Anda di halaman 1dari 31


Skenario Kedua
Minggu Ketiga

Nama Mahasiswa

: ............


: ............

Kelompok/ Tutor

: ........... / ..

Tim Kurikulum Pendidikan Preklinik

Program Pendidikan Dokter
Universitas Islam Malang

KELOID ,,,oh,,,

Susi pelajar SMU mengalami krisis kepercayaan diri akibat menderita Acne
vulgaris berat yang ditandai papule, pustule dan nodule. Susi akhirnya mendatangi
Dermatologist untuk mendapatkan pengobatan karena kondisi penyakitnya makin
parah. Seminggu menjalani pengobatan kondisinya berangsur membaik tetapi bekas
luka Acne vulgaris tidak dapat pulih seperti sedia kala, tampak adanya Scar tissue
dan Keloid pada wajah Susi. Keinginan Susi agar segera terbebas dari noda di
wajahnya diutarakan pada Dokter dan tindakan Operasi Plastik menjadi alternatif
pilihan. Susi menghadapi suatu dilema di satu sisi dia menginginkan wajahnya
kembali pulih tetapi di sisi lain harus siap menerima resiko munculnya Keloid baru
pada luka sayatan operasi.
A. Apa yang terjadi pada diri Susi bila dikaji secara Biomolekular ?
B. Bagaimana kajian Bioetika Kedokteran dan Agama pada kasus Susi ?


1. Krisis Kepercayaan Diri
2. Acne Vulgaris
3. Papule
4. Pustule
5. Nodule
6. Dermatologist
7. Scar Tissue
8. Keloid
9. Operasi Plastik
10. Biomolekular = molekul yang dihasilkan oleh sel hidup (protein, lemak dan
11. Biomedikal = biologis dan medis yang terkait dengan penerapan ilmu alam
(biologi, biokimia, biofisika dll) dalam ilmu kedokteran.



Mengapa Susi menderita Acne vulgaris ? (Faktor penyebab Acne vulgaris)

Bagaimana mekanisme terbentuknya Scar tissue dan Keloid di wajah Susi ?
Adakah hubungan Acne vulgaris dengan Scar tissue dan Keloid pada wajah Susi ?
Bagaimana proses terjadinya Wound Healing ?
Bagaimana bentuk-bentuk adaptasi sel setelah terjadi Injuri ?
Bagaimana upaya pencegahan terbentuknya Scar tissue dan Keloid ?
Bagaimana saran dokter terhadap tindakan operasi plastik bila ditinjau dari sisi
Bioetika Kedokteran ?
h. Bagaimana tindakan operasi plastik bila ditinjau dari sisi nilai-nilai Agama ?

Bacalah tentang :
1. Injury persisten
2. Inflamasi kronis
3. Wound healing
4. Adaptasi sel


1. Memahami proses terjadinya Wound Healling
2. Memahami mekanisme pembentukan Scar tissue dan Keloid.
3. Memahami bentuk-bentuk adaptasi sel
4. Memahami peran adaptasi sel (sisi positif dan negatif)
5. Memahami upaya penghambatan pembentukan Scar Tissue atau Keloid.
6. Memahami peran gangguan adaptasi sel terhadap patogenesa penyakit
7. Mahasiswa dapat menjelaskan konsep Bioetika Kedokteran dan nilai-nilai Agama


Radiasi, Iritan
Benda Tajam, Suhu

M.O / Alergen



Free Radikal


PG, Bradikinin,
Histamin, IL-10, Leeukotrien




Kerusakan Katup
Extravasasi Cairan

Hipoxia, Acidosis
Kematian PMN, Steril Pus
Kerusakan Sel

Kerusakan Limfatik



Functio Lesa



WOUND HEALING 1st atau 2nd








Jumlah Sel

Ukuran Sel


Ukuran Sel

Sel Berubah

Jumlah Sel



Koagulasi Faktor >>
Vasokontriksi >>

Mediator Inflamasi >>
(TNF, IL-1, PG, TGF)

Hormon & GF >>
Enzim >>

Degradasi Kolagen <<
Remodeling Kolagen <


OH*, O2*, H2O2

Proliferasi Fibroblast >

Sintesa Kolagen III >>
Kolagen III I <<

Kolagen >>
Jaringan Normal <<



Glikosaminoglikan >>
Neokolagenase <<




Hole Scar
Valley Scar

Hole Scar
Valley Scar




Rolling Scar

Rolling Scar
Thickened Scar

Acne vulgaris (commonly called acne) is a common skin condition, caused by changes in
pilosebaceous units, skin structures consisting of a hair follicle and its associated
sebaceous gland, via androgen stimulation. It is characterized by noninflammatory
follicular papules or comedones and by inflammatory papules, pustules, and nodules in its
more severe forms. Acne vulgaris affects the areas of skin with the densest population of
sebaceous follicles; these areas include the face, the upper part of the chest, and the back.
Severe acne is inflammatory, but acne can also manifest in noninflammatory forms.[1] Acne
lesions are commonly referred to as pimples, blemishes, spots, zits, or simply acne.
Acne occurs most commonly during adolescence, affecting more than 89% of teenagers,
and frequently continues into adulthood. The cause of acne in adolescence is generally an
increase in male sex hormones, which people of both genders accrue during puberty.[2] For
most people, acne diminishes over time and tends to disappearor at the very least
decreaseafter one reaches one's early twenties. There is, however, no way to predict how
long it will take to disappear entirely, and some individuals will carry this condition well
into their thirties, forties and beyond.[3]
The face and upper neck are the most commonly affected, but the chest, back and
shoulders may have acne as well. The upper arms can also have acne, but lesions found
there are often keratosis pilaris, not acne. Typical acne lesions are comedones,
inflammatory papules, pustules and nodules. Some of the large nodules were previously
called "cysts" and the term nodulocystic has been used to describe severe cases of
inflammatory acne.[4]
Aside from scarring, its main effects are psychological, such as reduced self-esteem[5] and,
according to at least one study, depression or suicide.[6] Acne usually appears during
adolescence, when people already tend to be most socially insecure. Early and aggressive
treatment is therefore advocated by some to lessen the overall impact to individuals.[5]

1. Causes of acne
Acne develops as a result of blockages in follicles. Hyperkeratinization and formation of a
plug of keratin and sebum (a microcomedo) is the earliest change. Enlargement of
sebaceous glands and an increase in sebum production occur with increased androgen
(DHEA-S) production at adrenarche. The microcomedo may enlarge to form an open
comedone (blackhead) or closed comedone (whitehead). Whiteheads are the direct result of
skin pores becoming clogged with sebum, a naturally occurring oil, and dead skin cells. In
these conditions the naturally occurring largely commensal bacteria Propionibacterium
acnes can cause inflammation, leading to inflammatory lesions (papules, infected pustules,
or nodules) in the dermis around the microcomedo or comedone, which results in redness
and may result in scarring or hyperpigmentation.[10]

Primary causes
Acne is known to be partly hereditary. Several factors are known to be linked to acne:

Family/Genetic history. The tendency to develop acne runs in families. For

example, school-age boys with acne often have other members in their family with
acne as well. A family history of acne is associated with an earlier occurrence of
acne and an increased number of retentional acne lesions.[11]

Hormonal activity, such as menstrual cycles and puberty. During puberty, an

increase in male sex hormones called androgens cause the follicular glands to get
larger and make more sebum.[12]

Inflammation, skin irritation or scratching of any sort will activate inflammation.

Stress. While the connection between acne and stress has been debated, scientific
research indicates that "increased acne severity" is "significantly associated with
increased stress levels."[13] The National Institutes of Health (USA) list stress as a
factor that "can cause an acne flare."[14] A study of adolescents in Singapore
"observed a statistically significant positive correlation [] between stress levels
and severity of acne."[15]

Hyperactive sebaceous glands, secondary to the three hormone sources above.

Bacteria in the pores. Propionibacterium acnes (P. acnes) is the anaerobic

bacterium that causes acne. In-vitro resistance of P. acnes to commonly used
antibiotics has been increasing.[16]

Use of anabolic steroids.[17]

Exposure to certain chemical compounds. Chloracne is particularly linked to toxic

exposure to dioxins, namely Chlorinated dioxins.[citation needed]

Chronic use of amphetamines or other similar drugs.[18]

Several hormones have been linked to acne: the androgens testosterone,

dihydrotestosterone (DHT) and dehydroepiandrosterone sulfate (DHEAS), as well as
insulin-like growth factor 1 (IGF-I).
Development of acne vulgaris in later years is uncommon, although this is the age group
for Rosacea which may have similar appearances. True acne vulgaris in adult women may
be a feature of an underlying condition such as pregnancy and disorders such as polycystic
ovary syndrome or the rare Cushing's syndrome. Menopause-associated acne occurs as
production of the natural anti-acne ovarian hormone estradiol fails at menopause. The lack
of estradiol also causes thinning hair, hot flashes, thin skin, wrinkles, vaginal dryness, and
predisposes to osteopenia and osteoporosis as well as triggering acne (known as acne
climacterica in this situation).


The popular belief that chocolate intake, in and of itself, is a cause of acne is not supported
by scientific studies.[19][20] As discussed below, various studies point not to chocolate, but to
the high glycemic nature of certain foods containing simple carbohydrates as a cause of
acne. Chocolate itself has a low glycemic index.[21]

Recently, three epidemiological studies from the same group of scientists found an
association between acne and consumption of partially skimmed milk, instant breakfast
drink, sherbet, cottage cheese, and cream cheese.[22][23][24] The researchers hypothesize that
the association may be caused by hormones (such as several sex hormones and bovine
insulin-like growth factor 1 (IGF-1)) or even iodine[25] present in cow milk.

The long-held belief that there is no link between diets high in refined sugars and
processed foods, and acne, has recently been challenged.[26] The previous belief was based
on earlier studies (some using chocolate and Coca-Cola) that were methodologically
flawed.[26][27][28] The recent low glycemic-load hypothesis postulates that rapidly digested
carbohydrate foods (such as soft drinks, sweets, white bread) produce an overload in blood
glucose (hyperglycemia) that stimulates the secretion of insulin, which in turn triggers the
release of IGF-1.[26] IGF-1 has direct effects on the pilosebaceous unit (and insulin at high
concentrations can also bind to the IGF-1 receptor)[29] and has been shown to stimulate
hyperkeratosis and epidermal hyperplasia.[30] These events facilitate acne formation. Sugar
consumption might also influence the activity of androgens via a decrease in sex hormonebinding globulin concentration.[31][32]
In support of this hypothesis, a randomized controlled trial of a low glycemic-load diet
improved acne and reduced weight, androgen activity and levels of insulin-like growth
factor binding protein-1.[33] High IGF-1 levels and mild insulin resistance (which causes
higher levels of insulin) had previously been observed in patients with acne.[34][35][36] High
levels of insulin and acne are also both features of polycystic ovarian syndrome.[26]
According to this hypothesis, the absence of acne in some non-Westernized societies could
be explained by the low glycemic index of these cultures' diets.[37] It is possible that genetic
reasons account for there being no acne in these populations, although similar populations
(such as South American Indians or Pacific Islanders) do develop acne.[38][39] Note also that
the populations studied consumed no milk or other dairy products.[40]
Further research is necessary to establish whether a reduced consumption of high-glycemic
foods, or treatment that results in increased insulin sensitivity (like metformin) can
significantly alleviate acne, though consumption of high-glycemic foods should in any case
be kept to a minimum, for general health reasons.[41] Avoidance of "junk food" with its high
fat and sugar content is also recommended.[42]

Vitamins A and E
Studies have shown that newly diagnosed acne patients tend to have lower levels of
vitamin A circulating in their bloodstream than those who are acne free.[43] In addition
people with severe acne also tend to have lower blood levels of vitamin E.[44]

Acne is not caused by dirt. This misconception probably comes from the fact that
blackheads look like dirt stuck in the openings of pores. The black color is not dirt but
simply oxidized keratin. In fact, the blockages of keratin that cause acne occur deep within
the narrow follicle channel, where it is impossible to wash them away. These plugs are
formed by the failure of the cells lining the duct to separate and flow to the surface in the
sebum created there by the body. Built-up oil of the skin can block the passages of these
pores, so standard washing of the face could wash off old oil and help unblock the pores.

2. What is Scar Tissue ?

Adhesions (scar tissue) is a dead fibrotic tissue that forms mostly in muscles, tendons,
ligaments, fascia, and joints.
Scar Tissue occurs as a result of injury , surgery, or repetitive motion. When a muscle,
tendon, or ligament is torn (strained or sprained) or nerve is damaged, healing occurs in
three stages called the inflammatory response: acute inflammation, repair, and remodeling.
In acute inflammation, redness, swelling, heat and pain occur. This phase lasts
approximately 72 hours. After the inflammation recedes, repair begins. The damaged
tissues heal with adhesions or scar tissue formation rather than the formation of brand new
When a muscle tightens up-- through a repetitive motion such as typing, or after it has been
injured-- swelling occurs, and it restricts the oxygen supply to the muscles and connective
tissues (hypoxia). The lack of oxygen also causes scar tissue to form.
That scar tissue can adhere to muscle fibers, preventing them from sliding back and forth
properly. It can adhere to connective tissues, limiting the flexibility of a muscle or joint.
And it can adhere to nerve cells, leading to carpal tunnel syndrome, chronic back pain, and
other conditions.
Scar tissue can bind up many layers of muscle and connective tissue, causing varying
degrees of limited movement and pain.
Research has proven scar tissue to be weaker, less elastic, more prone to future re-injury
and as much as 1000 times more pain sensitive than normal, healthy tissue. Chronic pain is
the result, pain that could remain for years after the initial injury.
To avoid the formation of adhesive scar tissue after an injury, surgery, or excessive
muscle's overuse, healing must take place in the presence of a full range of movement.
Scar tissue forms as skin heals after an injury or surgery. The amount of scar tissue may be
determined by the size, depth, and location of the wound; the age of the person;
heredity; and skin characteristics.
The color of a scar may be pale pink, brown, or silvery. Some people tend to get scars
more easily, and scars are more likely to form after wounds on certain parts of the body.
Guaranteed effective all natural Scar Removal

How scarring occurs

A scar is a natural part of the healing process. Skin scars occur when the deep, thick layer
of skin (the dermis) is damaged. The worse the damage is, the worse the scar will be. Most
skin scars are flat, pale and leave a trace of the original injury that caused them. The
redness that often follows an injury to the skin is not a scar, and is generally not permanent.
The time it takes for it to go away may, however, range from a few days to, in some serious
and rare cases, a few years. Various treatments can speed up the process in serious cases.
Scars form differently based on the location of the injury on the body and the age of the
person who was injured. To mend the damage, the body has to lay down new collagen
fibers (a naturally occurring protein that is produced by the body by fibroblasts). In
wounded tissue these fibers are over expressed with collagen, but not so in non wounded
tissue. Stable forms of topical vitamin C have been shown to improve collagen

formation[2]. Recent research has also implicated the gene product osteopontin in scarring
and University of Bristol have developed a gel that inhibits the process[3] [4].
An injury does not become a scar until the wound has completely healed. And because the
wounded body tissue over expresses collagen on the fibers and cannot re-build, the new
tissue will have a different texture and quality than the surrounding normal tissue. This
collagen producing process results in a fortuna scar.
Transforming Growth Factors (TGF) play a critical role in scar development and current
research is investigating the manipulation of these TGFs for drug development to prevent
scarring from the emergency adult wound healing process. As well, a recent American
study implicated the protein Ribosomal s6 kinase (RSK) in the formation of scar tissue and
found that the introduction of a chemical to counteract RSK could halt the formation of
Cirrhosis. This treatment also has the potential to reduce or even prevent altogether other
types of scarring.[5]

Abnormal scars
Two types of scars are the result of the body overproducing collagen, which causes the scar
to be raised above the surrounding skin. Hypertrophic scars take the form of a red raised
lump on the skin, but do not grow beyond the boundaries of the original wound, and they
often improve in appearance after a few years. Keloid scars are a more serious form of
scarring, because they can carry on growing indefinitely into a large, tumorous (although
benign) growth.
Keloid scars can occur on anyone, but they are most common in dark-skinned people. [6]
Keloid scars can be caused by surgery, an accident, by acne or, sometimes, from body
piercings. In some people, keloid scars form spontaneously.
Although they can be a cosmetic problem, keloid scars are only inert masses of collagen
and therefore completely harmless and non-contagious. However, they can be itchy or
painful in some individuals. They tend to be most common on the shoulders and chest.
Alternately, a scar can take the form of a sunken recess in the skin, which has a pitted
appearance. These are caused when underlying structures supporting the skin, such as fat
or muscle, are lost. This type of scarring is commonly associated with acne, but can be
caused by chickenpox, surgery or an accident.
Scars can also take the form of stretched skin. These are called striae and are caused when
the skin is stretched rapidly (for instance during pregnancy, significant weight gain or
adolescent growth spurts), or when skin is put under tension during the healing process,
(usually near joints). This type of scar usually improves in appearance after a few years.

Scar keloid Jaringan

With the skin's constant ability to shed old cells and create new ones, cuts, wounds and
incisions are repaired. However, it is this very process that also results in scars of all shapes
and sizes. While a visible scar may be the end to the healing process, the results vary with
the individuals and methods used to help the body speed skin repair.
A scar is growth of collagen beneath the skin that is formed as the result of wound healing;
therefore, every cut or injury to the skin heals to form a scar. A scar usually takes 12 to 18
months to fully mature. Not all scars are the result of wounds, burns, surgeries and
Skin diseases caused by bacteria, fungus, or viruses can also result in scarring. For
example, acne often leaves a variety of scars, and stretch marks are a form of scars
caused by weight loss or growth. Early in the process, scars are red or dark and raised, but

will become paler and flatter over time. It can take up to 24 months for a scar to develop
and mature to its stable form and appearance.
There are three different types of scars --- atrophic, hypertrophic, and keloids. Atrophic
scars are depressed and cause a valley or hole in the skin. Hypertrophic scars are elevated
and will subside with time.
Keloids are actually non-malignant tumors formed by scar tissue that exceeds the
boundaries of an original incision or injury. Keloidal scars are elevated, expansive and
continue to grow. In addition to appearance, location and orientation are also important
considerations in determining scar type. If a scar is thickened, does not invade normal
tissue, and lies across the relaxed skin tension lines (creases in the skin), then it is a
hypertrophic scar. If it is elevated and invading normal tissue, then it is a keloid scar.
Keloids have the appearance of a raised amorphous growth and are frequently associated
with pruritus and pain.. Microscopy observation reveals randomly organized collagen
fibers in a dense connective tissue matrix. In normal scars, the collagen bundles are
arranged parallel to the skin surface.
An hypertrophic scar is a widened or unsightly scar that does not extend beyond the
original boundaries of the wound. Unlike keloids, an hypertrophic scar reaches a certain
size and subsequently stabilizes or regresses. Similar to keloids , hypertrophic scars are
associated with adverse wound healing factors.

Scars and the Skin Repair Process

The removal or reduction of scars, lesions, and stretch marks from the skin depends on a
process called "skin remodeling". The skin is designed to heal wounds quickly to prevent
blood loss and infection. Scars are manufactured from a rapidly formed "collagen glue"
that the body deposits into an injured area for protection and strength. In ideal skin healing,
wounded skin is rapidly closed, and then the healed area is slowly reconstructed to remove
the residual collagen scars and blend the skin area into nearby skin.
Scar collagen is removed and replaced with a mixture of skin cells and invisible collagen
fibers. This remodeling may continue in a skin area for ten years.
In children the remodeling rate is high and scars are usually rapidly removed from injured
skin areas. But as we reach adulthood, this rate diminishes and small scars may remain for
One way to accelerate remodeling is to induce a small amount of controlled skin
damage with a needle, laser, acid, or other means, and then let the body repair
processes rebuild the skin area.
A second method is to use enzymes and fibroblast proliferators to increase the body's
natural rebuilding processes and obtain even better final results. Fibroblasts are the cells in
the basal membrane of the skin and they are the precursors of all the structural elements of
healthy skin, including those that provide tensile strength and elasticity to skin. Enzymes
dissolve or "digest" damaged and dying cells.

A keloid (also known as a "keloidal scar"[1]:1499) is a type of scar, which depending on its
maturity, is composed of mainly either type III (early) or type I(late) collagen. It is a result
of an overgrowth of granulation tissue (collagen type 3) at the site of a healed skin
injury which is then slowly replaced by collagen type 1. Keloids are firm, rubbery lesions
or shiny, fibrous nodules, and can vary from pink to flesh-colored or red to dark brown in
color. A keloid scar is benign, non-contagious, and usually accompanied by severe

itchiness,[citation needed] sharp pains,[citation needed] and changes in texture. In severe cases, it can
affect movement of skin.
Keloids should not be confused with hypertrophic scars, which are raised scars that do not
grow beyond the boundaries of the original wound.
Keloids expand in claw-like growths over normal skin. They have the capability to hurt
with a needle-like pain or to itch without warning, although the degree of sensation varies
from patient to patient.
If the keloid becomes infected, it may ulcerate. The only treatment is to remove the scar
completely. However, the probability that the resulting surgery scar will also become a
keloid is high, usually greater than 50%.
Keloids form within scar tissue. Collagen, used in wound repair, tends to overgrow in this
area, sometimes producing a lump many times larger than that of the original scar.
Although they usually occur at the site of an injury, keloids can also arise spontaneously.
They can occur at the site of a piercing and even from something as simple as a pimple or
scratch. They can occur as a result of severe acne or chickenpox scarring, infection at a
wound site, repeated trauma to an area, excessive skin tension during wound closure or a
foreign body in a wound. Keloids can sometimes be sensitive to chlorine.
Biologically, keloids are fibrotic tumors characterized by a collection of atypical
fibroblasts with excessive deposition of extracellular matrix components, especially
collagen, fibronectin, elastin, and proteoglycans. Generally, keloids contain relatively
acellular centers and thick, abundant collagen bundles that form nodules in the deep dermal
portion of the lesion. Keloids present a therapeutic challenge that must be addressed, as
these lesions can cause significant pain, pruritus (itching), and physical disfigurement.
They may not improve in appearance over time and can limit mobility if located over a
Keloids affect both sexes equally, although the incidence in young female patients has been
reported to be higher than in young males, probably reflecting the greater frequency of
earlobe piercing among women. There is a fifteen times higher frequency of occurrence in
highly pigmented people. It is speculated that people who possess any degree of African
descent, regardless of skin color, may be especially susceptible to keloid occurrences.
Scars are always formed to reconnect skin that has been damaged. Initially, they may be
red or dark and rose after the wound has healed but will become paler and flatter naturally
over time, resulting in a flat, pale scar.. Details on scar reduction at: biological wound
For reasons that are yet to be fully understood some people form raised scars that are red
and thick and may be itchy or painful and others develop scars that extend beyond the site
of an injury, called keloid scars .
Keloid scars are actually thick, puckered, itchy clusters of scar tissue that grow beyond the
edges of a wound or incision and rarely regress. They occur when the body continues to
produce tough, fibrous protein (known as collagen) after a wound has healed.
Keloid scars can result from any type of injury to the skin, including scratches, injections,
insect bites, tattoos or surgery procedures. Keloid scars can appear anywhere on the body,
but most commonly occur over the breastbone, on earlobes and on shoulders.
Hypertrophic scars sometimes are difficult to distinguish from keloid scars histologically
and biochemically, but unlike keloids, hypertropic scars remain confined to the injury site
and often mature and flatten out over time. Both types of scars secrete larger amounts of

collagen than normal scars, but typically the hypertrophic type exhibits declining collagen
synthesis after about six months. However, hypertrophic scars contain nearly twice as
much glycosaminoglycan as normal scars, and this and enhanced synthetic and enzymatic
activity result in significant alterations in the matrix which affects the mechanical
properties of the scars, including decreased extensibility that makes them feel firm.
As with hypertrophic scarring, people who have developed one keloid scar are likely to be
prone to this condition in the future and should alert their doctor or surgeon if they are
likely to need injections or to have any form of surgery.
Atrophic scars are characterized by a thinning and diminished elasticity of the skin due to a
loss of normal skin architecture. An example of an atrophic scar is striae distensae, also
known as stretch marks.

When the skin is damaged it produces growth factors,

inhibitors of tumors and proteins.
Following cutaneous injury or wounding, growth factors are produced to stimulate the
regeneration of tissue and to induce the creation of antimicrobial peptides. The growth
factor response ceases after regeneration of the tissue, when the physical barrier protecting
against microbial infections is re-established.
Skin wounds healing is a vital process involving proliferation of cellular elements with
accompanying synthesis of extracellular matrix that results in replacement of an open skin
wound with tissue. With the completion of the dynamic process of wound healing, a scar
remains in place of the wound. Although scar differs from normal uninjured skin, a normal
scar returns functionality to the skin. However, that scar restores tensile strength to only
approximately 80% of normal uninjured skin and stands out in appearance from the normal
surrounding skin.
The process of wound healing, however, can go awry. The wounds of some people undergo
aberrant healing, resulting in the formation of abnormal scars known as keloids or
hyperthropic scars. After a wound has occurred to the skin, both skin cells and connective
tissue cells (fibroblasts) begin multiplying to repair the damage. The fibroblasts form a
framework upon which the skin cells can migrate into and fill in the wound. It is the
balance between the rate of replication of fibroblasts versus skin cells that is important
here. If the fibroblasts replicate too quickly, they can form a dense network that is not as
easily penetrated by the skin cells and that results in a large scar. If the skin cells keep up
with the fibroblasts, then little scar tissue is formed and the skin has a more normal
appearance after the wound has healed.
Scar tissue is the fibrous connective tissue which forms a scar; it can be found on any
tissue on the body, including skin and internal organs, where an injury, cut, surgery or
disease has taken place, and then healed. Thicker than the surrounding tissue, scar tissue is
paler and denser because it has a limited blood supply; although it takes the place of
damaged or destroyed tissue, it is limited in function, including movement, circulation, and
sensation. Other than with minor cuts and scrapes, scarring is a common result of any
bodily damage.
Scar tissue in the skin is inferior to healthy, normal skin for several reasons: sweat glands
are damaged or destroyed, hair does not grow back, and there is less resistance to
ultraviolet radiation. Skin scars are normally flat and pale, illustrating the history of the
injury which caused them, yet often a body will produce too much fibrous tissue, resulting
in an extra thick or raised scar.

Hypertrophic scars form as red lumps on the skin but stay within the confines of the
original wound. Keloid scars may cover the original wound but then continue to grow,
causing a type of tumorous growth. Hypertrophic and keloid scars can occur in anyone, but
are more common in younger and dark skinned people. In rare cases, keloid scars form
without warning or injury.
Scars (also called cicatrices) are areas of fibrous tissue that replace normal skin (or other
tissue) after injury. A scar results from the biologic process of wound repair in the skin and
other tissues of the body. Thus, scarring is a natural part of the healing process. With the
exception of very minor lesions, every wound (e.g. after accident, disease, or surgery)
results in some degree of scarring.[citation needed]
Scar tissue is not identical to the tissue that it replaces and is usually of inferior functional
quality. For example, scars in the skin are less resistant to ultraviolet radiation, and sweat
glands and hair follicles do not grow back within scar tissue. A myocardial infarction,
commonly known as a heart attack, causes scar formation in the heart muscle, which leads
to loss of muscular power and possibly heart failure. However, there are some tissues (e.g.
bone) that can heal without any structural or functional deterioration.

3. Acne vulgaris & Scars Tissue or Keloid

Skin diseases caused by bacteria, fungus, or viruses can also result in scarring. For
example, acne often leaves a variety of scars, and stretch marks are a form of scars
caused by weight loss or growth. Early in the process, scars are red or dark and raised, but
will become paler and flatter over time. It can take up to 24 months for a scar to develop
and mature to its stable form and appearance. Acne often leaves small scars where the skin
gets a "volcanic" shape.
Physical acne scars are often referred to as "Icepick" scars. This is because the scars tend to
cause an indentation in the skin's surface. There are a range of treatments available.
Although quite rare, the medical condition Atrophia Maculosa Varioliformis Cutis also
results in "acne like" depressed scars on the face.

Ice pick scars: Deep pits, that are the most common and a classic sign of acne

Box car scars: Angular scars that usually occur on the temple and cheeks, and can
be either superficial or deep, these are similar to chickenpox scars.

Rolling scars: Scars that give the skin a wave-like appearance.

Hypertrophic scars: Thickened, or keloid scars.

4. Wound Healing
Wound healing is a complex and dynamic process of restoring cellular structures and tissue
layers. The human adult wound healing process can be divided into 3 distinct phases: the
inflammatory phase, the proliferative phase, and the remodeling phase. Within these 3
broad phases is a complex and coordinated series of events that includes chemotaxis,
phagocytosis, neocollagenesis, collagen degradation, and collagen remodeling. In
addition, angiogenesis, epithelization, and the production of new glycosaminoglycans
(GAGs) and proteoglycans are vital to the wound healing milieu. The culmination of these
biological processes results in the replacement of normal skin structures with fibroblastic
mediated scar tissue. For more information on wound healing, visit Medscape's Wound
Management Resource Center.

This process can go awry and produce an exuberance of fibroblastic proliferation with a
resultant hypertrophic scar, which by definition is confined to the wound site. Further
exuberance can result in keloid formation, where scar production extends beyond the area
of the original insult. Conversely, insufficient healing can result in atrophic scar formation.
Click here to complete a CME activity on evidence-based medicine in wound care.

Types of Wound Healing

Although various categories of wound healing have been described, the ultimate outcome
of any healing process is repair of a tissue defect.
Primary healing, delayed primary healing, and healing by secondary intention are the 3
main categories of wound healing. Even though different categories exist, the interactions
of cellular and extracellular constituents are similar.
A fourth category is healing that transpires with wounds that are only partial skin

Categories of Wound Healing

Category 1
Primary wound healing or healing by first intention occurs within hours of repairing a fullthickness surgical incision. This surgical insult results in the mortality of a minimal number
of cellular constituents.
Category 2
If the wound edges are not reapproximated immediately, delayed primary wound healing
transpires. This type of healing may be desired in the case of contaminated wounds. By the
fourth day, phagocytosis of contaminated tissues is well underway, and the processes of
epithelization, collagen deposition, and maturation are occurring. Foreign materials are
walled off by macrophages that may metamorphose into epithelioid cells, which are
encircled by mononuclear leukocytes, forming granulomas. Usually the wound is closed
surgically at this juncture, and if the "cleansing" of the wound is incomplete, chronic
inflammation can ensue, resulting in prominent scarring.
Category 3
A third type of healing is known as secondary healing or healing by secondary intention. In
this type of healing, a full-thickness wound is allowed to close and heal. Secondary healing
results in an inflammatory response that is more intense than with primary wound healing.
In addition, a larger quantity of granulomatous tissue is fabricated because of the need for
wound closure. Secondary healing results in pronounced contraction of wounds.
Fibroblastic differentiation into myofibroblasts, which resemble contractile smooth muscle,
is believed to contribute to wound contraction. These myofibroblasts are maximally
present in the wound from the 10th-21st days.
Category 4
Epithelization is the process by which epithelial cells migrate and replicate via mitosis and
traverse the wound. This occurs as part of the phases of wound healing, which are
discussed in Sequence of Events in Wound Healing. In wounds that are partial thickness,
involving only the epidermis and superficial dermis, epithelization is the predominant
method by which healing occurs. Wound contracture is not a common component of this
process if only the epidermis or epidermis and superficial dermis are involved.

Overview of Wound Healing

The amalgam of coordinated events that constitute the process of wound healing is quite
complex. The steps in the procession of wound healing include inflammation, the
fibroblastic phase, scar maturation, and wound contracture.2,3 Wound contracture is a
process that occurs throughout the healing process, commencing in the fibroblastic stage.2
The inflammatory phase occurs immediately following the injury and lasts approximately
6 days. The fibroblastic phase occurs at the termination of the inflammatory phase and can
last up to 4 weeks. Scar maturation begins at the fourth week and can last for years.2
An analogous system depicts the 4 phases as hemostasis, inflammation, granulation, and
remodeling in a continuous symbiotic process.4 This is the phase system used in this text.

Sequence of Events in Wound Healing

Following tissue injury via an incision, the initial response is usually bleeding. The cascade
of vasoconstriction and coagulation commences with clotted blood immediately
impregnating the wound, leading to hemostasis, and with dehydration, a scab forms. An
influx of inflammatory cells follows, with the release of cellular substances and
mediators. Angiogenesis and re-epithelization occur and the deposition of new cellular
and extracellular components ensues.
Initial phase - Hemostasis
Following vasoconstriction, platelets adhere to damaged endothelium and discharge
adenosine diphosphate (ADP), promoting thrombocyte clumping, which dams the wound.
The inflammatory phase is initiated by the release of numerous cytokines by platelets.
Alpha granules liberate platelet-derived growth factor (PDGF), platelet factor IV, and
transforming growth factor beta (TGF-b), while vasoactive amines such as histamine and
serotonin are released from dense bodies found in thrombocytes. PDGF is chemotactic for
fibroblasts and, along with TGF-b, is a potent modulator of fibroblastic mitosis, leading to
prolific collagen fibril construction in later phases. Fibrinogen is cleaved into fibrin and the
framework for completion of the coagulation process is formed. Fibrin provides the
structural support for cellular constituents of inflammation. This process starts immediately
after the insult and may continue for a few days.
Second phase - Inflammation
Within the first 6-8 hours, the next phase of the healing process is underway, with
polymorphonuclear leukocytes (PMNs) engorging the wound. TGF-b facilitates PMN
migration from surrounding blood vessels where they extrude themselves from these
vessels. These cells "cleanse" the wound, clearing it of debris. The PMNs attain their
maximal numbers in 24-48 hours and commence their departure by hour 72. Other
chemotactic agents are released, including fibroblastic growth factor (FGF), transforming
growth factors (TGF-b and TGF-a), PDGF, and plasma-activated complements C3a and
C5a (anaphylactic toxins). They are sequestered by macrophages or interred within the
scab or eschar.5
As the process continues, monocytes also exude from the vessels. These are termed
macrophages. The macrophages continue the cleansing process and manufacture various
growth factors during days 3-4. The macrophages orchestrate the multiplication of
endothelial cells with the sprouting of new blood vessels, the duplication of smooth muscle
cells, and the creation of the milieu created by the fibroblast. Many factors influencing the
wound healing process are secreted by macrophages. These include TGFs, cytokines and
interleukin-1 (IL-1), tumor necrosis factor (TNF), and PDGF.

Third phase - Granulation

This phase consists of different subphases. These subphases do not happen in discrete time
frames but constitute an overall and ongoing process. The subphases are "fibroplasia,
matrix deposition, angiogenesis and re-epithelialization".4
In days 5-7, fibroblasts have migrated into the wound, laying down new collagen of the
subtypes I and III. Early in normal wound healing, type III collagen predominates but is
later replaced by type I collagen.
Tropocollagen is the precursor of all collagen types and is transformed within the cell's
rough endoplasmic reticulum, where proline and lysine are hydroxylated. Disulfide bonds
are established, allowing 3 tropocollagen strands to form a triple left-handed triple helix,
termed procollagen. As the procollagen is secreted into the extracellular space, peptidases
in the cell wall cleave terminal peptide chains, creating true collagen fibrils.
The wound is suffused with GAGs and fibronectin produced by fibroblasts. These GAGs
include heparan sulfate, hyaluronic acid, chondroitin sulfate, and keratan sulfate.
Proteoglycans are GAGs that are bonded covalently to a protein core and contribute to
matrix deposition.
Angiogenesis is the product of parent vessel offshoots. The formation of new vasculature
requires extracellular matrix and basement membrane degradation followed by migration,
mitosis, and maturation of endothelial cells. Basic FGF and vascular endothelial growth
factor are believed to modulate angiogenesis.
Re-epithelization occurs with the migration of cells from the periphery of the wound and
adnexal structures. This process commences with the spreading of cells within 24 hours.
Division of peripheral cells occurs in hours 48-72, resulting in a thin epithelial cell layer,
which bridges the wound. Epidermal growth factors are believed to play a key role in this
aspect of wound healing.
This succession of subphases can last up to 4 weeks in the clean and uncontaminated
Fourth phase - Remodeling
After the third week, the wound undergoes constant alterations, known as remodeling,
which can last for years after the initial injury occurred. Collagen is degraded and
deposited in an equilibrium-producing fashion, resulting in no change in the amount of
collagen present in the wound. The collagen deposition in normal wound healing reaches a
peak by the third week after the wound is created. Contraction of the wound is an ongoing
process resulting in part from the proliferation of the specialized fibroblasts termed
myofibroblasts, which resemble contractile smooth muscle cells. Wound contraction occurs
to a greater extent with secondary healing than with primary healing. Maximal tensile
strength of the wound is achieved by the 12th week, and the ultimate resultant scar has
only 80% of the tensile strength of the original skin that it has replaced.


- Terdiri dari Fisiologik dan Patologik.
- Atrofri (Ukuran mengecil).
- Hipertrofi (Ukuran Membesar)
- Hiperpalsia (Ukuran bertambah)
- Metaplasia (Perubahan Jenis Sel).
- Pengecilan sel oleh karena menghilangkanya substansi sel sehingga jaringan mengecil.
Penyebab :
* Beban/Kurang aktivitas
* Persarafan Menghilang
* Aliran Darah berkurang
* Kekurangan Nutrisi.
Pembesaran sel dan organ oleh karena peningkatan struktur protein/organel
Fisiologik : uterus hamil, Patologik : Penyakit jantung hipertensi.
Penyebab : Kebutuhan meningkat, Rangsang hormonal, Beban meningkat.
- Fisiologik :
* Hormonal : Proliferasi kelenjar mammae
* Kompensatorik : Pengangkatan jaringan/penyakit.
- Patologik :
* Oleh karena stimulasi hormon/faktor pertumbuhan.
* Hiperplasia endometrium
* Virus
- Perubahan Reversibel tipe sel matur menjadi sel matur lainnya.
- Perokok :
* Epitel saluran nafas
* Jaringan lunak : Penulangan
Penyebab Jejas :
1. Hipoksia
2. Agen fisik.
3. Kimia / Obat
4. Mikroorganisme
5. Reaksi imunologil
6. Defek genetika
7. Ketidakseimbangan nutrisi
8. Penuaaan.
Jejas Sel terdapat Yang Reversibel dan Ireversibel
Hidrpopic Swelling :
- Tersering
- Akibat Gangguan fungsi pompa Na/K

- Sel membengkak, sitoplasma pucat, organel membengkak.

- Organ membesar dan lebih berat
Akumulasi Selular :
- Penimbunan substansi intrasel normal. Mis : lemak dihati
- Penimbunan substansi intra sel abnormal oleh karena gangguan metabolisme.
- Penimbunan pigmen/partikel yang tidak dapat dihancurkan.
Apoptosis :
- Proses fisiologik/patologik
- Mengenai satu sel
- Sel melisut
Nekrosis :
- Kematian sel
- Jejas terlalu berat dan lama sehingga tidak dapat diperbaiki.
- Inti sel mula-mula menjadi mengecil, hiperkormatik (piknotik).
- Kemudian kromatin mengalami lisis (kariolisis)
-akhirnya pecah (karioeksis)
Bentuk-bentuk Adaptasi Sel
1. Adaptasi dari Sel

Respon dari proses normal


Perubahan sel menyesuaikan dng lingkungan guna bertahan hidup sesuai

lingkungan yg berubah

Langkah-langkah Penyesuaian

Receptor binding, signal transduction, protein transcription, translation,


2. Bentuk Adaptasi sel.

b. Atrofi (Atrophy)
Definisi : pengisutan ukuran sel akibat kehilangan bahan sel penurunan fungsi sel
Atrofi Organ

Atrofi sel (selnya hidup)

Apoptosis (selnya mati)

Berkurangnya beban kerja
Hilangnya persarafan

Berkurangnya perbekalan darah

Nutrisi yg tidak memadai
Hilangnya rangsang hormon/endokrin
Mekanisme Biokimia
Penurunan sintesis protein
Peningkatan katabolisme protein
Perubahan Histologi
Penurunan ukuran sel
Peningkatan autofagi vacuole
Peningkatan badan residu (lipofuscin)

c. Hipertrofi (Hypertrophy)
Definisi : penambahan ukuran dari sel-sel penambahan ukuran dari organ.

Pembesaran pada organ ini pada sel yg tidak mampu bermitosis.

Oleh karena peningkatan fungsi/rangsang hormon

Peningkatan Sintesa Protein dari interaksi hormon dan Inti DNA

Peningkatan Organela sel

Contoh :

o Otot Skeletal dengan latihan

o Miokardium pada hipertensi

Sebab :
o Kenaikan tantangan fungsional

Otot skeletal pada latihan

miokardium pada hipertensi

o Stimulasi Spesifik hormonal

Uterus pada kehamilan

d. Hiperplasi (Hyperplasia)
Definisi : penambahan jumlah sel pada organ atau jaringanan
Hiperplasia dan Hipertrofi sering timbul bersamaan

Hormonal (mammae selama kehamilan)

Kompensasi (partial hepatektomi)

o Kelebihan hormonal / growth factor
Peningkatan absolute atau relative dari estrogen yg melebihi progesterone-endometrial hyperplasia
o Proses kontrol tetapi menyuburkan Cancer, stimulasi hormonal yang
berlebihan pada infeksi virus (papilloma viruses)

e. Metaplasia
Definisi : perubahan yg reversibel dimana bentuk sel dewasa menjadi sel dewasa
yang lain
Pemograman Genetic kembali dari stem sel (epithelial dan Mesenchymal)

Metaplasia Skuamosa epitel Respirasi

Merokok sigarete

Defisiensi vitamin

A Gastric Metaplasia

Epitel esofagus bag bawah

gastric reflux kronis

Metaplasia Mesenkhimal (tak jelas merupakan reaksi adaptasi)

o Tranformasi Fibroblasts menjadi osteoblasts atau chondroblasts

Mekanisme Adaptasi Sel

1. Adaptasi Terhadap Peningkatan Beban Kerja Sel

2. Adaptasi Terhadap Penurunan Beban Kerja Sel

Berdasarkan 2 bagan di atas maka dapat disimpulkan bahwa sel beradaptasi terhadap
cedera ada 3 cara yaitu :
1. Menambah atau mengurangi ukuran sel (hipertrofi dan atrofi).
2. Menambah atau mengurangi jumlah sel (hiperplasia dan involusi).
3. Merubah ukuran sel (metaplasia).

6. Reducing of Scar Tissue

Regulates dermal fibroblast proliferation and excess collagen, and thus helps to prevent
and reduce keloid scars and hyperthropic scarring. Acts as a potent antioxidant and antiinflammatory. Regulates blood vessel formation and oxygenation within the skin so
that fewer nutrients get into the scar tissues. Halts keloid scar itching. Smoothes old
surgery scars and also rough and dry skin.
Surgical procedures can be used to improve or minimize the appearance of scars, restore
function, and correct disfigurement resulting from an injury, lesion, or previous surgery.
Surgical revision is usually delayed until the scar lightens in color. It takes several months
or even a year after a wound has healed for the scar to lighten in color. Surgery to revise
scars can be done while the patient is awake or sleeping.
Medications (topical corticosteroids, anesthetic ointments, and antihistamine creams) can
reduce the symptoms of itching and tenderness.
No treatment for keloids is considered to be 100% effective. Some of the treatments that
are currently available are described below. These treatments have varying degrees of
effectiveness. All the invasive methods of treatment like surgery carry a serious risk of the
keloid recurring and becoming bigger than it previously was.

Mederma Contains allium cepa.

Contractubex Gel / Hexilak Gel These gels contain allium cepa extract, heparin
and allantoin. Developed for the treatment of post-thyroidectomy scars, these gels
are now indicated for the treatment of all post traumatic (burns, acne, piercings) or
post surgery scars and keloids. Treatment is simple but requires perseverance. } The
earlier the initiation of treatment, the better the prognosis.

Natural treatments Some scar treatments contain mucin from the snail helix
aspersa mller. The secretion from the snail regulates the skin healing and scar
formation process. Topical application of treatments with this ingredient on keloid
scars regulates and/or decreases dermal fibroblast proliferation and excess collagen
production, and thus prevents and reduces keloid scars and hyperthropic scars.[citation

Surgery Surgery requires great care during and after the operation. Keloids that
return after being excised may be larger than the original. There is a 50% chance of
recurrence after surgical removal. However, keloids are less likely to return if
surgical removal is combined with other treatments. Surgical or laser excision may
be followed by intralesional injections of a corticosteroid. Plastic closure of the
skin including techniques such as v-plasty or w-plasty to reduce skin tension are
known to reduce recurrence of keloids following excision.

Dressings Moistened wound coverings made of silicone gel (such as Dermatix)

or silastic have been shown in studies to reduce keloid prominence over time. This
treatment is safe and painless, although some patients may experience increased
itchiness from wearing the dressing for an extended period of time.

Steroid injections Steroid injections are best used as the scar begins to thicken or
if the person is a known keloid former. A series of injections with triamcinolone
acetonide or another corticosteroid may reduce keloid size and irritation. However,
injections are often uncomfortable and in large and/or hard scars can be difficult to
perform, requiring local anesthetic for people over 16, and full anesthetic for people
under. The treatment area can become very painful as the anesthetic wears off.

Compression Compression bandages applied to the site over several months,

sometimes for as long as six to twelve months, may lead to a reduction in the size
of the keloid. This is the best treatment for preventing new scars.

Cryosurgery Cryosurgery is an excellent treatment for keloids which are small

and occur on lightly pigmented skin. It is often combined with monthly cortisone
injections. The use of cryotherapy is limited since it causes skin blanching. It
freezes the skin and causes sludging of the circulation beneath, effectively creating
an area of localized frostbite. There is a slough of skin and keloid with reepithelization.

Radiation therapy Electron beam radiation can be used at levels which do not
penetrate the body deeply enough to affect internal organs. Orthovoltage radiation
is more penetrating and slightly more effective. Radiation treatments reduce scar
formation if they are used soon after a surgery while the surgical wound is healing.
This is one of the most effective procedures.[2]

Laser therapy This is an alternative to conventional surgery for keloid removal.

Lasers produce a superficial peel but often do not reduce the bulk of the keloid. The
use of dye-tuned lasers has not shown better results than that of cold lasers. A
relatively new approach is to combine laser therapy with steroid injections.

Newer treatments Drugs that are used to treat autoimmune diseases or cancer
have shown promise. These include alpha-interferon, 5-fluorouracil and bleomycin.
However, there is a need for further study and evaluation of this treatment

7. Treatments for skin scars

Scars can never be completely removed. Many doctors advise their patients to use vitamin
E supplements or creams to speed the healing process and keep the scar tissue suppler.
Surgeries are available to remove scars, but any surgery will always make a new scar: the
former scar may be less obvious, but it will not go away completely. Surgery is not
recommended for hypertrophic or keloid scarring, as there is the risk of recurrence
and worse scarring.
Currently no scar can be completely removed,[7] although healing in embryos and some
animals even after extended injuries can occur without scarring.[8] Therefore all treatments
will leave a trace, but a number of approaches have been tried with silicon gel sheeting and
steroid injections having the most widely accepted role in general scar treatment.[9]
In historical sequence, corticosteroid therapy by injection into the scars was introduced in
the 1960s, from the early 1970s pressure garment therapy was introduced for widespread
burn scars, and silicone gel sheets from the 1980s.[10]

Needling is an inexpensive process where the scarred area is continuously needled to
promote collagen formation. Once needled the area is allowed to fully heal, and needled
again if required depending on the intensity of the scar. Scarring needles and needling
rollers are available for home use; however, needling should not be done on parts of the
face or areas where major nerves are located without professional medical supervision.
Needling at home must also be done in line with hygienic and sterilization requirements.

Pressure garments
Pressure garments should be used only under supervision by a medical professional. They
are most often used for burn scars that cover a large area, this treatment is only effective on
recent scars.
Pressure garments are usually custom-made from elastic materials, and fit tightly around
the scarring. They work best when they are worn 24 hours a day for six to twelve months.
It is believed that they work by applying constant pressure to surface blood vessels and
eventually causing scars to flatten and become softer.

A long term course of steroid injections under medical supervision, into the scar may help
flatten and soften the appearance of keloid or hypertrophic scars.
The steroid is injected into the scar itself; since very little is absorbed into the blood
stream, side effects of this treatment are minor. However, it does cause thinning of the scar
tissue so it does carry risks when injected into scars caused by operations into ruptured
tendons. This treatment is repeated at 4-6 week intervals.Topical steroids are ineffective.[11]

Silicone sheeting and gel

Silicone scar treatments improve scar appearance and are often used to prevent and treat
hypertrophic scarring. The exact mechanism of action is unknown though some studies

suggest a manipulation of local ionic charges or a decrease in production of proinflammatory substances like TGF2.[12]
Dimethicone silicone gel appears to be is as effective as silicone sheeting in improving scar

Dermabrasion involves the removal of the surface of the skin with specialist equipment
and usually involves a general anaesthetic. It is useful with raised scars, but is less effective
when the scar is sunken below the surrounding skin.

Collagen injections
Collagen injections can be used to raise sunken scars to the level of surrounding skin. Its
effects are however temporary, and it needs to be regularly repeated. There is also a risk in
some people of an allergic reaction.

Laser surgery & resurfacing

The use of lasers on scars is a new form of treatment. Several cosmetic lasers have been
FDA approved for the treatment of acne scars by using laser resurfacing techniques.
Vascular lasers have been proven to greatly reduce the redness of most scars 610 weeks
after the initial treatment. It has been theorized that removing layers of skin with a carbon
dioxide or Erbium:YAG laser may help flatten scars. Scarring caused by acne (left), and
photo 1 day after scar revision surgery. Area around sutures is still swollen from surgery

Surgical excision of hypertrophic or keloid scars is often associated to other methods such
as pressotherapy or silicone gel sheeting. Lone excision of keloid scars however shows a
high recurrence rate close to 45%. A clinical study is currently ongoing to assess the
benefits of a treatment combining surgery and laser-assisted healing in hypertrophic or
keloid scars.

Low-dose, superficial radiotherapy, is used to prevent re-occurrence of severe keloid and
hypertrophic scarring. It is usually effective, but only used in extreme cases due to the risk
of long-term side effects.

Natural remedies
Research shows the use of vitamin E and onion extract as a treatment for scars is
ineffective. Vitamin E causes contact dermatitis in up to 33% of users and in some cases it
may worsen scar appearance. [14][15] Vitamin C normalizes collagen production and
encourages the production of an organized, healthy collagen framework [16] which improves
scar appearance. Vitamin C and some of its esters also fade the dark pigment associated
with some scars. [17]

1. Tutor menggali kembali keberhasilan belajar mahasiswa melalui pertanyaan yang
mengarah pada kemampuan mahasiswa menjelaskan LO yang ada
2. LO nomor 1 s.d 6 minimal 68% dikuasai. Terapi dan proses hukum minimal 58%
3. Harap melakukan pemeriksaan pencapaian kompetensi pada tutorial III dengan
menanyakan mahasiswa satu persatu.

1. Silbernagl.S, Lang.F., 2003, Teks & Atlas Berwarna Patofisiologi, Penerbit Buku Kedokteran
EGC, Jakarta.

2. Robbins, 1999, Pathologic Basic of Disease, Sixth edition, Saunders Company, Philadelphia.
3. Dale MM., 1994, Textbook of Immunopharmacology, Third edition, Blacwell Science, London.
4. Abbas,A.K., 1997, Cellular and Molecular Immnunology, Third edition, Sauders Company,

5. Underwood., J.C.E, 2004, General and Systematic Pathology, Fourth Edition, Toronto.
6. Porth, 1986, Pathophysiology Concepts of Altered Health States, Second edition, Philadelphia.
7. Walter, John B., 1982, Principles of Disease, second edition, Saunders Company, Toronto.
8. ^ a b c d e f g h i j k l m n o p q Cotran; Kumar, Collins. Robbins Pathologic Basis of Disease.
Philadelphia: W.B Saunders Company. 0-7216-7335-X.

9. ^ Wiedermann U, et al (1996). "Vitamin A deficiency increases inflammatory responses.".

Scand J Immunol. 44 (6): 578-84. PMID 8972739.
10. ^ Serhan CN, Savill J (2005). "Resolution of inflammation: the beginning programs the end".
Nat. Immunol. 6 (12): 11917. doi:10.1038/ni1276. PMID 16369558.
11. ^ Bastard J et al (2000). "Elevated levels of interleukin 6 are reduced in serum and
subcutaneous adipose tissue of obese women after weight loss". J Clin Endocrinol Metab 85
(9): 3338-42. PMID 10999830.
12. ^ Mohamed-Ali V et al (2001). "beta-Adrenergic regulation of IL-6 release from adipose tissue:
in vivo and in vitro studies". J Clin Endocrinol Metab 86 (12): 5864-9. PMID 11739453.
13. ^ Clment K et al (2004). "Weight loss regulates inflammation-related genes in white adipose
tissue of obese subjects". FASEB J 18 (14): 1657-69. PMID 15522911.
14. ^ M Stitzinger (2007). Lipids, inflammation and atherosclerosis (pdf). The digital repository of
Leiden University. Retrieved on 2007-11-02

15. Halliwel B., Gutteridge JM., 1999, Free Radical in Biology and Medicine, Third edition,
Oxford Science Publication, Oxford

16. Born V., Schwartz J., 1997, Vascular endothel Physiology, Pathology and therapeutic
Opportunities, Schattauer, Stuttgart.

17. Bloom W and Fawcet D.W. : A Textbook of Histology. 10 th ed. Philadelphia, WB Saunders
Co., 1978.

18. Coopenhaver W.M. and Johnson D.D. : Baileys Textbook of Histology. 7th ed. Baltimore, The
Williams Walkins Co. 1978.

19. Junquira L.C. and J Carneiro : Basic Histology. 3th ed. Lange Med. Publ. 1980.
20. Robbins, 1999, Pathologic Basic of Disease, Sixth edition, Saunders, Philadelphia.
21. Woywodt, Alexander ; Bahlmann, Ferdinand H,, Circulating Endothelial Cells : Life,
death, detachment and repair of the Endohelial Cell Layer. Nephrol.Dial. Transplant 17 : 17281730.

22. Lum H., Roebuck KA., 2001, Oxidant Stress and Endothelial Cell Dysfunction, Am.J Physiol
Cell Physiol 280 : C719-C741.

23. Carlos, Luiz., Carneiro, Jose., 2003, The circulatory System. Chapter 11. Basic Histology, Text
and atlas. 10th edition. Lange Medical Books McGraw-Hill Companies.

24. Dale MM., 1994, Textbook of Immunopharmacology, Third edition, Blacwell Science, London.
25. Dejana, Elisabetta. Corada, Monica., 1995, Endothelial Cell to Cell Junction. Review
FASEB. Vol 9.