Inflammation and repair /orthodontic courses by Indian dental academy

AND
REPAIR
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiantalacademy.comwww.indiantalacademy.com

Clinical dentistryClinical dentistry will be able to adapt to a rapidly changing world only ifwill be able to adapt to a rapidly changing world only if
it is based upon a sound understanding of the structure, metabolismit is based upon a sound understanding of the structure, metabolism
and function of the oral tissues. Such understanding should not only beand function of the oral tissues. Such understanding should not only be
of the healthy and normal tissues but also include a knowledge ofof the healthy and normal tissues but also include a knowledge of
effects of microbiological and pathological interactions with the tissueseffects of microbiological and pathological interactions with the tissues
so that proper treatment plan can be done.so that proper treatment plan can be done.

Contents Of The Seminar.Contents Of The Seminar.
1. Introduction.
2. Definition.
3. Types of inflammation.
4. Causes of inflammation.
5. Cardinal signs of
inflammation.
6. Microscopic features of
inflammation.
7. Mediators of inflammation.
8. Regulation of inflammation.
9. The inflammatory cells.
10. Morphology of inflammation.
11. Systemic effects of
inflammation.
12. Fate of acute inflammation.
.
13. Chronic inflammation.
a) General features.
b) Granulomatous
inflammation.
14. Healing.
a) Regeneration.
b) Repair.
15. Wound healing.
16. Healing of specialized tissues.
17.Inflammatory conditions of the
oral cavity.
18. Prosthodontic considerations.
19. References from Journals.
20. Bibliography.

Definition-
inflammation can be defined as the local response of a living tissue
to any injury due to any agent.
or
Inflammation can also be defined as a dynamic process by which
living tissues react to injury.
or
It is a body defense reaction in order to eliminate or limit the spread of
injurious agent as well as to remove the consequent necrosed cells
and tissues

Types of inflammation.Types of inflammation.
Depending upon the defense capacity of the host & duration of
response, inflammation can be classified as
1.Acute inflammation-
is of short duration & represents the early body
reaction & is usually followed by repair .
2. Chronic inflammation-
is of longer duration & occurs after the causative agent
of acute inflammation persists for a long time.

Causes of inflammation.Causes of inflammation.
Physical Chemicals
Trauma Heat or cold Radiation Acids organic poisons
Infective Immunological
Bacteria Viruses Parasites Antigen-antibody cell-mediated

Cardinal signs of inflammation.Cardinal signs of inflammation.
1.Calor(Heat) 2. Rubor(Redness) 3.Tumour(Swelling) 4.Dolor(Pain)
5.Functio laesa(Loss of function)

Acute inflammation.Acute inflammation.
Vascular events-alteration in the
microvasculature is the earliest
response to tissue injury. These
include haemodynamic changes
and changes in the vascular
permeability.
Transient vasoconstriction
Persistent progressive vasodilatation
Increase in local hydrostatic pressure
Slowing or stasis
Leucocytic margination

Altered vascular permeabilityAltered vascular permeability
Mechanisms of altered vascular
permeability.
1.Contraction of the endothelial cells.
2.Retraction of the endothelial cells.
3.Direct injury to the endothelial
cells.
4.Endothelial injury mediated by
leucocytes.

Cellular events.Cellular events.
The cellular events consists of two processes
A. Exudation of leucocytes.
B.Phagocytosis.
A. Exudation of leucocytes-the escape of
leucocytes from the lumen of
microvasculature to the interstitial tissue.
Changes leading to migration of
leucocytes are-
1. Changes in the formed elements of the
blood-
in the early stages of inflammation the
rate of flow of blood is increased due to
vasodilatation. But subsequently there is
stasis of blood stream. The central
stream of cells widens & the peripheral
plasma zone becomes narrow due to
exudation. This is known as
margination.As a result of this
redistribution the neutrophils of the
central column come close to the vessel
wall which is known as pavementing.

2.Adhesion or rolling-
the peripherally marginated
neutrophils stick briefly to the endothelial cells
lining the vessel wall or roll over it. Injury leads to
neutralization of the normal negative charge of the
leucocytes and endothelial cells so as to cause
adhesion.
3.Emigration-
Neutrophils move along the endothelial
surface till a suitable site between the cells is found
where neutrophils throw out cytoplasmic
pseudopods. Subsequently, cross the basement
membrane by damaging it locally with secreted
collagenases & escape into the extra vascular
space, this is known as emigration.
Escape of red cells through the
gaps takes place which is called as diapedesis
responsible for the hemorrhagic appearance of the
inflammatory exudate.

4.chemotaxis-
the chemotactic factor mediated emigration of
leucocytes after crossing the several barriers to reach the interstitial
tissues is called as chemotaxis.
the agents acting as potent chemotactic substances for
leucocytes are
1.Leukotriene B4
2.Platelet factor 4
3.Components of the complement system(c5a in particular)
4.Cytokines-IL8
5.Soluble bacterial products.
6.Chemotactic factor for CD4 cells.

PhagocytosisPhagocytosis
Phagocytosis is defined as the process of
engulfment of a solid particulate matter by
the cells. The cells are called phagocytes.
There are two main types of phagocytic
cells
1. Polymorphonuclear neutrophils which
appear in acute inflammatory response
and are also called as microphages.
2. Circulating monocytes & fixed
mononuclear phagocytes called as
macrophages.
Phagocytosis involves 4 steps
1.Attachment stage(Opsonisation)
2.Engulfment stage
3.Secretion or degranulation stage
4.Killing or Degradation stage

1.Attachment stage or Opsonisation
To bond the bacteria & the
cell membrane of the phagocytic cell, the
microorganisms get coated with opsonins
which are naturally occurring factors in the
serum.
The opsonins present in the serum are IgG
opsonin & C3b opsonin.
2.Engulfment stage-
By formation of pseudopods
around the particle, enveloping it in a
phagocytic vacuole. Eventually the plasma
membrane enclosing the phagocytic
vacuole breaks the cell surface and the
lysosomes of the cell fuse with the vacuole
and form phagolysosome or phagosome.

3.Degranulation stage-The preformed granule
products of PMN’s are discharged. Specific or
secondary granules of PMN’s are released
with interlukin2,TNF,superoxide oxygen,
hydrogen peroxide,hypochlorous acid.
4.Killing or degradation stage-This stage of killing
& digestion of the microorganisms by the
phagocytes as scavenger cells is done. The
microorganisms are degraded by the
hydrolytic enzymes. The antimicrobial agents
act by either of the following mechanisms
A) Oxygen dependant mechanism
B) Oxygen independent mechanism
C) Nitric oxide mechanism

A. Oxygen dependant mechanism-
in this mechanism the microorganisms are
killed by the production of reactive oxygen metabolites such as O2’,H2O2,
HOCL,HOI,HOBR.In this mechanism there is production of Hypohalous
acid which is a more potent antibacterial agent than H2O2.
B. Oxygen independent mechanism-
Some agents released from the granules of
the phagocytic cells do not require oxygen for bactericidal activity. These
include lysosomal hydrolases,defensins and cationic proteins.
C. Nitric oxide mechanism-
Nitric oxide is produced by the endothelial cells
as well as by activated macrophages and has potent fungicidal and anti-
parasitic action.

CHEMICAL MEDIATORS OF INFLAMMATIONCHEMICAL MEDIATORS OF INFLAMMATION
SOURCE MEDIATOR ACTIONS
Cell
derived
Mastcells,Basophil
Platelets
Histamine Permeability
Platelets Serotonin Permeability
Inflammatory cells Lysosomal enzymes,
PAF
Prostaglandins
Cytokines
NO & O2 metabolites
Tissue damage
Permeability
Fever
Antibacterial
Tissue damage
Plasma
derived
Clotting &
Fibrinolytic system
Fibrin split products Permeability
Kinin system Kinin,Bradykinin Permeability
Complement
system
Anaphylotoxins permeabilitywww.indiantalacademy.comwww.indiantalacademy.com

REGULATION OF INFLAMMATIONREGULATION OF INFLAMMATION
Damaging effects are kept in check by the host mechanisms so as
to resolve inflammation as seen in hypersensitivity reactions. These
include
1.Acute phase proteins-
these are α1−antitrypsin,protease inibitor,haptoglobin,
C-reactive protein, serum amyloid A & P component. These are
synthesized in the liver & they are released in response to
inflammation.APP combined with systemic features of fever &
leucocytosis is termed as ‘acute phase response'. Deficiency of
these APP leads to severe form of disease in chronic & repeated
inflammatory response.
2. Corticosteroids-
The endogenous glucocorticoids act as
anti-inflammatory agents. Their levels are raised in infection and
trauma by self regulating mechanism.

3.Free cytokine receptors-
the presence of free receptors for cytokines in
the serum correlates directly the disease activity.
4. Suppressor T-Cells-
these inhibit the function of T & B cells
5. Anti-inflammatory chemical mediators-
these are PGE2 and Prostacyclin which have
both pro-inflammatory as well as anti-inflammatory actions.

The inflammatory cellsThe inflammatory cells
Polymorpho nuclear neutrophils
Initial phagocytosis, acute inflammatory cell
Monocyte/macrophage
Bacterial phagocytosis
Chronic inflammatory cell
Regulates Lymphocyte response
Lymphocyte
Humoral & cell mediated response
Regulates Macrophage response

Eosinophil
Allergic states
Parasitic infestations
PGE2 synthesis
Reactive O2 metabolites
Mast cell
Receptor for IgE anti-
bodies
Histamine,
leukotreins,
PAF
Plasma cell
Anti-body synthesis

FACTORS DETERMINING VARIATION INFACTORS DETERMINING VARIATION IN
INFLAMMATORY REPONSEINFLAMMATORY REPONSE
1 .Factors involving the organisms
I) Type of injury & infection
II) Virulence
III) Dose
IV) Portal of entry
V) Product of the organisms
2. Factors involving the Host
I) General health of the host
II) Immune state of the host
III) Leucopenia
IV) Type of tissue involved
V) Local host factors
3. Type of exudation
I) Serous
II) Fibrinous
III) Purulent
IV) Haemorrhagic
V) Catarrhal
4. Necrosis
I) Gas Gangrene
II) Acute appendicitis

MORPHOLOGY OF ACUTE INFLAMMATIONMORPHOLOGY OF ACUTE INFLAMMATION
1.Pseudomembranous inflammation-
it’s a inflammatory response
of the mucous surface to toxins of
diphtheria or irritant gases. As a result of
denudation of the epithelium, plasma
exudes on the surface where it
coagulates & together with the necrosed
epithelium forms a false membrane.
2.Ulcer-
Ulcers are local defects on
the surface of an organ produced by
inflammation. Common sites of
ulcerations are the stomach,
duodenum,intestinal ulcers in typhoid,
ulcers of the legs due to varicose veins.

3.Suppuration(Abscess formation)-
Accompaniment by intense
neutrophilic infiltrate in the inflamed tissue
results in tissue necrosis. A cavity is formed
which is called an abscess & contains a
purulent exudate such as a Boil or Furuncle
which is an acute inflammation of the hair
follicles in the dermal tissues.
4.Cellulitits-
it’s a diffuse inflammation of soft
tissues resulting from spreading effects of
substances like hyaluronidase released by
some bacteria.
5.Bacterial infection of the blood-
a) Bacteraemia
b) Septicemia
c) Pyaemia

SYSTEMIC EFFECTS OF INFLAMMATIONSYSTEMIC EFFECTS OF INFLAMMATION
The systemic effects of inflammation are
1.fever-
This occurs due to bacteraemia mediated by the
release of factors like prostaglandins,interleukin-1 and
tumour necrosis factor.
2.Leucocytosis-
In bacterial infections there is neutrophilia,in viral
infections lymphocytosis & in parasitic infestations
eosinophilia.

3.Lymphagitis-Lymphadenitis-
The affected lymph may show hyperplasia of the lymphoid
follicles & proliferation of mononuclear phagocytic cells in the
sinuses of the lymph nodes.
4.Shock-
occurs in severe cases wherein there is massive release of
cytokine & TNF-α in severe tissue injury or infection resulting in
profuse systemic vasodilatation, increased vascular permeability &
intravascular volume loss. The net effect of these changes is
hypotension & shock. Systemic activation of the coagulation
pathway may occur leading to micro thrombi through the body &
result in disseminated intravascular coagulation, bleeding and
death.

FATE OF ACUTE INFLAMMATION.FATE OF ACUTE INFLAMMATION.
1.Resolution-
It means complete return to normal tissue following acute
inflammation. This occurs if tissue changes are slight & the cellular
changes are reversible e.g.-resolution of lobar pneumonia.
2.Healing by scarring-
This takes place when the tissue destruction is extensive so
that there is no tissue regeneration but actually there is healing by
fibrosis.
3.Progression to suppuration
When the pyogenic bacteria cause severe tissue necrosis,
inflammation progresses to suppuration. Mixture of
neutrophils,bacteria,fragments of necrotic tissue, cell debris & fibrin
comprise pus which is contained in a cavity to form abscess.
4.Progression to Chronic inflammation.-
The acute inflammation may progress to chronic inflammation
in which processes of inflammation & healing proceed side by side.www.indiantalacademy.comwww.indiantalacademy.com

CHRONIC INFLAMMATIONCHRONIC INFLAMMATION
Chronic inflammation can be defined as a prolonged process in which tissue
destruction and inflammation occur at the same time.

Causes of Chronic inflammation
1.Chronic inflammation following Acute inflammation-
When the tissue destruction is extensive or the
bacteria survive & persist in small numbers at the site of
inflammation.
e.g.Osteomyelitis,Pneumonia terminating in lung abscess.
2.Recurrrent attacks of acute inflammation-
when recurrent bouts of acute inflammation culminate
in chronicity of the process.
e.g. recurrent urinary tract infection leading to chronic
pyelonephritis.
3.Chronic inflammation starting de novo-
when the infection of the organisms of low
pathogenicity is chronic from the beginning.
e.g. infection with Mycobacterium tuberculosis.

GENERAL FEATURES OF CHRONIC INFLAMMATIONGENERAL FEATURES OF CHRONIC INFLAMMATION
1.Mononuclear cell infiltration.
Infiltrated by mononuclear inflammatory cells
like phagocytes, circulating monocytes,
macrophages & giant cells.
2.Tissue destruction or necrosis.
Tissue destruction & necrosis are
common in many inflammatory lesions & are
brought about by activated macrophages by
release of a variety of biologically active
substances.
3.Proliferative changes.
As a result of necrosis, proliferation of
small blood vessels & fibroblasts is
stimulated resulting in formation of
inflammatory granulation tissue eventually
leading to healing by fibrosis.

Types Of Chronic InflammationTypes Of Chronic Inflammation
1.Nonspecific inflammation-when the irritant substance produces
a non-specific chronic inflammatory reaction with formation of
granulation tissue and healing by fibrosis
e.g. Chronic ostomyelitis,Chronic ulcer.
2.Specific-When the injurious agent causes a characteristic histologic
tissue response
e.g.Tuberculosis,Leprosy,Syphilis.
According to histological findings these are again classified
into
1.Chronic nonspecific inflammation-It is characterized by
nonspecific cell infiltration
e.g. chronic osteomyelitis,Actinomycois.
2.Chronic Granulomatous inflammation-It is characterized by
formation of granulomas
e.g.Tuberculosis,Leprosy,Actinomycosis,Sarcoidosis.www.indiantalacademy.comwww.indiantalacademy.com

Granulomatous InflammationGranulomatous Inflammation
Granuloma is a circumscribed lesion
composed predominantly of modified
macrophages called epitheloid cells
and rimmed at the periphery by
lymphoid cells.
Giant cells- Formed by the fusion of
adjacent epitheloid cells & may have
20 or more nuclei.
The giant cells are weakly phagocytic
but produce secretory products which
help in removing the invading agents.

Examples of some Granulomatous inflammationsExamples of some Granulomatous inflammations
Conditions Etiologic agent Features
1.Tuberculosis M.Tuberculosis Tuberculous granulomas with central
caseating necrosis.
2.Syphilis Treponema
pallidum
Gummas composed of histiocytes,
plasma cell infiltration, central necrosis
3.Cat scratch
disease
Coccobacillus Lymphadenitis,reticuloendothelial
hyperplasia,granulomas with central
necrosis.
4.Actinomycosis Actinomycosis
Israeli
Cervicofacial lesions
5.Foreign body
granulomas
Talc,suture,oils,
wood splinter etc
Non caseating granuloma with foreign
body giant cells

Healing and repairHealing and repair

Injury to the tissue may result in cell death & tissue destruction.
Healing is the body response to injury in an attempt to restore the normal
structure & function.
Healing occurs in the following phases
REMOVAL OF DEAD TISSUE
INFLAMMATION HEALING
SPECIALIZED TISSUE
(REGENERATION)
REPLACEMENT BY
FIBROUS TISSSUE
(SCARRING)

Regeneration involves two processesRegeneration involves two processes
1.Proliferation of surviving cells to replace lost tissue.
2.Migration of surviving cells into the vacant space.
The factors which control healing & repair are complex & they include the
production of variety of growth factors
Damaged epithelial cells Platelets Macrophages
Specialized cell regeneration Fibroblast activation Angiogenesis
(epidermal growth factor) (transforming growth (angiogenic
factor β) factor)
Growth factors and cytokines

RepairRepair
Repair is the replacement of injured tissue by fibrous tissue.The processes
involved in repair are
1.Granulation tissue formation
2. Contraction of wounds
Takes place by the participation of mesenchymal cells
(consisting of connective tissue stem cells,fibrocytes& histiocytes),
endothelial cells, macrophages, platelets & parenchymal cells of the injured
organ. www.indiantalacademy.comwww.indiantalacademy.com

Granulation tissue formationGranulation tissue formation
Granulation tissue derives its name
from the slightly pink appearance of the
tissue. Each granule corresponds
histologically to proliferation of new
blood vessels which are slightly lifted
on the surface by a thin covering of
fibroblasts and young collagen.
Phases involved in formation of
granulation tissue.
Phase of inflammation
Phase of clearance
Phase of in growth of granulation
tissue
angiogenesis(neovascularization)
Fibrous tissue formation

Contraction of woundsContraction of wounds
The wound starts contracting after 2-3 days & the process is completed by
14th
day, during this period the wound is reduced by approximately 80% of its
original size.Contracted wound results is rapid healing since lesser
surface area of the injured tissue has to be replaced.
Mechanism
Dehydration as a result of removal of fluid by drying of wound
Contraction of collagen proceeds at a stage when the collagen content of the
granulation tissue is very small
Myofibroblasts migrate and their active contraction decreases the size of the
defect, these cells contain actin & myosin & thereby causing formation of new
tissue and contraction takes place.

WOUND HEALINGWOUND HEALING
Regeneration & repair is accomplished in one of the
following two ways
1.Healing by first intention (primary union)
2.Healing by secondary intention (secondary union)

HEALING BY FIRST INTENTIONHEALING BY FIRST INTENTION
This occurs in clean, incised wounds with good
opposition of the edges.
Immediately blood clot & debris fill in the defect
2-3 hours early inflammation close to the edges with
mild hyperemia & few PMN’s
2-3 days macrophagic activity removing the
clot. Proliferation of blood vessels & fibroblastic activity

10-14 days scab loose & epithelial covering
complete.
Fibrous union of the edges
Weeks: scar tissue still hyperemic with good
fibrous
union but not of full strength
Months-years: Devascularisation & Remodeling of
collagen by enzymatic action. Scar is minimal &
merges with the surrounding tissues

HEALING BY SECONDARY INTENTIONHEALING BY SECONDARY INTENTION
This occurs in open wounds particularly when there has
been significant loss of tissue because of necrosis or
infection
Early stages the cavity is filled with blood &
clot. Acute inflammation at the junction of the
living tissues.
A few days later contraction of the wound takes place with
a single sheet of epithelial cells between the surface of
the debris & the underlying living tissue.
1 week: granulation tissue formation
2 weeks: Epithelial covering complete with capillaries less
prominent.
Months: There is a varying depth on the skin surface with
thick collagenous scar tissue becoming less vascularwww.indiantalacademy.comwww.indiantalacademy.com

COMPLICATIONS OF WOUND HEALINGCOMPLICATIONS OF WOUND HEALING
Contracture is due to the
thickening & shortening of the
collagen bundles & may cause
serious cosmetic & functional
disability, particularly in deep &
extensive burns & around the
joints of the muscles if seriously
damaged.
Occasional complications may
occur at the edges & base of the
wound in which granulation tissue
may form in excess and prevent
proper healing. www.indiantalacademy.comwww.indiantalacademy.com

FACTORS INFLUENCING HEALNGFACTORS INFLUENCING HEALNG
These can be divided into local factors & systemic factors
A. Local factors
i) Infection
ii) Poor blood supply
iii) Foreign bodies
iv) Movement
v) Exposure to ionizing radiation delays granulation tissue
formation
vi) Exposure to ultra violet light facilitates healing
vii) Type, size & location of injury
B. Systemic factors
i) Age
ii) Nutrition
iii) systemic infections
iv) Cortisteroids act as anti-inflammatory agents.
v) Uncontrolled diabetics
vi) Hematological disturbanceswww.indiantalacademy.comwww.indiantalacademy.com

HEALING OF SPECIALIZED TISSUESHEALING OF SPECIALIZED TISSUES
Healing of Nervous tissue-
1.Central nervous system-The nerve cells of brain,
spinal cord and the ganglia once destroyed cannot be
healed. The damaged neuroglial cells however may
show proliferation of astrocytes called gliosis.
2.Peripheral nervous system- The peripheral nerves
show regeneration, mainly from proliferation of
Schwann cells and fibrils from the distal end.
The myelin sheath & the axon of the intact distal
nerve undergo Wallerian degeneration upto the next
node of Ranvier towards the proximal end.
Sprouting of fibrils takes place from the viable axon.
In 6-7 weeks the peripheral stump consists of tube
filled with elongated Schwann cells.
Once the fibrils from the proximal stump enter the old
neural tube it develops into a new functional axon.

HEALING OF MUSCLE
All three types of muscle fibres have a limited capacity to regenerate
1. Skeletal muscle- On injury the cut ends of the fibres are held
together by stromal connective tissue. The injured site is filled with
fibrinous material,PMN’s & macrophages.
If the muscle sheath is intact sarcolemmal tubes containing
histiocytes appear along the endomysial tube which in about 3
months time restores properly the oriented muscle fibres
If the muscle sheath is damaged it forms a disorganized
multinucleate mass & scar composed of fibro vascular tissue.
2. Smooth muscle-Non-striated muscle has limited regenerative
capacity e.g. appearance of smooth muscle in the arterioles as
granulation tissue.
3. Cardiac muscle-Destruction of the heart muscle is replaced by
fibrous tissue & in situations where the endomysium of the individual
cardiac fibre is intact regeneration may occur in young patients.

HEALING OF MUCOSAL SURFACESHEALING OF MUCOSAL SURFACES
The cells of the mucosal surfaces have a very good regeneration
capacity and are replaced continuously as the blood supply is excellent
and promotes healing due to rapid differentiation of cells.

INFLAMMATORY CONDITIONS OF THE ORAL CAVITYINFLAMMATORY CONDITIONS OF THE ORAL CAVITY

Prosthodontic ConsiderationsProsthodontic Considerations
FIXED PARTIAL DENTURE
Factors of specific influence are
1.Ridge contact-Pressure free contact between
the pontic & the underlying tissues.
If any blanching of the tissues is observed
at the try in stage the pressure area should
be identified by disclosing medium & the
pontic recontoured until contact is entirely
passive.
This passive contact should be on the
keratinized mucosa.
Scraping of the cast should be avoided as
this may also cause positive ridge pressure.
2. Oral hygiene considerations-Patients must
be taught efficient oral hygiene techniques.

PONTIC MATERIALPONTIC MATERIAL
Glazed porcelain is generally considered the most biocompatible.
Well polished gold is smoother, less prone to corrosion & less retentive
to plaque than an unpolished or porous casting.
Regardless of the choice of the pontic material patients can prevent
inflammation around the pontic with meticulous oral hygiene.
OCCLUSAL FORCES
Reducing the buccolingual width of the pontic by as much as 30% has
been suggested as a way to reduce the occlusal forces on & thus the
loading of the abutment teeth.
Reducing the pontic width may be desired as it facilitates plaque
control
measures by lessening the lingual contour.
USE OF SOFT TISSUE MODELS
Use of soft tissue models will help the technician to fabricate the
prosthesis by the adequate guidance of the soft tissue contours.

COMPLETE DENTURESCOMPLETE DENTURES
1.Soft tissue hyperplasia-it is the response of the soft tissues under or
around the complete denture due to fibro epithelial response to
complete denture wearing. The causes are
a) Trauma from denture wearing b) Gradual residual ridge resorption
c) Habits & duration of wear d) Excessive forces on limited segments
of the dental arches because of lack of balancing contacts in
eccentric jaw positions.
2.Epulis fissuratum- Hyperplasia occurring around the dentures leading
to a fibrous growth which occurs due to ill-fitting or over extended
dentures.
3. Denture stomatitis -is a chronic inflammation of the denture bearing
mucosa caused due to ill-fitting dentures or Para functional
habits.
Effective management of all these conditions can be done by
A) Oral and denture hygiene accompanied by tissue rest.
B) Antifungal therapy .
C) Surgical excision of papillomatosis.www.indiantalacademy.comwww.indiantalacademy.com

Subpontic osseous hyperplasia: A literature review
J.P.D:1991:66;638-41
The proposed etiologies for this condition are
1.FPD acting as a stimulus to osseous proliferation.
2.Chronic irritation produced by the pontic initiates the subperiosteal
growth.
3.Functional stresses on bone during mastication.
4.Stress generated electrical potentials of the bone.

CONCLUSIONCONCLUSION
The mouth represents one of the most complex areas of the body with
regard to the broad range of disorders affecting it. By virtue of its partial
Ectodermal and Endodermal origin, the oral mucosa may show
manifestations of the systemic diseases. Oral mucosa is extremely
sensitive to metabolic disturbances perhaps only paralleled by the
bone
marrow and thus serves as an excellent marker for such disorders.
The modern concept of practicing dentistry is to
recognize these basic etiological factors & pathological changes
occurring in the oral tissues as it is a significant diagnostic aid
representing the patient’s general medical status.
“ FACE IS THE MIRROR OF THE MIND AND THE ORAL CAVITY IS
THE MIRROR OF THE WHOLE BODY”

BIBLIOGRAPHYBIBLIOGRAPHY
1.Text of Pathology-Harshmohan 4th
edition
2. Pathology illustrated-Peter.S.Macfarlene 5th
edition
3. Text of Pathology –Robbins
4. Pathology in dentistry-Shefield
5. Gen. & systemic Pathology-Underwood 2nd
edition
6. Colour atlas of Oral pathology-Robinson & miller 4th
edition
7. Colour atlas of common oral diseases- Robert.P.Langlais
8. Oral bio-science-Fergusson
9. Oral medicine – Tyldessly & Field 4th
edition
10.Essentials of Oral pathology & Oral Medicine- R.A.Cawson
11.Contemporary Fixed Prosthodontics-Rosenstiel 3rd
edition
12.Prosthodontic treatment for edentulous Patients-Bouchers
10th
edition

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Inflammation and repair /orthodontic courses by Indian dental academy

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