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1
INFLAMMATION
AND HEALING
Dr. Rupali PG – CODS , Davangere
& DENTAL IMPLICATIONS
2
INTRODUCTION - History General features of inflammation
Classification of inflammation
ACUTE INFLAMMATION – Stimuli Vascular Events & Cellular Events Morphology of acute inflammation CHEMICAL MEDIATORS OF INFLAMMATION
CHRONIC INFLAMMATION – causes features
DENTAL ASPECTS OF INFLAMMATION
DENTAL ABSCESS
3
WOUND HEALING
Introduction
Regeneration & Repair
Healing by primary intention & secondary intention
Healing in oral tissues - Extraction socket Re-implanted tooth Alveolar bone Newer concepts in healing
Factors affecting healing
4
INTRODUCTION
"A localised protective response
elicited by injury or destruction of
tissues , which serves to destroy ,
dilute or wall off both infective agent
and injured tissue.
According to ROBINSINFLAMMATION is a complex reaction to injurious agent such as microbes and damaged , necrotic cells that consist of vascular responses , migration , and activation of leukocytes and systemic reaction
5
HISTORICAL HIGHLIGHTS
Egyptian Papyrus , 3000 BC
CELSUS , Roman Writer - 1 AD - CARDINAL SIGNS
JOHN HUNTER , 1793 – “ Inflammation is not a disease but a salutary effect on host”
JULIUS CONHEIM-1st used microscope to observe inflamed blood vessels & cells
6
SIGNS OF INFLAMMATIONGIVEN BY CELSUS
• REDNESS
• SWELLING
• HEAT
• PAIN
Rubor
Tumor
Dolor
Calor
• LOSS OF FUNCTION FUNCTIO LAESA
BY VIRCHOW
7
CLASSIFICATION
ACUTE INFLAMMATION
CHRONIC
INFLAMMATION
8
ACUTE INFLAMMATION
An acute condition is one with a rapid onset and/or a short course
INFECTIONS :Bacterial / viral /
parasitic & microbial toxins
Trauma : Blunt / penetrating
Physical / chemical agents
eg thermal injury
Foreign body eg sutures / splinters
Immune reactions / hypersensitivity
reactions
9
ACUTE INFLAMMATION
Alteration in vascular calibre/HEMO-DYNAMIC
change
Structural changes in micro-
vasculature
Emigration of leukocytes &
accumulation in focus of injury
10
ACUTE INFLAMMATION
VASCULAR CHANGES HEMODYNAMIC CHANGES /
Change in vascular flow & calibre
CHANGE IN VASCULAR PERMEABILITY
11
ACUTE INFLAMMATION
HEMODYNAMIC CHANGES / Change in vascular flow & calibre
Begin earlyDevelop at varying rates…..severity…
Transient vasoconstriction
Vasodilation
Increased permeability of microvasculature
Stasis
Emigration of leukocytes
12
TRANSIENT VASOCONSTRICTION
Arterioles 3-5 sec. in mild injury………5 minutes ; severe injury
13
PERSISTENT PROGRESSIVE VASODILATION
• 1st involves arteriole ………then other capillary bed• seen in 1st 30 min.• Results in Incr. blood vol. in microvascular bed
• By mediators - Nitric oxide (NO) - Histamine
Heat
Redness
14
INCREASED PERMEABILITY OF MICROVASULATURE
• Contraction of endothelial cells - Histamine
• Retraction of endothelial cells – cytokine IL – 1 , TNF
• Direct injury to endothelial cells
• Endothelial injury mediated by leukocytes
• Leakage from new blood vessels
15
STASIS
Increased vascular permeability leads to loss of fluid from microvasculature
Concentration of red cells in small vessels
Slower blood flow
STASIS
16
LEUCOCYTIC MIGRATION & EMIGRATION
Stasis is followed by peripheral orientation of leucocytes along vascular endothelium
LEUCOCYTIC MIGRATION
Movement of leucocytes in extracellular space through gaps b/w endothelium.
EMIGRATION
17
CELLULAR EVENTS
18
CELLS OF INFLAMMATION
19
Neutrophils Macrophages
20
CELLULAR EVENTS
Deliver leukocytes to site of injury
To perform their ‘FUNCTION’
ACTIVATE
Ingest offending bacteria
Kill bacteria & other microbes
Get rid of necrotic tissue & foreign substance
21
CELLULAR EVENTS
DELIVERY OF LEUKOCYTES TO SITE OF INJURY
• Margination • Rolling• Adhesion
IN THE LUMEN
CHEMOTAXIS
PHAGOCYTOSIS
FUNCTION
22
CELLULAR EVENTS • Margination • rolling• Adhesion
IN THE LUMEN
MARGINATION
23
• Margination • Rolling• Adhesion
IN THE LUMEN
CELLULAR EVENTS
ROLLING
Leukocytes now tumble along the endothelium
Have a TRANSIENT adhesion with endothelium
24
• Migration • Rolling• Adhesion
IN THE LUMEN
CELLULAR EVENTS
ADHESION
25
TRANS- MIGRATION
CELLULAR EVENTS
‘ TRANS ‘ across
PSEUDOPODIA
SQUEEZE THROUGH INTER-ENDOTHELIAL JUNCTION
LIE B/W ENDOTH. CELLS & BASEMENT MEMBRANE
‘across’ the endothelial wall..
26
EMIGRATION
CELLULAR EVENTS
EXTRA-VASCULAR SPLACE
Leukocytes lodged b/w BASEMENT MEMBRANE & ENDOTHELIUM
Release COLLAGENASES ….cause local defect in membrane
27
EMIGRATION
CELLULAR EVENTS
DIAPEDESIS
EXTRA-VASCULAR SPLACE
28
CHEMOTAXIS
CELLULAR EVENTS
Along chemical gradient
29
CHEMO-ATTRACTANTS
EXOGENOUS SUBSTANCES
ENDOGENOUS SUBSTANCES
Bacterial Products :a) Peptides – N – formyl
methionine terminal amino acid
b) Lipids
a) LTB-4b) PF-4c) Components of
complement systemd) Cytokine : IL – 1, 5 , 6e) Monocyte chemoattractant proteinf) Chemotactic factor
for CD-4 cellsg) Eotaxin chemotactic
factor for eosinophils
CELLULAR EVENTS
30
6 to 24 hours 24 to 48 hours
CELLULAR EVENTS
In chemotaxis…..
31
CELLULAR EVENTS
PHAGOCYTOSIS
RECOGNITION AND ATTACHMENT OF PARTICLE
ENGULFMENT WITH FORMATION OF PHAGOCYTIC VESICLE
DEGRANULATION STAGE
KILLING & DEGRADATION STAGE
32
CELLULAR EVENTS
RECOGNITION AND ATTACHMENT OF PARTICLE 1
CHEMO-TACTIC AGENTS
‘ OPSONINS ‘
Ig G
C3b Opsonin
Lectins
MANNOSE RECEPTOR
SCAVENGER RECEPTOR
33
ENGULFMENT WITH FORMATION OF PHAGOCYTIC VESICLE2
CELLULAR EVENTS
Fig 10.6 harsh mohan pg 101
PHAGO-LYSO-SOME
34
DEGRANULATION STAGE3
CELLULAR EVENTS
Mononuclear phagocyte also secrete enzymes eg • IL-2 , 6-TNF• Arachidonic acid metabolites (Prostaglandin , leukotriene , platelet activating
factor• Oxygen metabolites
Preformed granule stored products of PMNs are released into phagolysosome
35
KILLING & DEGRADATION STAGE4
CELLULAR EVENTS
OXYGEN – DEPENDENT BACTERICIDALMECHANISM
OXYGEN–INDEPENDENT MECHANISM
36
KILLING & DEGRADATION STAGE
OXYGEN – DEPENDENT MECHANISM
Production of reactive oxygen metabolites
NADPH oxidase ESSENTIAL ENZYME
H2O2
37
MYELO - PEROXIDASES AZUROPHILLIC GRANULES contain
MPO – DEPENDENT KILLING MPO – INDEPENDENT KILLING
H202 HOCl + H2O
MORE POTENT ANTIBACTERIAL AGENT
MPO
H2O2 Performs the action
weaker
38
OXYGEN – INDEPENDENT MECHANISM
CELLULAR EVENTS
Followed by :
Lysosomal hydrolases
Permeability increasing factors
Defensins
Cationic proteins
39
MORPHOLOGY OF ACUTE INFLAMMATION
40
MORPHOLOGY OF ACUTE INFLAMMATION
ACUTE
INFLAMMATION
PSEUDO-
MEMBRANE
BACTERIAL
INF. OF
BLOOD
CELLULITIS
ULCER
ABSCESS
41
SYSTEMIC EFFECTS OF ACUTE INFLAMMATION
FEVER LEUCOCYTOSISLYMPHANGITIS - LYMPHADENITISRigors chills
Malaise , anorexiaIncreased pulse rate
42
LYMPHATICS IN INFLAMMATION filters the extravascular fluids
in inflammation…. lymph flow is inc. and helps drain the edema fluid from extravascular space
LYMPHATICS
LYMPHANGITIS
DRAINING LYMPH NODES
LYMPHADENITIS
43
CHEMICAL MEDIATORS OF INFLAMMATION‘ MEDIATOR ‘ : one that reconciles differences b/w disputants
CHEMICAL MEDIATORS : chemical substances that mediate the process of inflammation………..
44
CHEMICAL MEDIATORS OF INFLAMMATION
Present in plasma in precursor form
Must be activated to acquire biologic properties
Pr. In intracellular granules
Major cellular sources Platelets Neutrophil Monocyte / macrophage
45
CHEMICAL MEDIATORS OF INFLAMMATION
CELL DERIVED MEDIATORS
VASO – ACTIVE AMINES
HISTAMINE
SOURCE : 1) Mast cells in C.T adjacent to blood vessels
2) Blood basophils 3) Platelets STIMULI : Injury Immune reactions Fragments of complement - C3a , C5a Neuropeptides eg substance P Cytokines IL – 1 , 8
SEROTONIN
SOURCE : 1) Platelets 2) Enterochromaffin cells
STIMULI : Platelet aggregation after contact with collagen , thrombin
46
ROLE IN INFLAMMATION
Dilation of arterioles
Permeability of vasculature
47
CHEMICAL MEDIATORS OF INFLAMMATION
ARACHIDONIC ACID METABOLITES
A fatty acid with 2 main sources : Directly through diet
Through conversion of essential fatty acid
Arachidonic acid ARACHIDONIC ACID METABOLITES
Cyclo – oxy- genase pathway
Lipo – oxy- genase Pathway
CYCLO – OXY- GENASE PATHWAY
Prostaglandin - PGD2 , E2 , F2
Thromboxane A2
Prostacyclin
LIPO – OXY – GENASE PATHWAY
5 – HETE
Leukotrienes
48
CHEMICAL MEDIATORS OF INFLAMMATION
LYSOSOMAL COMPONENTS
PRIMARY SECONDARY
MPO
ACID HYDROLASES
NEUTRAL PROTEASES
LACTOFERRIN
LYSOZYME Alk. Phosph Collagenase
• ACID PROTEASE
• COLLAGENASE
• ELASTASE
• PLASMINOGEN ACTIVATOR
49
CHEMICAL MEDIATORS OF INFLAMMATION
CYTOKINES
• proteins produced mainly by- activated lymphocytes & macrophages , also from endothelium, epithelium & connective tissue cells.
TNF and IL - 1• major cytokines that mediate inflammation.
• Produced mainly by activated macrophages
STIMULI : • Immune reactions, • physical injury & variety of inflammatory stimuli.• endotoxins & other microbial products
50
NITROUS OXIDE
CHEMICAL MEDIATORS OF INFLAMMATION
Released by activated neutrophils and macrophages
Superoxide , hydrogen peroxide , hydroxl ion
ACTION : Endothelial cell damage- inc. vascular permeability Damage to cells and tissue matrix by activating protease and inactivating anti-protease
6 OXYGEN METABOLITES
mediates in vascular dilation
51
MEDIATORS BRINGING ABOUT ROLLING & ADHESION
SELECTINS
INTEGRINS
IMMUNOGLOBULIN SUPERFAMILY
ADHESION MOLECULES
• P – Selectins• E – Selectins• L – Selectins
• ICAM – 1• VCAM - 1
52
CHEMICAL MEDIATORS OF INFLAMMATION
PLASMA DERIVED MEDIATORS
KININ SYSTEM
CLOTTING SYSTEM
COMPLEMENT SYSTEM
FACTOR XII
53
PLASMA DERIVED MEDIATORSFACTOR XII
FACTOR XIIa
FIBRINOLYTIC SYSTEM
CLOTTING SYSTEM KININ SYSTEM
PLASMIN FIBRIN BRADYKININ
COMPLEMENT SYSTEM
C3a , C5a
54
FATE OF ACUTE INFLAMMATION
ACUTE INFLAMMATION
RESOLUTION
HEALING BY SCARRING
PROGRESSION TO SUPPURATION
PROGRESSION TO CHRONIC
INFLAMMATION
55
CHRONIC INFLAMMATION
Inflammation of prolonged duration (weeks to months) in which inflammation , tissue destruction and attempts at repair are proceeding simultaneously.
CAUSES
Following acute inflammation
Begin insidiously as a low – grade inflammation Persistent inf. By micro-organisms : tubercle bacilli ,
Prolonged exposure to toxic agents Auto - immunity
56
FEATURES OF CHRONIC INFLAMMATION :
CHRONIC INFLAMMATI
ON
Infiltration with mononuclear cells – macrophages ,lymphocytes , & plasma cells
Tissue destruction
Healing by Proliferation & connective tissue replacement of damaged tissue
57
INFILTRATION WITH MONO-NUCLEAR CELLS
58
• Incr. lysosomal enzymes
• Greater ability to phagocytose
ACTIVATION OF MACROPHAGE
Cytokine IFN - ɤ
Endotoxin , fibronectin chemical mediators
59
MACROPHAGE
IN ACUTE INFLAMMATION
IN CHRONIC INFLAMMATION
* Irritant eliminated – macrophage disappears
Persistent macrophage accumulation by following mechanisms :
1. )Recruitment from circulation – Chemotactic stimuli include :a) C5a b) Platelet derived growth factorc) Transforming growth factor
2.) Local proliferation of macrophages
3.) Immobilization of macrophages
60
TISSUE DESTRUCTION OR NECROSIS
CENTRAL
• ACTIVATED MACROPHAGES
Elastase Protease Collagenase Reactive oxygen radical Cytokine IL-1,8
61
PROLIFERATION
NEW BLOOD VESSELS
FIBROBLAST
Helps in healing of damaged tissue
62
63
INFLAMMATION OF PULP & PERIAPICAL TISSUE
PULPITIS
DEEP DENTAL CARIES
TOOTH FRACTURE
CRACKED TOOTH
SYNDROME
CHEMICAL CHANGES
THERMAL CHANGES
64
Involves enamel
Progresses to dentin
Invade pulp
65
REACTIONS OF PULP TO BACTERIAL INVASION
ᶲ Vascular changes take place inside blood vessels.
ᶲ PMNLs reach the area of inflammation
ANATOMICAL FEATURES OF PULP THAT TEND TO ALTER THE RESPONSE
Enclosure of pulp in rigid calcified walls - PREVENTS EXCESSIVE SWELLING …thus more painful.
Pressure leads to decr. Blood supply and ischaemia – does not get corrected since collateral circulation cannot develop through tiny apical foramina
66
HISTOLOGIC FEATURES OF PULPITIS
PULPITIS
ACUTE CHRONIC
VASCULAR EVENTS CELLULAR
EVENTS
MONONUCLEAR CELLS PREDOMINATE - chiefly plasma cells & lymphocytes.
Fibroblastic activity is evident
collagen fibres seen in bundles
• Continued vascular dilation
• Accumulation of oedemal fluid in connective tissue
• Pavementing Of PMNLs along endothelial wall
• Through quiescence of acute pulpitis
• Begin as chronic d/s from onset
67
UNTREATED PULPITIS
ACUTE CHRONIC
PULPITIS
UNTREATED
APICAL PERIODONTITIS
PERIAPICAL ABSCESS PERIAPICAL GRANULOMA
68
UNTREATED PULPITIS
APICAL PERIODONTITIS
• Inflammation of periodontal ligament around root apex..
INITIALLY
Changes localised around root apex…..since richly vascular
LATER – if irritant present
Resorption of bone – ABSCESS FORMATION
69
TYPES OF ABSCESS
PYOGENIC ABSCESS PYAEMIC ABSCESS COLD ABSCESS
• Commonest type
• mostly found in soft tissues
• eg periapical abscess
• occurs due to circulating bacterial emboli in blood
Abscess without signs of inflammationEg Tubercular abscess
70
ABSCESS FORMATION / SUPPURATION
Acute bacterial inf. + intense neutrophillic infiltrate
TISSUE NECROSIS
Cavity is formed called an ABSCESS
Contain purulent exudate called as PUS
SUPPURATION
71
PERIAPICAL ABSCESS
MICRO-ABSCESS
Rise in pressure with inflammatory exudate
Local tissue hypoxia
Localised destruction ….breakdown of leucocytes , bacteria & tissue
ABSCESS FORMATION PERIAPICAL ABSCESS
72
PERIAPICAL ABSCESS
Disintegrating PMNLsViable leukocytes , lymphocytes , bacterial colonies
Dil. Blood vessels in adj. PDL and marrow spaces + serous exudate
73
PERIAPICAL ABSCESS( DENTO-ALVEOLAR ABSCESS / ALVEOLAR ABSCESS )
Tender on percussion
Will feel slightly extruded from socket
Fever & regional lymphadenitis
INFLAMED PERIODONTIUM
74
ACUTE PERIAPICAL ABSCESS
CHRONIC FORM
PERIAPICAL ABSCESS
Takes the path of least resistance in tissuesSINUS
FISTULA / PARULIS / GUM
BOIL
75
WOUND HEALING
76
WOUND : Anatomic or functional interruption in continuity of a tissue that is accompanied by cellular damage and death
INTRODUCTION
MAY BE INFLICTED BY :
Physical injury Chemical injury Biologic injury
Series of co-ordinated processes directed towards restoring the injured tissue of body to as near normal as possible is termed as WOUND HEALING
77
GOAL
a.) to restore continuity b/w wound edges
b.) To re-establish tissue functionREGENERATIONREPAIR
Biologic process by which both structure and function of disrupted or lost tissue is completely restored.
Biologic process whereby continuity of disrupted or lost tissue is regained by new tissue which does not restore structure & function
78
REGENERATION
• Healing by proliferation of parenchymal cells,
• results in complete restoration of the original tissues
Cell growthCell differentiationCell-matrix interaction
GROWTH FACTORS1. Epidermal2. Fibroblast3. Platelet derived4. Endothelial5. Transforming
79
REPAIR
Healing by conn. Tissue Fibrosis and scarring
Phase of inflammationPhase of clearancePhase of ingrowth of granulation tissue
80
TYPES OF WOUND HEALING
PRIMARY SECONDARY TERTIARY
81
HEALING BY PRIMARY INTENTION / FIRST INTENTION
Conditions:• Clean and uninfected wounds• Surgically incised• Edges are Approximated• Without much loss of tissue
82
Initial Hemorrhage:
Acute inflammatory Response:
Epithelial changes:
Organization :
HEALING BY PRIMARY INTENTION / FIRST INTENTION
83
Initial hemorrhageINJURY SEVERES VASCULATURE
Leads to extravasation of plasma , platelets , erythrocytes and leukocytes
Initiates coagulation cascade
that produces blood clot
84
INFLAMMATORY RESPONSE
Begins within 24 hrs with appearance of polymorphs from margin of incision
From 3rd day Polymorphs replaced with macrophages
85
Basal cells from both cut margins start proliferating and migrating towards incisional space in form of epithelial SPURS
A well approximated wound is covered by layer of epithelium in 48 hrs
By 5th day a multilayered new epidermis is formed.
PROLIFERATIVE PHASE – involves epithelial changes
86
Organisation starts by 3rd day
5th day : new collagen fibrils start forming which dominate till healing is complete
In 4 weeks Scar tissue formed
SCAR TISSUE
• Scanty cellular and vascular elements• few inflammatory cells
REMODELLING PHASE – involves ORGANISATION
87
CONDITIONS:
Open wound with a large tissue defect
Having extensive loss of cells and tissue
Wound is not approximated by sutures
HEALING BY SECONDARY INTENTION
88
Initial Hemorrhage:
Acute inflammatory Response:
Epithelial changes:
Granulation tissue:
Wound contraction:
89
GRANULATION TISSUE
INFLAMMATION CLEARANCE INGROWTH OF GRANULATION TISSUE
ANGIOGENESIS FIBROGENESIS
• Neutrophils and monocytes
• Autocatalytic enzymes
90
Wound Healing in Oral Mucosa
MOIST ENVIRONMENT
UNUSUAL ANATOMIC SITUATION
COUNTLESS MICROORGANISMS
MARKED CAPACITY FOR REGENERATION
EASY REMODELLING OF SCAR TISSUE
fibroblasts in oral mucosa are phenotypically different from those of skin & more closely resemble fetal fibroblasts .
91
HEALING OF EXTRACTION SOCKETHealing Of Extraction Socket
Consists of erythrocytes & leucocytes in mesh of fibrin
STAGE 1 : coagulation
STAGE 2 : Granulation tissue
STAGE 3 : Connective Tissue collagen & reticuloendoth. fibres
STAGE 4 : Bone DevelopmentBegins at 7th post op dayBy 40th day socket almost completely filled with WOVEN bone
STAGE 5 : Epithelial RepairBegins at 4th post op day ; completes by 24th day
92
COMPLICATIONS - Healing Of Extraction Socket
FIBROUS UNION
• Occurs when tooth xtn accompanied with both buccal and lingual periosteum loss.
• RADIOGRAPHIC FEATURES : well circumscribed radiolucent area in site of previous xtn
May be mistaken for residual infection
• HISTOLOGIC FEATURES : dense bundles of collagen with occasional fibrocytes and few blood vessels
• TREATMENT : excision of wound may ……..
93
DRY SOCKET
• Most common and painful complication• Occurs due to disintegration / loss of blood
clot• CLINICAL F :
• Foul odour• Severe throbbing type of pain
‘DRY’TREATMENT
• AIM : to keep socket clean to protect exposed bone
• Irrigation with mild warm antiseptic
Palliative socket dressing of ZOE – iodoform gauze
94
HEALING OF RE-IMPLANTED TOOTH
oCLOT b/w root n ruptured PDL
oFIBROBLAST PROLIFERATION on pdl remnants on bone side
oRECONNECTION – occurs by collagen fibres extending from cementum to alveolar bone
oREATTACHMENT OF EPITHELIUM – by 7th day
o2-4 weeks - complete regeneration of pdl
Healing Of RE-IMPLANTED tooth
95
Healing Of GINGIVA
Mainly by regeneration
1-2 weeks
96
Healing Of ALVEOLAR BONE
RESPONSE : resorption and remodelling
CHRONIC INFECTIONRESORPTION
GRANULATION
ACUTE INFECTIONABSCESS / CELLULITIS
Inf. In marrow - OSTEOMYELITIS
97
Healing Of DENTIN-PULP COMPLEXPulp is highly specialised loose connective tissue with specific response to surgical and traumatic injuries and bacterial insult
PREDOMINANT CELL TYPES IN PULPAL REPAIR Fibroblasts - present uniformly throughout pulp Undifferentiated mesenchymal cells – located paravascularlyPULPAL VASCULATURE in healing :Within pulp…esp apically.. ARTERIO-VENOUS shunts are present
Control the tissue pressure during inflammation
When tissue pressure exceeds that of venules , a decrease in blood flow results
98
RESPONSE OF PULP2 BASIC RESPONSE DETERMINING HEALING OF PULPPULPAL WOUND
HEALING RESPONSEDEFENSE
RESPONSE
Damaged pulp tissue is healed by replacement with newly differentiated tissue
Aims at neutralising or controlling bacterial invasion
Depends upon type of progenitor cells involved
Eg. PDL derived progenitor cells – cementum deposition along RC walls Patent apical foramen - Sharpeys fibre insertion
Involves creating barrier against micro – org. by• granulation tissue• hard tissue – secondary
dentin / cementum
NOT ABSOLUTE
RESPONSE
99
FACTORS INFLUENCING WOUND HEALINGLOCAL FACTORS
UV X - RAY
INFECTION FOREIGN BODY MOBILITY
RADIATION
100
FACTORS INFLUENCING WOUND HEALING
SYSTEMIC FACTORS
SYSTEMIC CONDITIONS
AGE NUTRITIONAL DEFICIENCIES
BLOOD DYSCRASIAS
• Vitamin C , E , A• Proteins
101
Healing – NEW CONCEPTS
Healing of chronic wound can be enhanced by one of the following methods
1. Topical application of growth factors.
2. Hyperbaric oxygen therapy.
Systemic
Local.
3. Electrical stimulation for wound healing
Direct current
Low frequency pulsed current (LFPC)
High voltage pulsed current (HVPC)
4. Topical application of cultured keratinocytes.
5. Vacuum assisted closure of the wound.
102
Conclusion……….
INFLAMMATION FORMS THE BASIS OF MOST OF THE CLINICAL COMPLAINTS…..
103
Refrences……..
1) Robbin’s & Cotron Pathological basis of diseases -7th edn.
2) Essential pathology for dental students –Harsh mohan,3rd edn.
3) Text book of oral pathology – Shafer 4th edn.
4) Textbook and colour atlas of traumatic injuries to the teeth—J.O.Andreasen, F.M.Andreasen 3rd edn.
5) Google search
104
THANK YOU