Repair l General pathology MCQs

 

Repair and healing by fibrosis ( granulation tissue ) or organization and type of wound intention  l General pathology MCQs for dental student

Healing by fibrosis

Granulation tissue:

• Transitory highly vascular tissue formed during repair process consist of capillary and fibroblast which mature to fibrous tissue

Mechanism of formation :

1. New capillaries arise as solid endothelial buds from capillaries at damaged area edge
2. Get hollowed & filled with blood ,anastomose and form capillary loop
3. New capillaries are highly permeable due to lack bm and give nutrition to proliferating fibroblasts
4. Fibroblast arise from resting fibrocytes and proliferate following capillaries from edge inward

Granulation tissue n/e:

• Red, granular ,velvety ,moist ,insensitive, fragile(bleed easily),resist to infection due to high amount of fluid exudate containing macrophage

Fate :

• Fibroblast produce g.s & 15 types of collagen fiber in all direction → compress and obliterates the capillaries
• Fibroblasts develops temporarily contractile microfilament in their cytoplasm as smooth muscle → myofibroblasts contract → lesion gets smaller(more seen in 2ry union of wound)→ fibroblasts change to fibrocytes
• Rearrangement(remodeling) of collagen fibers and fibrocytes regulary → give full strength of tissue
• Finally, avascular strong fibrous tissue is produced → scar

Healing by organization

• Organization: replacement of solid non living material (eg. Blood clot . Dead tissue) by fibrous tissue, examples(serofibrinous infl. ,thrombosis , hematoma , infarct area )

Healing of serofibrinous inflammation as serous sac:

1. The serous component of inflammatory exudate is absorbed
2. Fibrin &cellular exudate change to structurless mass which is removed by macrophage
3. Granulation tissue arise from subserosal surface and cover both surface    
4. Epithelization : serosal cells at the bare area edges proliferate and cover granulating surface
5. Maturation of granulation tissue to fibrous tissue

Effect: according to fibrosis extent:

• + → white patches in serous membrane
• ++ → band adhesion between two layers
• +++ → complete adhesion between the two layers

Healing of wound

• Wound contraction: the process by which the open wound full thickness is diminished by myofibroblast

Primary union of wound ( healing of 1ry intention):

1. Blood is clotted between the edges on the surface
2. It cause mild acute inflammation at edges
3. Inflammatory product remove rapidly by macrophage
4. The basal cell on both edges → proliferate to meet at center & divide to form the whole epidermis thickness
5. The remnant clot at the surface called scab → separate within 10-14 days
6. The gap filled by granulation tissue originated from edges
7. At the 5th day → granulation tissue   maturation to fibrous tissue
8. Fibrocyte and collagen fiber arranged parallel to the surface

2ry union  of wound ( healing of 2ry intention)

• The same except the following:
• Necrotic debris, clots, inflammatory  cells are more extensive
• Pus may exist and longer period
• The gap filled with granulation tissue up to basal layer of epidermis level
• Wound contraction is the major difference → an action occur by myofibroblast

Complication of repair

painful scar :

•  as neuroma stump

implantation dermoid:

• Dip down of epithelium into underlying tissue form it

squamous cell carcinoma :

• Rarely develops in scar

too less cellular proliferation :

1. Ulcer
2. Sinus
3. Fistula
4. Incisional hernia: due to stretching of weak scar

too much cellular proliferation:

• Proud flesh: extensive granulation tissue that protrude skin level causing block epithelialization
• Keloid: extensive scaring due to collagen degeneration defect , more common in young and negroes individual
• Cause: imbalance between collagen synthesis & its destruction by collagenase enz ( seems to be inherited in some patient)
• N/E : firm , raised scar with claw like process
• M/E : dense hyalinized collagen bundles running parallel to surface
• Prognosis: spread progressively then cases , may recur after removal , may cays squamous carcinoma

fibrosis can harm patient: 

1. skin scar may be disfiguring
2. Scar contraction → hollow organ stricture
3. Heart valve scar → stenosis or incompetence
4. Arterial wall scar → aneurysm
5. Liver fibrosis→ cirrhosis
6. Fibrous ankylosis of joint
7. Cerebral scar → cerebral irritation & epilepsy
8. Fibrous adhesion in peritoneum

control repair mechanism

 cell-cell interaction ( contact inhibition ) :

• direct contact between similar cell → suppresses division & motility

• in wound, absence of contact inhibition, so cells migrate to cover wound surface 2)collagen synthesis and degradation:

• the net collagen accumulation depend on collagen synthesis & degradation by collagenase enzyme

cell-ECM interaction:

• important for cell attachment, locomotion, migration, proliferation and differentiation ECM consist of :

1. collagen (main structural protein forming most component of BM)
2. fibronectin & laminin (adhesive protein bind cell mm with collagen and fibrin)

4-chemical mediators : cell growth is controlled by growth stimulation(trephones) and inhibition(chalones)

• chalones:

1. formed of living cells & inhibit mitosis in neighboring cells of same type
2. tissue destrucion → - - chalones locally → adjacent living cells will proliferate

• trephones:
• they stimulate mitosis of living cell , include

1. EGF (epidermal growth factor) : ++ epithelial cell and fibroblast proliferation
2. PDGF(platelet derived …): ++fibroblast, smooth muscle, monocytes proliferation  
3. FGF( fibroblast …): ++ fibroblast & angiogenesis proliferation
4. alpha TGF ( transforming …)
5. beta TGF , TNF (tumor necrosis factor) : increase collagen synthesis