2008

DEPPRIYAANCA SAXENAA SEMINAR

JAIPUR DENTAL COLLEGE
REPORT
ART FINAL YEAR BDS
2007-08

W
MEN
T OF
OU
PERI
ND
ODO
NTIC
HES
ALI
NG
ONTENTS –
1. INTRODUCTION
2. HEALING BY FIRST INTENTION (WOUNDS WITH OPPOSED
EDGES)
3. HEAIING BY SECOND INTENTION (WOUNDS WITH
SEPARATED EDGES)
4. WOUND STRENGTH
5. LOCAI AND SYSTEMIC FACTORS THAT INFLUENCE WOUND
HEALING
6. PATHOLOGIC ASPECTS OF WOUND REPAIR
7. HEALING FOLLOWING PERIODONTAL THERAPY
a). HEALING FOLLOWING SCALING & ROOT PLANING

b) HEALING FOLLOWING Curettage

c) HEALING FOLLOWING FLAP SURGERY

d) HEALING FOLLOWING OSSEOUS RESECTION

e) STAGES OF HEALING OF IMPLANTS

8. SUMMARY
 WOUND HEALING
INTRODUCTI ON
Wound healing is a complex but
orderly phenomenon involving a
number of processes:
1. Induction of an acute
inflammatory process by the initial injury
2. Regeneration of parenchymal cells
3. Migration and proliferation of both parenchymal and
connective tissue cells
4. Synthesis of ECM proteins
5. Remodeling of connective tissue and parenchymal
components
6. Collagenizaton and acquisition of wound strength
.
Healing by First Intention (Wounds With
Opposed Edges)
1. The least complicated example of wound repair is the healing
of a clean, uninfected surgical incision approximated by surgical
sutures
2. The incision causes death of a limited number of epithelial
cells and connective tissue cells as well as disruption of
epithelial Basement Membrane continuity.
3. The narrow incisional space immediately fills with clotted
blood containing fibrin and blood cells, dehydration of the
surface clot forms the well- known scab that covers the wound.
4. a) Within 24 hours, neutrophils appear at the margins of the
incision, moving toward the flbnn clot.
b)The epidermis at its cut edges thickens as a result of
mitotic activity of basal cells, and within 24 to 48 hours,
spurs of epithelial cells from the edges both migrate and
grow along the cut margins of the dermis, depositing BM
components as they move.
c) They fuse in the midline beneath the surface scab, thus
producing a continuous but thin epithelial layer.
5. By day 3, the neutrophils have been largely replaced by
macrophages. Granulation tissue progressively invades the
incision space. Collagen fibers are now present in the margins
of incision, but at first these are vertically oriented and do not
bridge the incision.
Epithelial cell proliferation continues, thickening the epidermal
covering layer.
6. By day 5,
a) The incisional space is filled with granulation tissue.
b)Neovascularization is maximal.
c) Collagen fibrils become more abundant and begin to bridge
the incision.
d)The epidermis recovers its normal thickness, and
differentiation of surface cells yields a mature epidermal
architecture with surface keratinization.
7. During the second week,
a) There Is Continued Accumulation Of Collagen And
Proliferation Of Fibroblasts.
b) The leukocytic infiltrate, edema, and increased vascularity
have largely disappeared. At this time, the long process of
blanching begins, accomplished by the increased
accumulation of collagen within the incisional scar,
accompanied by regression of vascular channels.
c) By the end of the first month, the scar comprises a cellular
connective tissue devoid of inflammatory infiltrate, covered
now by intact epidermis.
d)The dermal appendages that have been destroyed in the
line of the incision are permanently lost.
e) Tensile strength of the wound increases thereafter, but it
may take months for wounded area to obtain maximal
strength. Although most skin lesions heal efficiently, the
end product may not functionally perfect. Epidermal
appendages do not regenerate and there remains a dense
 connective tissue scar in place of the mechanically efficient
meshwork of collagen in unwounded dermis.

HeaIing by Second Intention (Wounds

With Separated Edges)
When there is more extensive loss of cells and tissue, as occurs
in infarction, inflammatory ulceration, abscess formation and
surface wounds that create large defects, the reperative
process is more complicated .The common denominator in all
these situations is a large tissue defect that must be filled.
Regeneration of parenchymal cells cannot completely
reconstitute the original architecture. Abundant granulation
tissue grows in from the margins to complete the repair. This
form of healing is red to as secondary union or healing by
second intention. Secondary healing differs from primary
healing in
several respects:
1. INEVITABLY, large tissue defects initially have more fibrin d more
necrotic debris and exudate that must be removed.
Consequently the inflammatory reaction is more intense.
2. Much larger amounts of granulation tissue are formed, when
a large defect occurs in deeper tissues, such as in viscous ,
granulation tissue with its numerous scavenger white cells
bears the full responsibility for its closure because drainage
to the surface cannot occur.
3. Perhaps the feature that most clearly differentiates primary
from secondary healing is the phenomenon of wound
contraction, which occurs in large surface wounds.
Contraction has been ascribed, at least in part, to the
 presence of myofibroblasts, altered fibroblasts that have the
ultrastrucrural characteristics of smooth muscle cells.
4. Whether a wound heals by primary or secondary intention is
determined by the nature of the wound, rather than by
healing process itself

Wound Strength
a) When sutures are removed , usually at the end of the first
week, wound
b) srength is
approximately 10% of
the strength of
Unwounded skin, but it
increases rapidly over
the next 4 weeks.
c) This rate of increase
then slows at
approximately third
month after the original
incision and then reaches plateau at about 70 to 80% of
the tensile strength of unwounded skin, which may persist
for life.
d) The recovery of tensile strength results from increased
collagen synthesis exceeding collagen degradation during
the first 2 months and from structural modifications of
collagen fibers (cross- linking, increased fiber size).

LocaI and Systemic Factors That Influence Wound

Healing
SYSTEMIC FACTORS INCLUDE THE FOLLOWING:
 a) NUTRITION has profound effects on wound healing rrotein
deficiency, for example, and particularly vitamin C
deficiency inhibit collagen synthesis and retard healing.
b) METABOLIC status can change wound healing. Diabetes
mellitus, for example, is associated with delayed healing.
c) CIRCULATORY status can regulate wound healing. Inadequate
blood supply usually caused by arteriosclerosis or venous
abnormalities that retard venous drainage also impair
healing.
d) HORMONES, such as glucocorticoids, have well-documented
anti-inflammatory effects that influence various
components of inflammation and fibroplasia; additionally,
these agents inhibit collagen synthesis.
LOCAL FACTORS THAT INFLUCENCE HEALING
INCLUDE THE FOLLOWING:
a) INFECTION is the single most important cause of
delay in healing.
b) MECHANICAL FACTORS, such as early motion of wounds,
can
delay healing.
c) FOREIGN BODIES, such as unnecessary sutures or fragments of
steel, glass, or even bone, constitute impediments to
healing.
d) SIZE, LOCATION, AND TYPE OF WOUND INFLUENCE HEALING. Wounds in richly
vascularized areas, such as the face, heal faster than those
in poorly vascularized ones, such as the foot. As we have
discussed, small injuries produced intentionally heal faster
than larger ones caused by blunt trauma.
Pathologic Aspects of Wound Repair
Complications in wound healing can arise from abnormalities in
any of the basic repair processes.
These aberrations can be grouped into three general
categories:
(1) deficient scar formation,
(2) excessive formation of the repair components, and
(3) formation of contractures.
Examples of each of these types of healing abnormalities are :
1. Dehiscence or rupture of a wound is most common after
abdominal surgery and is due to increased abdominal pressure.
This mechanical stress on the abdominal wound can be
generated by vomiting, coughing, or ileus.
2. Wounds can ulcerate because of inadequate vascularization
during healing. For example, lower extremity wounds in
individuals with atherosclerotic peripheral vascular disease
typically ulcerate

3. Non-healing wounds also form in areas devoid of sensation.

These neuropathic ulcers are occasionally seen in patients with
diabetic peripheral neuropathy
4. Excessive formation of the components of the repair process
can also complicate wound healing.
5. Aberrations of growth may occur
even in what may begin initially as
normal wound healing. The
accumulation of excessive amounts
of collagen may give rise to a raised
tumorous scar known as a KELOID, or hypertrophic scar .
6. Another deviation in wound healing is the formation of
excessive amounts of granulation tissue, which protrudes above
the level of the surrounding skin and in fact blocks re-
epithelialization. This has been called EXUBERANT GRANULATION (or
PROUD FLESH).

7. Contraction in the size of a wound is an important part in the

normal healing process. An exaggeration of this process is
called a CONTRACTURE and results in deformities of the wound and
the surrounding tissues.

HEALING FOLLOWING
PERIODONTAL THERAPY
1.HEALING FOLLOWING
SCALING & ROOT PLANING
Immediately after Scaling of Teeth the epithelial attachment will be
severed & junctional & crevicular epithelium Partially removed.
Numerous polymorphonuclear leucocytes can be seen between
residual epithelial cells & crevicular surface in about 2 hrs. There is
dilation of blood vessels, oedema & necrosis in the lateral wall of
the pocket. The remaining epithelial cells show very little pre-
mitotic activity at that time. 24 hrs. After scaling a widespread &
intense labeling of the cells have been observed, in all areas of the
remaining epithelium& in 2 days the entire epithelium is covered
by epithelium. In 4-5 days a new epithelial attachment may appear
at bottom of sulcus. Depending on the severity of inflammation &
the depth of the gingival crevice, complete epithelial healing
occurs in 1-2 weeks. Immature collagen fibers occur within 21
days. Following scaling, root planning & curettage procedure
healing occurs with the formation of a long, thin junctional
epithelium with no connective attachment.

2. HEALING FOLLOWING CURETTAGE

A blood clot forms between the root surface & the lateral wall of
the pocket, soon after the curettage. Large number of
polymorphonuclear leucocytes appear in the area shortly after the
procedure.This is followed by rapid proliferation of granulation
tissue.
Epithelial cells proliferate along the sulcus. Epitheliasation of the
inner surface of the lateral wall is completed in 2-7 days. The
junctional epithelium is also formed in about 5 days.Healing results
in the formation of a long junctional epithelium adherent to the
root surface.
3. HEALING FOLLOWING FLAP
SURGERY
Immediately after suturing of the flap
against tooth surface a clot forms
between the 2 tissues. The clot consists
of fibrin reticulum with many
polymorphonuclear leukocytes,
erythrocytes & remnants of injured
clots. At edge of flap numerous
capillaries are seen.
1-3days after surgery space between flap & tooth surface & bone
appears reduced & the epithelial cells along border of the flap start
migrating.
By 1 week after surgery, epithelial cells have migrated &
established an attachment to root surface by means of
hemidesmosomes. The blood clot is replaced by granulation tissue
proliferating from the gingival connective tissue, alveolar bone 7
periodontal ligament.
By 2nd week collagen fibers begins to appear. Collagen fibers gets
arranged parallel to root surface rather than at right angles. The
attachment between soft tissue & tooth surface is weak.
By end of one month following surgery the epithelial attachment is
well formed& the gingival crevice is also well epithealised. The
long junctional epithelium forms the attachment of soft tissues to
root surface.
In cases where MUCOPERIOSTEAL FLAP has been reflected,
superficial bone necrosis have been observed during first 3 days.
Osteoclastic Resorption occurs in that areawhich reaches its peak
at 4-6 days. Osteoblastic Remodelling occurs subsequently. Loss
of alveolar bone height by about 1 mm may be expected after
healing.
4. HEALING FOLLOWING OSSEOUS RESECTION
Osseous surgery initiates a
inflammatory response. Elevation of
Mucoperiosteal Flap results in
temporary loss of nutrient supply to
the bone.In additition surgical
resection of bone also contributes to
inflammatory changes. Necrosis of
the alveolar crest & osteoclastic
resorption of the bone takes place
initially. The osteoclastic
resorption is followed by bone deposition & remodeling. The initial
loss in bone height is compensated to some extent by the repair
and remodeling. Thus final loss in bone height is clinically
insignificant.
Osteoblastic activity is even seen after 1 yr. post-operatively. As
mucoperiosteum is sutured back on to alveolar process the
osteoclastic activity doesn’t lasts for long.

5. STAGES OF HEALING OF IMPLANTS

a. Wooven Bone Formation: When bone matrix is exposed to
extra-cellular fluid, non-collagenous proteins & growth factors are
set free & initiate repair. Wooven bone is first formed & bridge a
gap within a few days. Wooven bone formation dominates the first
4-6 weeks.
b. Lamellar Bone Formation : From 2nd month post-operatively the
microscopic structure of bone changes to lamellar or parallel
fibered bone.
c. Bone Remodelling : It begins around 3rd month post-operatively.
Initially rapid remodeling occurs which slows down & continues for
rest of the life.

SUMMARY
The healing wound, as a prototype of tissue repair, is a
dynamic and changing process .The early phase is one of
inflammation, followed by a stage of fibroplasia, followed by
tissue remodeling and scarring. Different mechanisms occurring
at different times trigger the release of chemical signals that
modulate the orderly migration, proliferation, and
differentiation of cells and the synthesis and degradation of
ECM proteins. These proteins, in turn, directly affect cellular
events and modulate cell responsiveness to soluble growth
factors. The magic behind the seemingly precise orchestration
of these events under normal conditions remains beyond our
grasp but almost certainly lies in the regulation of specific
soluble mediators and their receptors on particular cells; cell-
matrix interactions; and a controlling effect of physical factors,
including forces generated by changes
BIBLIOGRAPHY
1. PATHOLOGIC BASIS OF DISEASES
2. WILLIAM F GANGING, REVIEW OF MEDICAL
PHYSIOLOGY
3. NEWMAN, TAKEI, FERMIN, A. CARRANZA

4. GYTON, TEXTBOOK OF PHYSIOLOGY

5.