11. INFLAMMATION DENTISTRY IN SIMPLER TERMS.ppt

What Is Inflammation?
Inflammation is a process by which your body's white blood cells and the things they make protect you from infection from outside invaders, such as bacteria and viruses.

But in some diseases, like arthritis, your body's defense system -- your immune system -- triggers inflammation when there are no invaders to fight off. In these autoimmune diseases, your immune system acts as if regular tissues are infected or somehow unusual, causing damage.

1. GENERAL PATHOLOGY
INFLAMMATION

2. INFLAMMATION
Inflammation
Inflammation is the reaction of vascularised living tissue to local injury
Causes of inflammation
1.) Mechanical eg: cutting, crushing
2.) Chemical eg: acids, alkalis, bile etc
3.) Physical eg: sun, heat, electricity
4.) Infection eg: bacteria, viruses, fungi, parasites
5.) Necrosis eg: around infarcts [ vital reaction]
6.) Immune orallergic eg: rhinitis, dermatitis
Clinical Signs Of Inflammation= Response To Injury
Redness (Rubor)
Heat (Color)
Pain (Dolor)
Swelling (Tumor)
Loss of function

3. INFLAMMATION

4. MICROSCOPIC FEATURES
OF INFLAMMATION
In order:
Arteriolar dilatation: sometimes preced by transient vasoconstriction
Increased in blood flow: through arterioles, capillaries and vessels
Increased permeability:of microvessels allows for the
Exudation: of fluid through permeable vessels
Concentration or packing of red cells in vessels due to fluid loss. This
results in increased viscosityof the blood
Slowing or complete cessation of blood flow
Peripheral marginationor pavementing of white cells which stick to the
endothelium in microvessels. Adhesion takes place by virtue of cells
adhesion molecules (CAM)
Emigrationof white cells by activepassage through vessel wall into the
inflammatory focus, first polymorphonuclearleucocytes, then monocytes
together with passiveescape of red blood cellsforced out with them by
process known as Diapedesis
(see diagram at lecture)

5. White cells find their way to site of injury by
process of chemotaxis
Chemotatic agents are bacterial products,
components of complement system(C5a,
components of the lipoxygenase pathway
of arachordonic acid metabolism especially
leukotriene B4
Polymorphonuclearcytes are characteristic
histological finding in acute inflammation

6. THESE CHANGES CAN BE
SUMMED UP AS:
Vascular: active hyperaemia
Exudative: fluid orcellular exudate.
Oedema, space occupied by fluid
separating fibres and cells
Fibrin precipitation
Accumulation of white cells,
especially PMN in and on vessel
walls and in tissues

7. VASCULAR
PERMEABILITY
 3 types of this response can be described
 1.) Immediate Transient
 Response which comes immediatelyafter injury
 Lasts for 15-30 minutes
 Brought about by histamine and other chemical mediators
 Leakage occurs from gaps in small venules
 2.) Immediate Sustained
 More severe injury to all small vessels (arterioles, venules and capillaries)
 E.g. severe burn
 Necrosis of endothelial cells occur and leakage for several days until damage vessels are thrombosed e.g. repaired
 3.) Delayed Prolonged
 Leakage may take some hours to develop and lasts for hours or days
 Affects capillaries and venules
 E.g. sunburn, moderate heat xray
 Other causes will be bacterial toxins and delayed hypersensitivity reactions
 Increased hydrostatic pressure leads to fluids leaving permeable vessels either by pinocytosis, gaps in intercellular
junctions of endothelial cells which are opened up by the chemical mediators of inflammation
 Fluid part of exudates = to plasma in composition
 Fluid/ exudates acts by:
 Diluting toxins
 Transporting antibiotics, drugs to site of inflammation
 Precipitating fibrin to wall off the area ant to aid phagocytosis

8. IMMEDIATE TRANSIENT

9. IMMEDIATE SUSTAINED

10. Lymphaticsdilate and drain oedemafluid
and waste products from
the inflamed area
An immune response maybe evoked by
transport of macrophages containing
antigenic material to the lymph nodes
Drainage lymph nodes maybe enlargened
and tender

11. CLINICAL CARDINAL
SIGNS OF INFLAMMATION
Can Be Related To Vascular Changes:
1.) Redness And Heart
Increased blood supply with vascular dilation
2.) Swelling
Due to oedema caused by the exudation of fluid from vessels
into the tissues
3.) Pain
Maybe due to oedema causing increased tissue tension and
pressure on nerve endings. Release chemical mediators of
inflammation (such as bradykinin) may also, cause pain
4.) Loss
Of function may occur following the swellingand the pain or
following inflammatory destruction of tissue

12. CLINICAL CARDINAL
SIGNS OF INFLAMMATION

13. CHEMICAL MEDIATORS
OF INFLAMMATION
1.) Vasoactive Amines
E.g. histamine and 5-hydroxy tryptamine
Released by mast cells in tissue and basophils in blood and platelets
following certain stimuli e.g. trauma, IgE hypersensitivity, release of
fragments of complement (C3a and C5a)
2.) The Complement System
System activate by antigen-antibody complexes (classic pathway) or variety
of substances such as bacterial toxins (alternate globulins)
C3a and C5a increase vascular permeability
C5a exert chemotatic influence
Acts as opsonins (C3b) and lyse the membranes of cells and organisms
3.) The Kinin System, The Coagulation System And Fibrinolytic System
Related systems maybe activated together by contact activation factor
(factor x11)

Contact Activation

14. CHEMICAL MEDIATORS
OF INFLAMMATION
Bradykinin
Increase in vascular permeability
Is a vasodilator
Causes pain
Plasmin
Activates C3to C3a, which is permeability
Spilt fibrin and increases vascular permeability
Lyses and fibrin formed
Conversion Of Fibrinogen To Fibrin
Increases vascular permeability
Has chemotatic effect

15. CHEMICAL MEDIATORS
OF INFLAMMATION

16. ARACHIDONIC ACID
METABOLITES
Leukotriences
Aid in chemotaxis
Vascular permeability is increased
Constriction
Vessels and bronchi
Prostacyclin
Anti aggregant and vasodilator
Thromboxane A2
Platelet aggregant and vasoconscritor
Prostaglandins
Vasodilators oedema

17. LEUKOTRIENES

18. IMPORTANT CELLS TO
REVISE IS:
1.) PolymorphonulearLeucocytes
Neutrophils
Esonophils
Basophils
2.) Mononuclear Phagocytes
3.) Lymphocytes
4.) Plasma Cells

19. INFLAMMATION
Inflammation can be classified according to the nature of the inflammatory
exudates:
One such type is SuppurativeInflammation
This inflammation is accompanied by pus
Localized collection of pus is known as an abscess
Abscess forms when the destructive inflammatory process is walled off, at
first by fibrin and inflammatory cells, and later by newly formed connective
tissue
If pus formation, continues after being walled off then it can be very painful
Whilst pus remains in situ, healing cannot easily take place
Pus must be removed and this can happen naturally because with increasing
tension the pus will tend to track between tissue planes to surface
Therefore, abscess must be incised and drained to minimize tissue damage
and relieve pain, as well as, reducing the chances of spread of infection due
to the trackingor pointing of the abscess

20. SUPPURATIVE
INFLAMMATION

21. CHRONIC INFLAMMATION
Is a prolonged process in which destruction
and inflammation are proceeding at the
same time as attempt at healing
Acute inflammation can be assumed to be
entering a chronic phase after it has
persisted for a week or two
Chronic inflammation although some
polymorphs are present, macrophages,
lymphocytes and plasma cells are the main
cells present

22. CHRONIC INFLAMMATION

23. HISTOLOGICAL FEATURES
OF CHRONIC
INFLAMMATION
1.) Exudation
Persistence of acute inflammatory changes
Continued tissue destruction
2.) Macrophage Accumulation
Macrophages presents in very large numbers
3.) Repair
Reparative granulation tissue can be formed
Granulation Tissue Consist of:
Newly formed capillaries and budding endothelial cells
Proliferating fibroblasts and collagen
Lymphocytes, plasma cells and other inflammatory cells
So called because when seen at bottom of healing wound granulation
tissue 6.)
has a red granular appeerance
May progress or nature to form proper fibrous tissue which will form a
scar

24. CLASSIFICATION OF
CHRONIC INFLAMMATION
1.) Non-Specific Chronic inflammation
Due to organisms of various sort or in response to foreign material
E.g. chronic ostemyelitis
Occurs in long bones of children or young adults
Follow acute inflammation in the bone
Increased tissue tension due to exudates is exerted against unyielding bone and there is
compression of blood vessels leading to ischaemia and necrosis of the actual bone
Pus is formed which tracks under the periosteum, further interfering with blood supply
Pus maybe discharges from the surface penetrating muscles and skin with formation of
sinuses
Dead bone acts as a foreign body in which organisms can continue to grow
At the same time, it prevents adequate draining of pus and delays healing
In chronic osteomyelitis, dead bone is known as Sequestrum
New bone formation can further prevent proper healing as it blocks drainage
End result is chronic supparative inflammation of bone or chronic osteomyelitis
This can cause death due to persistence of infection
Fortunately, due to antibiotics at an early stage and surgical treatment to bring about
drainage, the disease is no longer the danger it used to be

25. CLASSIFICATION OF
CHRONIC INFLAMMATION

26. GRANULATION OF
CHRONIC INFLAMMATION
E.g. TB (Refer To Notes)

27. GRANULATION OF
CHRONIC INFLAMMATION

28. EFFECTS OF CHRONIC
INFLAMMATION
1.) Systemic effects from chronic inflammation
similar to those in acute inflammation
Fever manifests as night sweats rather than
shivering and chills
Leucoytosis more likely to involved mononuclear
cells than polymorphs
Increased protein synthesis
Loss of appetite and weight loss
Tiredness, headaches and general feeling of being
are difficult to explain