Healing following pdl surgeries.pptx

HEALING FOLLOWING PERIODONTAL SURGERY

INTRODUCTION • Conventional periodontal therapy, usually

involves instrumentation in the inflamed dentogingival complex.

• Thus, the consequence of such therapeutic procedures depends largely on the cellular and molecular events associated with wound healing.

TERMINOLOGIES • Wound : Disruption of anatomical or functional

continuity of living tissues. • It can be due to physical, surgical, chemical, thermal,

microbial or immunological insult to the tissues.

• Wound healing: phenomenon by which body attempts to restore the tissue integrity by formation of new structures aimed to replace the defect.

• The new structure may more or less match the original structure.

• Repair: refers to the restoration of tissue architecture and function after an injury.

• Two types of reaction :

• Regeneration : some tissues are able to replace the damaged components and essentially return to a normal state

• Repair by scarring: if the injured tissue are incapable complete restitution , or the supporting structures are severely damaged ,repair occurs by laying down of connective tissue , a process termed healing that results in scar formation

GENERAL CONCEPTS – HEALING

HEALIING

• A cascade of events that involves the interaction of various cellular and molecular components that act in synchrony to effect wound closure

• The process can be understood as progressing through multiple stages, but realistically takes place as a continuum.

DIFFERENT TISSUES - DIFFERENT CAPACITIES TO HEAL

• High capacity• epithelial, lymphoid, hematopoietic, mesenchymal

tissues (fibroblasts, smooth muscle cells, osteoblasts, chrondrocytes, and endonthelial cells)

• Highly vascularized

• Low capacity• Nerve, muscle (skeletal and cardiac), cartilage

BASED ON THIS CRITERION, THE TISSUES OF THE BODY ARE DIVIDED INTO THREE

GROUPSContinuously dividing tissues

continuously being lost and repalced by maturation from stem cells and by proliferation of mature cells

Stable tissuesCells- quiescent and have only minimal replicative activity in their normal state capable of proliferating in response to injury

Permanent tissues

terminally differentiated and non proliferative post natal

TYPES OF HEALING

A. Primary Intention:

• When wound edges are directly next to one another

• Little tissue loss • Minimal scarring

occurs

B. Secondary Intention:• The wound is allowed to granulate • Granulation results in a broader scar • Healing process can be slower• Wound care must be performed

daily to encourage wound debris removal to allow for granulation tissue formation

• examples: gingivectomy, gingivoplasty,tooth extraction sockets, poorly reduced fractures.

C. Tertiary Intention • The wound is initially cleaned, debrided and

observed, typically 4 or 5 days before closure.• Presence of infection

The human adult wound healing process can be divided into 4 distinct but overlapping phases:

1. exudative phase (within hours)2. resorptive phase (day 0 to 4)3. proliferative phase (from day 3 up to 2

weeks)4. regenerative phase (from day 8 up to months)

Phase 1 and 2 -inflammatory phase.

EXUDATIVE PHASE

1. COAGULATION & CLOT FORMATION

• Hemostasis• Structural support• Provisional ECM• Early source of mediators of healing

•Immediately after a blood vessel is injured- vasoconstriction, • 10 to 20 minutes post-wounding - vasodilatation ( histamin, kinins, PGE2 and prostacyclin)

• Porousness of blood vessels increases

RESORPTIVE PHASE

Recruitment of PMNs (Early inflammatory phase) Recruitment of macrophages (Late inflammatory phase)

Polymorphonuclear cells

Attracted by fibronectin, growth factors, and kinins. Phagocytise debris and bacteria.Cleanse the wound Undergo apoptosis once they have completed their tasks - engulfed and degraded by macrophages.

Macrophages in healing:Growth factors - PDGF,VEGF,EGF,TGFB,FGF,IGF [M2 phenotype] - attract & support proliferation of fibroblasts, smooth muscle cells & endothelial cells - promotes matrix production & angiogenesis

Key role in transition from inflammation to granulation tissue formation

Phagocytose - PMNs, foreign & tissue debris, bacteria

PROLIFERATIVE PHASE

• Epithelial healing• Connective tissue healing• Fibroplasia• Formation of granulation tissue• Collagen deposition• Angiogenesis

• Wound Contraction

EPITHELIAL HEALING

• Mobilization of cells: achived by 2 distinct processes

• Migration: locomotion of epithelia cells

• Mitosis: mitotic growth of cells

• Regeneration of small wounds occur by migration alone• Large wounds need cell migration as well as new

cell supply by mitosis

Re-epithelialization

suprabasal keratinocytesare the first migratory cells sliding over thebasal keratinocytes.

• Basal and suprabasal cells from both the cut margins undergoes dedifferentiation and acquire potential for amoeboid movement

• Start proliferating and migrating towards the incisional space in the form of epithelial spurs.

• The movement of monolayer or sheets of cells during this migration is termed “streaming”

• Pattern: caterpillar track, frog leap phenomemon, sliding model

First keratinocytes to migrate- phagocytic

• Migration and proliferation of epithelial cells -Begins within 24 hours and Well approximated wound is covered by a layer of epithelium in 48 hours.

• For excised wound time depends upon its surface area• Cell migratory rate: 0.5-1mm/day

• contact from opposing edges: epithelial seal• Once seal is established- mitosis and definitive layers of

stratified squamous epithelium forms

CLINICAL SIGNIFICANCE

• Undisturbed healing of underlying C.T.• Inhibits loss of tissue fluid necessary for C.T. cells

and may affect repair• Tremendous increase in wound strength

B3 - inhibits the growth of primary human keratinocytes b1- stimulate keratinocyte motility by switching the cells from the differentiating to regenerative phenotype

CONNECTIVE TISSUE HEALING

• 4 processes• Production of new fibroblasts• Migration of these cells into the wounded area• Formation of new extracellular matrix• Remodeling of the extracellular matrix into the wound

FIBROPLASIA• Fibroblasts proliferate and migrate to the wound

area, adhering to fibronectin, deposit ground substance (later collagen) into the wound bed, secrete growth factors that attract epithelial cells to the wound site

• Granulation tissue begins to appear in the wound even during the inflammatory phase, and continues growing until the wound bed is covered, consists of new blood vessels, fibroblasts, endothelial cells, myofibroblasts, and the components of a new extra cellular matrix (ECM)

GRANULATION TISSUE FORMATION

• Begins with the formation of the epithelial seal

• According to Gillman (1955)• In shallow wound: onset of fibrogenesis occurs after

migration of the epithelial cells• Deep excised wound: first granulation tissue is built

up from the base and then epithelial migration occurs on this new C.T.

Granulation tissue formation

•Transient specialized organ of repair ,which replaces the PECM

• Microscopically, Fibroblasts + RBCs matrix + patent single cell lined capillaries surrounded by fibroblasts & inflm cells

•Fluid rich, source of growth factors & defensins

• On the granulation tissue frame work Migration & proliferation of fibroblasts Deposition of ECM by fibroblast

• Driven by PDGF, FGF-2,TGF-β ----- Inflammatory cells Activated endothelial cells• Cytokines like IL-1 & TNF

• Origin of matrix producing cells:

Surrounding CT Pericytes Bone marrow

• ‘Peripheral blood fibrocytes’ -Accumulate in early a/c phase -Antigen presenting cells -Secrete cytokines [immune response.hematopoesis,ECM synthesis]

COLLAGEN DEPOSITION

• one of fibroblast's most important duties is the production of collagen starting by the third post-wounding day

• collagen deposition increases the strength of the wound providing more resistance to traumatic injury

• cells involved in inflammation, angiogenesis, and connective tissue construction attach to, grow and differentiate on the collagen matrix

• Type III collagen predominates initially : 15-20% type III collagen

ANGIOGENESIS

• Functions of new formed blood vessels

• supply of oxygen and nutrients • transport of degradation products • cell settlement

• Angiogenesis process

• stimulation by chemical signals or hypoxia • endothelial cell proliferation • directional migration of endothelial cells • organisation and differentiation to form capillary tubes

At its peak, gran. tissue has more capillaries/unit vol than any other tissue

Growth factors inducing angiogenesis ----- VEGF,TGFB

Factors stabilizing vessels ----- Angiopoetin 1 &2 PDGF & TGFB

CONTRACTION

• Dehydration: removal of fluid by drying wound • Contraction of collagen• Discovery of myofibroblasts:

MYOFIBROBLAST

• Myofibroblasts move along fibronectin linked to fibrin in the provisional ECM in order to reach the wound edges and form connections to the ECM and they attach to each other and to the wound edges

• As the actin in myofibroblasts contracts, the wound edges are pulled together and fibroblasts lay down collagen to reinforce the contracted wound

MYOFIBROBLAST

• Differentiation of myofibroblasts - 6 - 15 days

• 70% of fibroblasts show α-smooth muscle actin

• Shape – fibroblasts Action – smooth muscle cells

• Reduces wound size by 40-80%

• After contraction –apoptosis →New normal CT fibroblasts emerge

Apoptosis begins at day 12, peaks at day 20 and resolves by day 60 after wounding

REGENERATIVE PHASE• Regenerative Phase, also called Remodeling or Maturation

Phase includes: • collagen

remodeling • blood vessel

apoptosis

TISSUE REMODELING• About 14 days post operatively wound is filled with fibers

that run in all direction and remodeling begins• Decrease in fibroblasts• Decrease in vascularity

• Remodeling consist of 2 distinct processes (homes,1959)• Resorption and changing of the orientation of these first

deposited fibers• Enlarging or increasing the numbers of oriented fibers

• Long lasting phase of repair

• Type III collagen, which is prevalent during proliferation, is gradually degraded and the stronger type I collagen is laid down

• Originally disorganized collagen fibers are rearranged, cross linked, and aligned along tension lines, the tensile strength of the wound increases

• After tissue remodeling is finished redundant blood vessels undergo apoptosis

GROWTH FACTORS IN PERIODONTAL WOUND HEALING

• Growth factors are polypeptide molecules, released by cells in the inflamed area, that regulate events in wound healing.

• Regulates connective tissue cell migration and proliferation and synthesis of proteins and other components of extra cellular matrix.

• Growth factors can be used to control events during periodontal wound healing (example: Promoting proliferation of fibroblasts from the periodontal ligament and favoring bone formation.)

HEALING AFTER PERIODONTAL PROCEDURES

CLINICAL REQUIREMENTS FOR EFFECTIVE HEALING

• The application of initial therapy prior to surgical intervention

• The selection of surgical approach specific for the cure of the particular inflammatory lesion

• The type of tissue environment that exists after surgery

• The degree of fibrosis of gingiva prior to and after surgery

• The method by which the surgical wound is protected in the postoperative period

• The maintenance of the dentition and the periodontium by the patient and the dentist daily and in periodic visits

SCALING AND ROOT PLANING

• Removes surface accretions

• Retards further accumulation of deposits

HEALING AFTER SRPDay 0 •Bleed and exudation of GCF will remove irritants

•Epi attachement is severed, acute inflammatory rxn in C.T

Day 1 •After an initial lag of 12-24 hrs, epi migration begins

Day 2 •Inflammation ↓, epithelialialization enhanced.

Day 5. •New epithelial attachment

1-2 wks •Residual retepegs involute•Clinically- gingival health

CURETTAGE(BLASS & LITE 1959)

• Involves removal of pocket wall

• Chemical and mechanical.

• The sharp curet or blade , however, has remained the method of choice

DURATION Connective tissue changes

Epithelial changes

Clinical changes

Immediately • Haemorrhage• a/c inflamm reac

• Removal of epthelial lining• Few cells may remain

• Blood&exudate

1st day • Marked inflamm • Epithelial migration begins (0.5-1mm/day)

• Edematous• Dislcoloration persists

2nd day • Inflamm • Vasularity

• Epithelium begins to cover the gingival corium

•Discoloration • Edema still +nt

4th-6th day • Chr inflamm• Collagenation • Matrix formation

• restoration of junctional &sulular epithelium

-

7th-10th day • Collagen formation& organisation

• Epithelium formation is complete

• Edema • Rigid&well adapted ginival wall

10th-14th day • Repair of conn tissue• vascularity

• Surface keratinization

• Normal color• Stippling appears• Gingival shrinkage

After 2 weeks • Mature collagen• New subsulcular & marginal vessels

-• Color,contour, consistency, texture.• Well adapted marginal gingiva

ULTRASONIC CURETTAGE• Epithelium- heat coagulation

• Immediately after – areas of coagulation – tissue discontinuity – fused collagen• Narrow band of necrotic tissue strips off the inner

lining of pocket• 3 days – epithelialisation occurs – lesser inflammation• 2 weeks – shorter & thinner epithelium – fewer rete pegs• Goldman (1980) – more satisfactory healing – healing is faster

CHEMICAL CURETTAGE

• Sodium sulphite, alkaline sodium hypochlorite, phenol.

• No control over magnitude of tissue destruction• More severe damage to underlying connective

tissue & bone

• Delayed healing

GINGIVECTOMY

• Elimination of suprabony pockets when underlying bone does not require therapy

• Elimination of gingival enlargements

• Surgical – scalpel – electrode • Produces an open surface wound• Heals by secondary intention

Duration Connective tissue

Epithelium Bone

Immediately Hemorrage,exudateBlood clot

Necrosis at wound margin

-

Few hours a/c inflamm reac Wound margin-Changes in prickle cell layer -

9-18 hours - Migration from prickle cell layer begins -

1st day PolybandCollagen fragmentationAngioblasts

Epithelialisation-centripetal fashion -

1st-3rd day - Hemidesmosomes &basement lamina

-

3rd-4th day Loss of clotGranulation tissue

- -

5th-14th day Disorganised conn tissuedilated blood vesselsAnastomis betw periodontal and gingival vessels

Epithelialisation~ completeNo rete pegs

Transient surface resorption(7-12 days)

14th-16th day Vascularity -

Reversal linesResorption continues

3-4 weeks Collagen formationOrganisation

Rete pegsDentogingival unitNew sulcus

Resorption ceasesCrestal bone level re-established

4-5 weeks - Complete repair -

By 7 weeks Complete repair - -

ELECTRO-SURGERY GINGIVECTOMY• Pope (1968)- delayed epithelialisation (by 4 days) - lack of bleeding and clot formation • Glickman&Imber(1970)- delayed healing - bone necrosis• Schneider&Zaki(1974)- no bleeding - transiently hyalinised C.T • Wilhelmsen et al(1976)- avoid contacting cemetum or

bone• Healing – fully rectified = conventional

LASER GINGIVECTOMY

• Advantages – minimal disturbance of surrounding tissues

– hemostatic effect – edema &pain – sterelisation of wound – minimal scarring

• Healing – delayed re epithelialisation – lesser inflammatory response – thermal necrosis – decreased wound contraction

CHEMOSURGERY GINGIVECTOMY• Chemicals – phenols – paraformaldehyde – potassium hydroxide

• Incomplete gingival remodelling• Delayed epithelialisation, connective tissue repair• Increased inflammation after chemical trauma• No control over the depth of action

FLAP SURGERY

• Periodontal flap – a section of gingiva and/or mucosa

surgically elevated fron the underlying tissue to

provide visibility and access to the root and bone

surface.

• Healing – both primary & secondary

• Reflection of epithelium and a layer of connective tissue

• Bone remains covered by a layer of connective tissue including periosteum

• Soft tissue including the periosteum is reflected to expose the underlying bone

FULL THICKNESS FLAP• Caffese ,Ramfjord& Nasjeleti (1968)

• Healing – 1st intention Ideal flap

adaptationMinimal surgical traumaNo intervening granulation tissueComplete within 21 days

2nd intention Intervening granulation tissueCommon in well adapted flaps

3rd intention Poor flap adaptationDelayed healing with complicationsNot complete even after 72 days.

Duration Healing 2 hours • No crevicular epithelium or epithelial attachment

• Narrow zone of necrosis on surgical surface of flap• Blood clot• Superficial necrotic changes on alveolar surface-empty lacunae

24 hours • Thick band of PMNL cells• Bone appears vital

2 days • Epithelial cells have started migrating• Blood clot & PMNL cells• Angioblasts & fibroblasts at alveolar crest• Superficial necrosis of bone• Cementoblasts -deranged for 1mm from wound surface

3 days • Epithelium makes contact with teeth surface• Thin blood clot• Inflammation• Connective tissue grows betw flap and bone• Collagen fibres within flap undergo necrosis• Granulation tissue starts forming

5 days • Granulation tissue is present• Osteoclasts (from marrow) – for 1mm over pdl membr side of bone• Cementoblasts – missing for 1mm apical to alv crest

Duration Healing 7 days • Formation of epithelial attachment begins

• Granulation tissue adheres the flap to underlyng bone• Severe osteoclastic activity (for 2-3 mm)

9 days • Crevicular epithelium & new epithelial attachment• Some cementoclastic activity• Osteoclastic activity over alveolar crest• Periodontal fibres replaced by vascular granulation tissue

14 days • Band of connective tissue betw flap & underlying bone• Free gingiva – vascular granulation tissue, no functional orientation• Alternative osteoclastic& osteoblastic activities• New periosteum – connective cells surrounded by immature collagen

21 days • Fully Epithelialised Gingival Crevice• Well Defined Epithelial Attachment• Functional Arrangement Of Supracrestal Fibres• Osteoblastic activity• Cementoblasts are normally arranged

35 days • Gingival Adaptation• Chronic inflammation in connective tissue

72 days • Total crevicular depth = 1mm• Parakeratinized free gingival margin• Periosteum appears normal• Functional orientation of gingival fibres(immature collagen)• Newly formed bone on tip of alveolar crest

PARTIAL THICKNESS FLAPS

• Lesser physical, biological & infective insult• Higher proliferative capacity of retained periosteum• Greater post-op edema• Healing depends on nature & thickness of periosteum

and retained connective tissue (min -0.5mm)• Heals faster with lesser destruction of alveolar bone• Ramjford & Costich (1968)

Duration Healing 1 weeks • Epithelium extends to margin of the clot and necrotic

debries• Rapid proliferation of granulation tissue• Rapid bone resorption

2 weeks • Complete epithelial coverage• Gingiva – vascular granulation tissue with subacute inflammation

3 weeks • Parakeratosis of gingival surface• Shallow new gingival crevice• Connective tissue parallel to root surface• Gingival fibers- no functional orientation• Diffuse chronic inflammation• Alternate areas of bone resorption and regeneration

4 weeks • Completely regenerated gingival tissue• Reparartive osteoblastic activity• Resorption lacunae on root surface- may extend into dentin

9 weeks • New epithelial attachment• Mild chronic inflammation• Bone formation continues

13 weeks • Epithelial covering is normal• Periosteal fibers – compressed & parallel to root surface• Slight resorption of cementum; undergoing repair

EFFECT OF THICKNESS OF BLOOD CLOT

• A thick coagulum has been associated with incomplete or imperfect adaptaion of soft tissue to the underlying bone

• Since the clot must be resorbed and replaced by connective tissue during healing thinner clot is more desirable than thick which retards the rapid attachment• The weakest part of adherence b/w flap and bone

occurs in area of the fibrin clot – not substantial enough to hold them together

APICALLY DISPLACED FLAP

• Introduced in 1950s – pocket elimination

– bone recontouring

– ing width of attached gingiva

• Can be partial/full thickness

• Costich & Ramjford (1968)

Healing sequence

Granulation starts covering the exposed boneSurface – acute inflammationPeriodontal membrane – chronic inflammationActive bone resorption starts

Thin layer of epitheliumGranulation tissue covers the wound surfaceSevere osteoclastic activity

Gingiva – parakeratinised epitheliumAppearance of shallow gingival crevice and epithelial attachmentConnective tissue – vasculat, young fibroblastsOsteoclasis &osteoblastosisNumerous resorption lacunae on cemental surface

Partially regenerated gingival tissueOsteoblastic activityAreas of root resorption undergoing repair

PEDICLE GRAFTS (WILDERMAN & WENTZ 1965)

Coronally displaced flap

Lateral pedicle

Double papilla

STAGE HEALINGAdaptaion(0-4 days)

Clot & thin fibrinous exudate betw flap and root surfacePMNLs in clot & connective tissueEpithelium at margins of flap proliferate – may contact tooth surface

Proliferation(4-21 days)

Connective tissue invades the fibrin layer6-10 days- fibroblasts apposed against root surfaceCollagen within the flap – oriented parallel to root surfaceThin collagen fibers adjacent to root (no fibrous union)Apical proliferation of epithelium- peaks at 10-14 daysOsteoclastic resorption (peaks at 6th day) - by 14th daySlight cemental resorption

Attachment(21-28 days)

Collagen fibers insert into new cementumCementoid deposition(by 28th day – along the entire root)Connective tissue attachmentNew gingival margin, sulcuc & epithelial attachmentOsteoblastic activity

Maturation(28-90 days)

Completely formed gingival sulcus and epithelial attachmentBone apposition at alveolar crest

DONOR SITEFull thickness Split thickness

Healing starts from periphery of woundSparing marginal gingiva of donor tooth prevents recession thereRecieves blood supply only through pdl vesselsGranulation tissue covers the woundOsteoclastic resorption on the pdl sideDehiscence if thin cortical platesEpthelialisation(centripetal fashion) – complete by 3 weeks

Retained periosteum and a layer of connective tissueIntact supraperiosteal vasculatureFaster healingMinimal bone resorption

FREE GINGIVAL GRAFT

Bjorn (1963) , Sullivan & Atkins (1968)

s zone of attached gingiva

can also be used over an extraction socket or osseous

graft (Ellegaard et al 1974).

success depends on survival of connective tissue

Oliver, Loe & Karring described the healing into 3 phases

Phase Healing

Initial phase(0-3 days)

• Thin layer of exudate Avascular plasmatic circulation(Foman 1960; Reese &Stark 1961)

• Epithelium gets desquamated

Revascularisation (2-11 days)

• Anastomosis betw graft & recipient site blood

vessels

• Capillaries proliferate in the graft tissue

• Fibrous union betw graft & conn tissue bed

• Re epithelialisation of the graft

Tissue maturation(11-42 days)

• Blood vessels in the graft reduce in no

• Epithelium matures-gets keratinised

• Functional integration – by 17th day

• Morphologically distinguishable for several

months

HEALING FOLLOWING SOFT TISSUE GRAFTS

Initial phase(0-3 days)

Revascularisation(2-11 days)

Tissue maturation (11- 42 days)

Pale – empty graft vesselsPink – vascularisation beginsSmooth & shiny – loss of epithelium

Thin grey veil like surface – new epitheliumNormal features – maturation of epithelium

SECONDARY CONTRACTION

• Upon healing, the graft may shrink by as much as

33% (Egli et al. 1975)

• Due to cicatrisation of tissues that unites it to the

recipient bed

• Thick graft on a rigid bed – maximum resistance to

shrinkage

Graft mobility

• Improper bed preparation - Too much loose tissue or muscle fibers left above the periosteum.• At this point, it is not necessary to redo the graft.• Raising a partial thickness flap that includes the

graft,removing the loose tissues above the periosteum,

andresuturing generally solves the problem.

BRIDGING PHENOMENA

• Collateral circulation• Essential for graft survival over the avascular

area (root surface)

CREEPING ATTACHMENT

• Goldman (1964) Post operative migration of gingval marginal

tissue in a coronal direction over a portion of previously denuded root.

• 0.12-3.5 mm ~ 2 years

• Favourable factors – narrow defect – +nce of interproximal bone – no gross malpositioning of

tooth – adequate plaque control

THICK VS THIN GRAFT

Sullivan and atkins- The two point collateral circulation present toward the coronal portion of a free graft over avascular root surface was insufficient to maintain tissue viability particularly in deep wide recessions

• Graft thickness would determine its behaviour during healing and its final character

• Thinner grafts (0.5-0.7mm) enhanced survival

• Thick graft with a thicker lamina propria → greater primary contraction causing blood vessels to collapse , retarding revascularization and reducing the likelihood of bridging.

• Once healed thicker grafts show superior resistance to frictional stress. Are recommended for areas with high susceptibility for gingival recession.

CONNECTIVE TISSUE GRAFTS• Healing is similar to FGG

Increased vasularity of connective tissue compared to FGGDouble blood supply (combined techniques) Recipient bed & overlying flap Faster healing

HEALING OF CTG

• 2nd day - epithelialization commences• 7 – 10 days - initial epithelialization completed• 4 weeks - keratinization commences

HEALING FOLLOWING GUIDED TISSUE REGENERATION

• GTR based on the principle of guiding the proliferation of the various periodontal tissue components during healing following periodontal surgery. (MELCHER)

• Placement of barrier covering the periodontal defects in such a way that gingival tissues are prevented from contacting the root surface during healing .

• Same time, space is formed between the barrier and root allowing periodontal ligament cells to produce new connective tissue attachment and bone cells to form new bone.

SANDER ET AL (1995) DESCRIBED HEALING OF PERIODONTAL LESIONS IN MONKEYS FOLLOWING THE GTR

1week• Coronal border of membrane - slightly exposed• Histological examination → furcation and proximal defects

contained partly disintegrated blood clot. • Most apical part of the defects → granulation tissue containing

inflammatory cells and blood vessels present. • Mean coronal regrowth of granulation amounted 0.9mm or 20%

of the maximal defects height and 1.5mm or 30% on the average in interproximal defects.

• A few collagen fibres were encountered in the tissue in the notch, but no instances were the collagen fibres inserted in to the newly formed cementum.

• At 3 week:• Histological examination: Newly formed tissue which has

proliferated considerably more coronally than in the one weeks specimens, but with great variation from one defect to another.

• Newly formed tissue in the central portion of the defects had primarily proliferated from the bone marrow of the interproximal and interradicular bone septum,

• Tissue adjacent to the root surfaces seem to originate from the periodontal space.

At 4 week:

• Partly filled with new connective tissue ,some inflammatory cells.

• New cementum in continuity with the old cementum . • New collagen fibres were inserted in to the newly

formed cementum• Notched area → inserting perpendicular to the surfaces,

in most apical part of the defects., • Bundles of collagen fibers were oriented in a mesiodistal

direction apically, where as those in the coronal part had no particular orientation.]

9 weeks: • Gingiva normal → consistency and color

• Bifurcation defects - partly or completely filled with new connective tissue + thin epithelial lining (coronal part of the defects. )

• New cementum with fibers inserting perpendicular to the surface had formed in the notch and to a varying degree also on the root surface coronally to the notch

HEALING FOLLOWING OSSEOUS SURGERY

REGENERATIVE

OSSEOUS AND MARROW AUTOGRAFTS

:

The process of repair of contiguous osseous autografts :• Ankylosis• Reattachment• Transplant resorption for the formation of new

bone.

Grafts: compact bone, cancellous bone and hematopoietic bone marrow.

COMPACT BONE :

Osteocytes present die , except the surface osteocytes . due to their close proximity to functioning capillaries or tissue fluids. Can possibly contribute to osteogenesis

• osteogenic layer (cambium) of periosteum , endosteum and marrow form new trabeculae & unite with the graft .

• After union of the graft and host , → resorption and replacement occur concurrently .

• Resorption - along the outer surface of the transplant and on the inner surface of haversian canals.

CANCELLOUS BONE TRANSPLANT

• Higher chance of osteocyte survival →covered with osteogenic cells• High production of surface cells ( osteoblasts) to

bone cells ( osteocytes).• Cancellous fragments →new centers for

osteogenesis if transplanted in to an area with an adequate vascular bed that provides surface cells with sufficient tissue fluid.

Healing Cancellous Cortical

Blood clot (1st week) Similar

Revascularisation

• Occurs within hrs• Marrow spaces – rapid degenration• Space for new channels• Complete within 2 weeks

• Slower rate• Not penetrated by vessels till 6th day• Complete within 1-2months

Repair • Initiated by osteoblats• Mesenchymal cell osteoblast • Osteoid deposited around cores of dead bone• Dead bone removed by osteoclasts• Transplant gets replaced by viable NEW bone.

• Initiated by osteoclasts• Bone apposition occurs only after 12 weeks

DRAGOO (1973)Duration Healing

3 days • Vascularity1 week • Resorption of grafted bone

• No evidence of periodontal membrane• Union betw the graft & existiong bone• Beginning of osteogenesis (osteoid)

3 weeks • Beginning of cementogenesis• Areas of calcification in conn tissue

8 weeks • Developing lamina dura and periodontal membrane• Further resorption of graft material• Cementogenesis• Beginning of attachment of sharpeys fibers to bone

3 months • New bone formation• Maturation of periodontal membrane with functional arangement.• Sharpeys fibers well inserted

4 months • Root resorption in some areas• Well oriented periodontal ligament• Lamina dura

6 months • Root resorption areas repaired• Many niduses of bone formation

RESECTIVE OSSEOUS SURGERY

• Osteoplasty

• Ostectomy

• Wilderman (1970) described the healing after

resective osseous surgery

Duration Healing

After 2 days Numerous empty lacunae – initial evidence of bone degenerationOsteoclasts & osteoblasts undergo enzymatic degradation

After 1 week Osteoclasts begin to appear – resorptionUndermining resorption ie from marrow spaces beneathe the exposed boneWidening of periodontal spaceIf bone septum was exposed – gets completely resorbed – lowering of the crestFew osteoclasts on periosteal surface

After 2 weeks Osteoclastic resorption begins to Bone apposition – osteoid depositionResorption on periosteal bone surface (2-3 weeks)

After 3 weeks Osteoid formation continuesNew bone – with entrapped osteocytesWoven bone (radicular interproximal, inter radicular)Waning of resorption

After 4 weeks Restoration of periodontal ligament widthRepair of boneRestoration of crestal height (interdental & furcation areas)

After 3 months Compact bone partially restoredLoss of bone height on redicular surfaces

After 6 months Slight bone apposition at bone crest, periodontal surface, periosteal surfacePresence of a definitive periosteum

HEALING AFTER ELECTROSURGERY

• Epithelium- Incision causes volatalisation of the cells in the line of delivered high frequency energy.

• Loss of cellular details secondary to lateral heat produced

• Subsequent wound healing is not affected adversely. (Krejci etal 1987)

Connective tissue –• Small denatured zone (100µm) resulting • Does not interfere with wound healing and

gradually disappear within 14 days (Kalkwarf etal 1981)• Misuse →delayed healing response ( Krejci etal)

HEALING AT IMPLANT SITE

osseointegrationFibro-osseous

integration

Biointegration

Fibro-osseous Integration

“tissue to implant contact- with healthy dense

collagenous tissue between the implant and the bone”

The fibers …

Osseo-integration

Direct connection b/w living bone & implant at light microscopic level

Meffert et al (1987)

Adaptive Biointegration osseointegration

Adaptive osseointegration – has osseous tissue approximating the surface of

the implant without apparent soft tissue interface at the light microscope level

Biointegration is a direct biochemical bone surface attachment

confirmed at the electron microscopic level

FACTORS AFFECTING WOUND HEALINGLocal factors

Infection Movement of the wound Poor blood supply Presence of foreign body X-ray irradiation Local application of

drugs/ointments Effect of smoking

Systemic factors

Malnutrition Metabolic disorders Hematologic disorders

• Malnutrition• vitamin C defeciency:• collagen cross linking and synthesis impaired

• vitamin B6 deficiency:• poor wound repair• impairs collagen cross linking

• vitamin E:• serves as a membrane stabilizer• plays role in anti bacterial action during healing.

• Vitamin A deficiency:• It is involved in fibroplasia,collagen synthesis and cross

linking&epithelialization.• Defeciency decreases collagen synthesis and

stability

• Protein deficiency:• It delays healing by intererfering the formation of

granulation tissue& collagen• Wound lacks tensile strength.• Synthesis of pro collagen is hampered

• Zinc defeciency• it is necessary for DNA and RNA polymerase enzyme which are

necessary for the replication of the cells.• it leads to delayed wound healing.

• Metabolic disorderDiabetes mellitus:wound healing in diabetes mellitus is delayed due to 1.neuropathy2.ischemia3.infection

• Haematological disorder:• it delays wound healing because of repeated haemmorhage of the

wound the leukopenia or functional abnormalities of leukocytes again delay the wound healing.

COMPLICATIONS

• Retarded epithelialization• Rough and irregular wound surface and tissue tags • Foreign substance embedded in the wound• Donor epithelium required for re-epithelialization is

distant to the wound site with temporal delay in epithelial coverage

• Hyperplastic connective tissue due to production of irregular granulation tissue or infection

Clinical consequences: bleeding and exudation, necrotic surface with fibrino- membranous cover, irregular hyperplastic hyperemic and edematous tissue

• Failure of epithelial keratinization

• Connective tissue edge of the incision lies on the alveolar mucosa

• Direct relationship between the connective tissue density rigidity and tightness of bond to underlying bone

• When it is associated or in contact with a dental surface or restoration

• Presence of bacterial plaque or debris

Clinical consequences: smooth and shiny gingival surface that is hyperemic, the

usual sharp demarcation between attached gingiva

• Flap displacement and avulsion

• Retardation or failure of tissue flap to reattach to bone or tooth and marginal aspect of the periodontal ligament

• Inadequate adaptation of flap due to• Inadequate no of sutures or improper placement, suture

breakage

• Bone exposure• Deficiency of vascularization

• Periodontal abscesses, pyogenic granulomas• Uncommon complication• More likely to occur in association with bone

exposure ,flap displacement , accidental impaction of calculus and foreign bodies

• Presence of systemic disease : diabetes mellitus , atherosclerosis

• Increased tooth mobility

APPLIED CLINICAL ASPECTS AND FUTURE APPROACHES TO ENHANCE WOUND HEALING

• Knowledge of growth factors, cell adhesion molecules and cytokines in the last two decades, understanding of the cellular and molecular biology of wound healing has improved significantly.

• Application of epidermal growth factor and TGF-a to burn wounds in animal models has been shown to enhance re-epithelialization

• Keratinocyte growth factor to skin wounds has been shown to have mitogenic effects on the healing epithelium

• Topical application of fibronectin in periodontal wound healing

• Systemic conditions such as diabetes → reduction in the availability of some of the growth factors →supplementing the appropriate growth factor may be beneficial.

• Recombinant growth factors to treat osseous defects → shows promising results

• Photobiomodulation - LLLT

BONE MORPHOGENIC PROTEIN

• Urist (1965)

• Protein extracted from bone containing multiple

osseopromoting factors

• Part of transforming growth factor-β superfamily

POLYPEPTIDES

• Osteoinducer + osteopromoter

• PepGen P-15 & OSA-117 MV

• Further studies required

ENAMEL MATRIX DERIVATIVES

Introduced in 1997

Composite of enamel matrix proteins

• Stimulates fibroblast proliferation

• Enhances growth of PDL cells

• Enhances expression of osteopontin osteoprotegrin, TGF-β1,

bone sialoprotein, BMPs

• Anti-inflammatory effects

CONCLUSION

• Wound healing is a complex process especially when compromised by local and systemic factors

• Only profound understanding of biological and clinical variables affecting the outcome of

periodontal treatment procedures will allow clinicians to manipulate biological and clinical factors

effectively in order to optimize the clinical result and increase the predicatbility of therapy.

REFERENCES

• Carranza’s clinical periodontology: 10th edition• Clinical periodontology Jan Lindhe-5th

edition.• Cell biology of gingival wound

healing:Periodontology 2000, Vol. 24, 2000, 127–152• Basic considerations of wound healing.

Periodontology 2000 vol19• General Pathology-Robins• Basic considerations of wound healing.

Periodontology 2000: vol19• Periodontal therapy: Goldman

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