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Biology of Scar Formation

Biology of Scar Formation

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Published by: rajs2010 on May 24, 2010
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The Biology of
"glue" is formed
highly organized sequence
of physio
The ability
of one
collagenous tissue
to weld
tissues,adapt to
their structural
impart tensile
strength, and permit
A knowledge of wound
healing enables the clinician
and implement
treatment strategies based
this overview
1) to address the
(inflammatory,fibroplastic, and remodeling), 2)to
discuss the
processes occurring
in each phase,3)to
review appropriate intervention methods based
on research findings, and
4) to describe complications
interfere with
of scar formation.
Phys Ther
69:1014-1024, 1989]
Key Words:
Cicatrix; Collagen; Hand injuries; Inflammation;
extremity,hand and
Maureen A HardyHow We Heal
in its most basic definition,is a disruption of unity. Primitive animals respond to this threat by mitosisof their cells; that is, they are capableof regenerating exact duplicates of themissing parts. Select organs in ourbody still retain this biological gift ofregeneration. Scratches and mildburns of the skin are healed by epidermal regeneration. Hepatocytes inthe liver are capable of regrowth following mild toxic conditions. Peripheral nerves heal by axoplasm regeneration distally to restore nerve tracts.The ability of these tissue examples toregenerate or "reduplicate" their original condition is limited to minorinjuries and healing under optimalconditions. Certainly, more devastating insults such as full-thicknessburns, cirrhosis, and large nerve gapsoverwhelm their limited regenerationpotential.Nature has provided us withanother means of survival. It is aninferior method compared withregeneration, but it is the primarymeans of repair for all vertebrates.Special cells in our body respond toinjury by forming a collagenous"glue."This body glue is called
granulation scar tissue
Maintenance of our well-being dependson our body's ability to sense a disruption of unity, signal the appropriate cells, and carry through thesequence of repair without complications. This review of scar biologypresents an overview of how healing occurs. Certainly, each component of the repair process is an areaof intense research efforts, both inthe clinic and in the laboratory.Although a comprehensive treatiseon each section is beyond the scopeof this manuscript, the reference listwill enable interested readers topursue further information.
Scar Characteristics
How is it possible for the body'srepair system to duplicate the original form and function of the injuredtissue with only one type of glue?Our body structures can be dividedinto at least 14 different types ofcollagen. Mature scar is formedfrom type-I collagen; yet it is thegreatest chameleon in its ability toimitate the structure of other collagen types. Somehow, the scarformed in dense tissue "senses" theneed for strength and attempts tomimic the surrounding tissue instructure. Likewise, scar, filling adefect in loose, flexible tissue, willchange in its last phase of healingto reproduce, as much as possible,these physical characteristics. Thus,in response to certain internal andexternal influences, scar does differentiate to become quasi-tissue-specific. Experience tells us thatoften this attempt by scar to blendin cosmetically and functionally isnot successful. Enhancing the potential of scar to duplicate the desiredoutcome is the basis for surgical,pharmacological, and therapeuticmanagement protocols.
M Hardy, MS, PT, is Director, Hand Management Center, St Dominic Hospital, 969 Lakeland Dr,Jackson, MS 39216-4699 (USA), and Instructor, School of Health Related Professions, University ofMississippi Medical Center, 2500 N State
Jackson, MS 39216.
Physical Therapy/Volume 69, Number 12/December 1989
The patient's wound-healing status iscertainly an integral part of each initial evaluation in acute care. However,a descriptive history of how the repairprogressed in a patient with well-healed scar will alert the clinician tocertain potential problems. Reports ofprolonged swelling, excessive skinsloughing, dramatic color or temperature changes, progressive pain, andparesthesias alert us to the presenceof associated complications. Theextent of wound infection or dehiscence may predict the amount of scarformed in the tissue. The durationand type of immobilization affects themobility and stability of the scar.Underlying disease processes and pre-injury medications can influence thetiming of repair.
Normal Wound-Healing Phases
All forms of trauma, to any tissue, anywhere in the body, signal the reparative sequence to begin. The sequenceof events is highly organized and predictable. One process is stimulated tobegin, and its completion in turn signals another cellular response untilthe wound is bridged by scar. Theultimate goal in collagen researchmay be the discovery of healing without scar formation. Until then, to prevent scar formation is to preventhealing.The response to injury, either surgically or traumatically induced, isimmediate. The wound then passesthrough three phases toward finalrepair:
the inflammatory phase,
 phase, and 3) theremodeling phase. The inflammatoryphase prepares the area for healing,the
 phase rebuilds thestructure, and the remodeling phaseprovides the final form.Timetables for the beginning and endof each phase must be understood asgeneral guides. Different tissues healat different rates, and even onewound can show various areas healing rapidly or slowly.
what point
healing complete?This question is important in determining return to work, the timing offurther surgical intervention, and permanent impairment ratings. Knowledge regarding injury time framescombined with objective appraisal ofthe scar give us our best basis onwhich to make these decisions.
Inflammatory Phase
Inflammation is a normal and necessary prerequisite to healing. Changesin vascular flow are responsible forthe clinical symptoms we use todetect an inflammatory response. Themajority of the specialized cellsinvolved in this phase of the wound-healing process come from ourblood. Obviously, any blood vesselsthat traversed the wound were cut atthe time of injury. These cut vesselspoured whole blood into the wound,which then coagulated, sealing off theinjured vessels and lymphatic channels, thus temporarily closing thewound.In addition to this direct blood vesselinjury, noninjured vessels dilate inresponse to chemicals released frominjured tissues. Most cells in injuredtissue release histamine. Histaminecauses brief vasodilation in neighboring noninjured vessels. This combination of whole blood exudate andserous transudate creates a reddened,hot, swollen, painful environment.Bradykinins, derived from plasma inthe area of the injury, contribute tomore prolonged vascular permeability. Prostaglandins, produced by allcells in the body, are released withany breach of cell membrane integrity. Certain prostaglandins furthercontribute to long-term vascular vasodilation. The fibrin plugs that clottedin the wound also form in the lymphatic vessels. Lymphatic
sblocked to seal off the wound andprevent the spread of infection. Thesechannels do not reopen until later inthe healing process.
The mast cells also release hyaluronicacid and other proteoglycans into thewound milieu, which bind with thewatery wound fluid to create a gel.
This gel then does not
 Theinflammatory edema fills all spaces inthe wound and surrounds all damaged or repaired structures, bindingthem all together as one unit, or onewound (Figure 1A). This type ofedema causes loss of dermal fat, thusthinning normal skin in the area.
This thinning of normal skin ishypothesized to be the cause of theclinical condition of fingertip "pencilpointing" that occurs followingchronic edema conditions.That some swelling in a wound isinevitable and needed is a fact. Yet abalance is needed. If there is noinflammation, healing does not begin.If too little inflammation occurs, healing is slow. If too much inflammationoccurs, excessive scar is produced.This inflammatory fluid, derived fromthe blood, is high in fibrinogen.
Fibrinogen coagulates in the woundand in the surrounding tissues thatare now
 filled.The coagulatedgel will later mature into a dense,binding scar (Fig. 1B). Excessiveswelling, therefore, must not be permitted. Primary wound care ensuresthat all blood vessels have beenrepaired, cauterized, or clotted.Hematomas, the result of ongoingbleeding in the wound, create extraexudate, a powerful stimulus to scarformation.
Secondary wound careaddresses the contribution made byinduced vasodilation, which continuesin relation to the severity of thewound. This serous transudate can bediminished by the classic "RICE" regimen of rest, ice, compression, andelevation. Pharmacological use of steroids and aspirin affects the transuda-tive edema.
Their action aids ininhibiting prostaglandin release. Allwounds, and even controlled surgicalprocedures, require edema care.Ward showed that the use of a tourniquet in hand surgery significantlyincreased hand edema, as comparedwith controls, as long as one monthpostoperatively.
Excessive inflammatory fluid alsoaffects joint positioning. Eyring andMurray performed joint distentionstudies by infusing saline in normalhands.
They found that each jointresponds to swelling by assuming aPhysical Therapy/Volume 69, Number 12/December 1989
(A) Shaded area
represents fluid
edema bathing allinjured
(B) the
wound fluid
has coalesced into one scar binding all
(C)scar absorption
reorganization has occurred through successful
predictable position to lessen tensionon joint receptors. The patient with aswollen hand characterized by a"dropped" wrist, extended metacarpophalangeal (MP) joints, flexed inter-phalangeal (IP) joints, and adductedthumb posture confirms their findings. Young et al
and deAndrade et
demonstrated further that swelling in a joint causes joint receptors tofire in a biased manner. They facilitatemuscle action that draws the joint intothe "comfortable" position and neuro-logically inhibit antagonistic muscles.These findings imply that hands inthis phase need to be supported andpositioned correctly through the useof external dressings and splints.Active exercise may be disadvantageous during this phase unless theedema is first reduced, thus removingthe inhibitory effect of distended jointreceptors.For healing to commence, two prerequisite events must occur: l)Thewound must be decontaminated(phagocytosis), and
2) a
new bloodsupply (neovascularization) must thenbe available. Each of these processeswill be described.
Within blood vesselsadjacent to the wound, white bloodcells begin to stick to the dilatedendothelial walls.
Chemical changesin the wound induce and attract thesecells to slip through the enlarged capillary pores and migrate to the site ofinjury. Anti-inflammatory steroids alsoact at this point by inhibiting theamount and mobility of
bloodcells.The main purpose of
portion ofthe phase is to prevent or rid thewound of infection. All wounds, evenunder meticulous sterile conditions,are contaminated. Fortunately, oursystem of defense is adequate to prevent minor contamination from developing into a major infection. Certainconditions can tip the scale in favor ofinfection developing: the type of bacteria present, presence of foreignobjects, necrotic tissue, poor oxygensupply, malnutrition, certain vitamindeficiencies, radiated tissues, andimmunosuppression.The first white blood cells to reachthe wound are polymorphonuclearleukocytes. These short-lived cellsbegin the process of phagocytosis byfixing to bacteria, extending theirmembrane around them, then enzy-matically dissolving and digesting theinvaders. In a few days, another typeof phagocyte will predominate andremain in the wound until all signs ofinflammation cease. This cell, themacrophage, has two important rolesin the process of repair.
First, it continues the important job of phagocyto
Second, the macrophage has beentermed the "director cell" of repairbecause of its influence on scar production. As a scavenger cell, the macrophage not only attacks and engulfsbacteria but also disposes of necrotictissue in the wound. It is capable ofphagocytosing in poorly nourishedtissues with low oxygen levels or canconsume oxygen at over 20% of thebasal rate for enhanced phagocytosis.Because ischemic tissues are moreprone to infection than normal
sues,the oxygen tension of thewound is a critical factor. Maintenanceof an adequate arterial oxygen supplyfor optimum phagocytosis is dependent on sufficient blood volume andpercentage of atmospheric oxygenbreathed, as opposed to local, topically applied oxygen.
As macrophages ingest microorganisms, they also excrete products ofdigestion. Ascorbic acid, hydrogenperoxide, and lactic acid are byproducts of phagocytosis. Hydrogenperoxide aids in controlling anaerobicmicrobial growth. Ascorbic acid andlactic acid are believed to be the substances that signal the extent ofdamage.
Build-up of these acids isinterpreted as a need for assistancefrom more macrophages. More macrophages produce more by-products.The net result of an increased macrophage population is a more intenseand prolonged inflammatoryresponse.
Physical Therapy/Volume 69, Number 12/December 1989

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