Inflammation ( part 3) l General pathology revision for dental student

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sequels of acute of inflammation 

Cellular chemical factor

• Various chemical mediators have roles in the inflammatory process. They may be circulating in plasma and require activation or they may be secreted by inflammatory cells. Many of these mediators have overlapping actions.

Amines       

• Release from mast cell , basophils & platelet (eg. Histamine & serotonin)

prostaglandin        

• Secreted from most tissues of the body and not stored.
• Derived from arachidonic acid via cyclo-oxygenase (COX) pathway
• Its action is delayed but prolonged and antagonized by Aspirin.

Leukotreines

• Secreted by neutrophils.
• Derived from arachidonic acid via lipo-oxygenase pathway Cytokines

cytokines     

• Produced by stimulated T lymphocytes or monocytes , e.g. Interleukin-1 (IL-l) & (IL-6), Interferon (INF) & Tumor necrosis factor (TNF).

Lysozomal enzyme:

•  Released from neutrophils, macrophages and platelets

O2  Free Radicals  :

• hydrogen peroxide (H2O2) or superoxide

Fibrinolytic system

• Dissolve fibrin

Coagulation (clotting ) system:

Convert fibrinogen to fibrin

Kinin system :

• Injury → acivate clotting factor XII ( hagmen factor) → convert prekallikerein to kallikerien → convert kininogen into bradykinin

Complement system :

• Consist of : plasma protein in inactive form in plasma , from C1 to C9 , activated by

classical pathway

• Trigged by fixation of C1 to ag-ab complex   

alternative pathway

• Trigged by activation of C3 by Ag-Ab complex or bacterial endotoxin
• N.B: main active complement system is C3a,C5a (anaphylatoxins)

Function of chemical mediators

1. Vasodilatation: due to  (histamine, Prostaglandin & Bradykinin).
2. ↑ vascular permeability (histamine, Bradykinin, C3a, C5a)
3. Chemotaxis (C3a, C5a & TNF).
4. Phagocytosis by (C3b which acts as an opsonizing agent.)
5. pain by ( bradykinin )             
6. fever & leukocytosis by ( IL-1 , TNF)

Acute suppurative inflammation

Definition :

• Severe acute inflammation characterized by pus formation.

Cause :

• Pyogenic bacteria (bacteria forming pus) as staphylococcus aureus, streptococcus pneumococcus & E-coli

PUS

• Is the fluid formed as a result of suppuration 

Pathogenesis of formation (3 factors required)     

• Prominent tissue necrosis: It is produced by:      

1. Bacterial toxins.      
2. Pressure of the inflammatory edema      
3. Thrombosis due to marked slowing of blood flow and endothelial injury.

• Excess neutrophil leucocytes. The pyogenic bacteria are Chemotactic to leucocytes.
• Presence of sufficient amount of proteolytic enzymes: Mainly produced by dead neutrophils (pus cells) and to less extent by necrotic tissue.         

Structure    

1. Living and dead bacteria.                                                
2. Living & dead neutrophils (pus cells)
3. Fragments of tissue debris from necrotic tissue.        
4. Inflammatory fluid exudate.
5. In old pus: macrophages, cholesterol crystals and fat globules are present.         

character    

1. Thick turbid fluid.                    
2. Odorless.                        
3. Alkaline PH
4. Viscous(due to  product of tissue destruction especially DNA)  
5. yellowish color (due to myeloperoxidase of neutrophils.)
6. Pus doesn’t clot on standing because its fibrin content is destroyed by the proteolytic enzymes   

1- ABSCESS

• localized suppurative inflammation resulting in the formation of an irregular pus-containing cavity 

sites :

• Occurs anywhere commonly in skin, lung, brain, kidney, liver         

pathogenesis        

• Early the abscess consists of two zone   

1. A central zone of necrosis.
2. A peripheral zone of acute inflammation

• Later, many neutrophils die and liberate their proteolytic enzymes→ liquefies central necrotic zone from the periphery & the abscess now is composed of three zones: 

1. central necrotic core.   
2. mid-zone of pus.
3. peripheral zone of acute inflammation (pyogenic membrane).

• The central necrotic core may disappear by more liquefaction →abscess enlarges by gradual destruction of the pyogenic membrane → staphylococci produce coagulase enzyme which helps fibrin formation → localizes the inflammation.   

    

N/E :

• Sub Cautenous abscess appears as localized tender swelling covered by red edematous skin with opaque yellow center.           

           

2-FURUNCLE

• Small abscess related to hair follicle, sebaceous or sweat gland due to staphylococci

Site     

• mainly hairy parts as face, axilla, Multiple neighboring boils are called furunclosis  

 

3-CARBUNCLE

• localized suppurative inflammation forming multiple communicating suppurative foci in the skin and S.C. fat discharging pus through several openings d.t staph cocci       

Site   

1. back of neck , scalp & buttoks
2. more common in diabetic patient       

Pathogenesis of carbuncle :

• Normally, S.C. fat is arranged in Columns separated by dense fibrous septa extending from deep fascia up to dermis,  When bacteria invade S.C. fat it will result in the formation of multiple communicating suppurative foci , They open on the surface at multiple points particularly at the base of hair follicles       

CELLULITIS (PHLEGMNOUS INFLAMMATION)

definition :

• Acute diffuse suppuration inflammation        

Site:  

• Loose connective tissue as areolar tissue of the orbit, scrotum and wall of the appendix       

Cause:

• streptococcus hemolyticus which produces two enzymes:               

1. Fibrinolysin (streptokinase) enzyme: Dissolves fibrin.               
2. Hyaluronidase enzyme: Dissolves hyaluronic acid of ground substances helping spread of bacteria & its toxins.     

pathology   

• The basic pathological changes are similar to those of abscess with the following differences:               

1. Failure of localization because of absence of fibrin.               
2. The necrosis is extensive and the separated dead masses are called sloughs.(more sloughs)               
3. Pus formation is slow→ Pus is thin in consistency & may contain many red cells (sanguineous).           

complication        

1. Lymphatic spread: leads to acute lymphangitis and lymphadenitis.   
2. Blood spread: leads to septicemia and pyemia