzadmehr
2001). A linear scar over the nose, for example,
may cause an indentation as it contracts, indent-
b
ing the thicker, softer sebaceous nasal skin
(Furnas and Farzadmehr 2001). Z-plasties or
W-plasties are occasionally indicated to improve
the aesthetic outcome.
Depressed Scars
Abnormal or disturbed collagen production can
cause anomalies of the cutaneous surface and
textural irregularities in the form of a depressed
scar (Fig.12.9). Furthermore, when mobile skin
adheres to immobile deep structures (e.g., mandibular area or after a tracheotomy) (Figs.12.10
and 12.11), xation and indentation of the scarred
skin result. Surgical separation of the deep from
the supercial scar through undermining and
interposition of supercial muscle/fascia between
the two portions is an effective way to tackle this
problem. In cases of larger depressed scars, surgical separation of the skin is followed by free fat
grafting or dermis-fat grafts, which satisfactorily
improves the surface contour (Fig. 12.11b–d).
Smaller depressions can be lled with the less
traumatic method of core fat grafts, as described
by Guyuron and Majzoub (2007).
Fat suspension injections obtained by vacuum-
assisted devices with cannula harvest and deliv-
12.3 Pathologic Responses toWound Healing
167
Fig. 12.8 (a, b)
Post-traumatic scar of
the left medial canthal
area with retraction, a
web, and a bridal band
Fig. 12.9 (a, b)
Depressed scars of the
left cheek. (c) Patient
with various posttraumatic of the face and
a depressed scar of the
left cheek. (d) The same
as (c) after scar
correction
ab
a
b
cd
ery techniques are also widely used grafting
methods. Long-term maintenance of autologous
fat grafts has been a matter of discussion. It may
be related to the traumatic handling of the graft
during the harvest and delivery steps of the procedure. The viability of aspirated fatty tissue
samples after centrifugation has been evaluated
in a study from Kentucky, which found that these
tissues have a suboptimal level of cellular function, indicative of potentially reduced survival
after transplantation (Pu et al. 2005).
Nontraumatic handling of fat grafts during both
the harvest and delivery steps has been shown in
experimental models to increase graft survival
(Fagrell etal. 1996) and should be the principle
which rules fat grafting in order to achieve a
more lasting outcome.
Injection of autologous platelet-rich plasma in
combination with phototherapy has recently been
reported as successful in treating depressed facial
scars (Oh etal. 2014). Furthermore, results from
an experimental study showed that injection of
autologous skin broblasts into the depressed
scar results in signicantly higher levels of col-
168
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12 Wound Healing Disturbances: TheUnfavorable Result
lagen type I and III in the dermal layer of the
injected skin as compared with those of the control, and type I collagen was signicantly higher
compared with type III. Reinjection of autologous skin broblasts could markedly improve the
repair (Zhao etal. 2016).
Occasionally, depressed scars are due to
underlying bony abnormalities (Fig. 12.12).
Thorough clinical investigation, and imaging
when indicated, avoids overlooking of such problems and leads to the correct mode of treatment.
Malaligned Scars
The inaccurate opposition and suturing of wound
edges lead to a malaligned or step-off scar. The
same phenomenon occurs when the sutured
edges have shifted from their original position.
Elliptical scar excision and wound edge realignment correct the step and improve the scar.
Trapdoor Scars
Scars that pucker above the skin surface in healing U- or V-shaped avulsion aps are called trapdoor scars. As the healing hemicircle contracts,
the skin may bulge with a “pin cushion” effect
(Furnas and Farzadmehr 2001). Staged excision
and resuturing or eventually a Z-plasty after redness and thickness have subsided has been used
for the correction of trapdoor scars.
Fig. 12.10 Depressed post-traumatic scar of the anterior
(tracheostomy) and lateral neck
Fig. 12.11 (a)
Depressed scar of the
left mandibular area. (b)
Dermis fat graft from
the lower abdomen. (c,
d) The inserted dermis
fat graft has
satisfactorily corrected
the depressed scar
a
cd
Anatomical Mismatch
Lacerations of the vermillion, the eyebrow, or the
nostril are occasionally closed inaccurately (Fig.
8.6). Scar excision and proper wound edge align-
ment or a small Z-plasty with the misplaced vermillion or brow forming one triangle and the
normal skin forming the other will correct the
b
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