Oedijani Santoso Bagian/SMF Gigi dan Mulut FK Undip/RSUP dr Kariadi Semarang

Factors Which Impede Healing (Systemic)

- Age - Mal-nourishment - Corticosteroids/NSAIDs - Diabetes - Anti-coagulants

Factors Which Maximize Healing (Systemic)

- Adequate nutrition - Calcitonin - Vitamin A - Glucosamine - Anabolic Steroids

Factors Which Impede Healing (Local)

- Prolonged immobilization - Rigid fixation - Excessive soft tissue gap - Excessive motion or stress/repeat injury

Factors Which Maximize Healing (Local)

- Electrical stimulation - Injectable growth factors - Surgical gap closure/surgical - Controlled motion

1. Primary Intention epithelization 24 hours

seals the wound from bacterial 2. Delayed Primary Closure contaminated wounds host inflammatory and immune responses 3. Secondary Intention natural biologic healing processes without surgical intervention epithelization & collagen deposition in the spontaneous closure of large open wounds

I. Inflammation : - vascular response - cellular infiltrate - neovascularization - synth granulation tissue II. Proliferation : - cell proliferation - collagen synthesis - endothelial cell proliferation - mature formation of granulation tissue - increase in mechanical strength III. Maturation : - collagen remodeling - increase in wound strength - decrease in vascularity - formation of scar tissue

1. Vascular Reaction
= Hemostasis deposition fibrin blood clot = Transient constriction local vessels 5-10mt leuko, erythro, platelet adherent to endothelium = vasoconstriction followed by active vasodilatation vasopermeability mediators : histamine, prostaglandin, norepinephrine permeability endothelial cells swell separation between themselves

2. Cellular Movement = PMN leukocytes , macrophage penetrated the vessel wall phagocytosis function 1-2 days = fibroblast and capillaries (neovascularization) appear 1-10 days = fibroblast glycosaminoglycans collagen

Cells Involved in Wound Repair

3. Chemotactic Mediators = subtances that promote migration of cells = can be through several mechanism and pathway : * complement system * immune system * phagocytotic system

Inflammation is an essential part of healing, but as an "all or nothing" response can be harmful. Excessive or prolonged inflammation excessive scar formation pain oedema secondary tissue ischaemia loss of movement and weakness

Physiotherapy aims to control inflammation:

prevent disruption of new blood vessels and collagen fibrils minimise bleeding promote collagen and ground substance synthesis reduce oedema ; protect healing tissue provide pain relief

Movement during inflammatory phase:

Improves blood flow Decreases swelling Relieves pain Increases phagocytosis Prevents joint stiffness and muscle weakness in related areas

1. Epithelization
= 3 separate but overlapping phases of epithelial activity : * migration * proliferation * differentiation = migration and proliferation of epithelial cells 24-48 hours after injury at the wound margin

NORMAL REPAIR

2. Fibroblast
= migrate along strands of fibrin deposited in blood clot proliferation glycosaminoglycans collagen

3. Collagen
Type I Fibroblast Bone,tendon,skin,dentin (90%) ligament, arteries, uterus Type II Chondrocyte Hyaline cartilage Type III Fibroblast arteries, spleen, intestine Smooth muscle Type IV Epithel Basement membrane

4. Tensile Strength = collagen deposition tensile strength = is defined as the load per cross-sectional area that can be supported by the wound = a sufficient quantity of collagen fibroblast in the wound diminishes disappearance of fibroblasts marks the end of phase II

Use therapeutic techniques to help control pain and swelling; reduce reliance on support and strapping; progress activity levels. Applying tension through exercise or manual therapy increase collagen synthesis, promote better collagen alignment increase tensile strength

Movement during proliferation phase:

Increases tensile strength Increases tissue metabolism Promotes extensibility of scar tissue Maintains and improves joint range of movement & muscle strength

= Microscopically : a random collagen fibers organized pattern = Loss of the size of collagenous mass depend on : physical factors (tension, pressure), oxygen supply, patients age = Interplay between collagen deposition and degradation : breakdown > production scar softer; Production > breakdown hypertrophy scar/keloid = after scar matured scar density fluid and volume

Physiotherapy aims to help the tissues regain as near normal structure and function as possible and control tissue overload by modifying intrinsic and extrinsic factors Achieve and maintain flexibility of healing tissues

Prevent unwanted adhesions [abnormal deposits of collagen that disrupt gliding between adjacent structures] Restore functional activity Address intrinsic and extrinsic causes

Movement during remodelling phase:

Restores full range of movement and muscle strength Counteracts scar contraction Restores function Restores confidence

= unique structure with several specific function = major reservoir of calcium = insertion of musc & protect vital soft tissue str = body support and strength, 1/10 body weight = extremely strong, has a flexible and elastic str = undergoing spontaneous regeneration = injured bony str regain preinjury strength & function

Local:
= Soft tissue injury

= Interruption of local blood supply = Interposition of soft tissue at fracture site = Bone death cause by radiation, thermal, chemical burn or infection

Systemic
= Malnutrition

= Smoking osteoblast nicotine vaso constr blood flow in fracture site = DM collagen defect = aging compromise in vascularity, osteoporosis

1. Primary intention occurs when:

excellent anatomic reduction, minimal / no mobility, good vascular supply at the fracture site 2. Secondary intention intermediate fibrous tissue is formed within the fracture gap through adaptation & remodelling form and function similar preinjury bone

= occurs when enough rigidity

= osteogenic cells and capillary proliferation in medullary bone on both sides of the fracture forming new bone = without intermediate cartilaginous callus formation = 2 way : gap healing and contact healing

1. Initial stage :
Hematoma formation concurrent with inflammatory response cellular proliferation (8-12 hours)fibroblast collagen + capillary network granulation tissue oxygen tension & pH cartilage

Secondary Bone Repair

2. Cartilaginous callus (Soft callus) = while external callus is forming internal callus between the bone ends also form = this area better blood supply, less necrosis osteoblast form an internal bony callus = callus strength & stiffness of bone especially resistance against bending & torsion, during the healing period

3. Bony callus (Hard callus ) = cartilaginous callus undergoes calcification = osteoblast deposit osteoid on calcified cartilage calcification processforming bone = initially, woven bone lamellar bone during final stage

4. Remodeling = familiar pattern of lamelar bone = osteoclast (resorption of bone) + remodeling factors (bone morphogenetic protein = BMP) as a mitogenic and transforming growth factor induce differentiation of mesenchymal cells bone formation

Secondary Bone Repair

1. Inflammatory reaction Hematoma stage (0-5 days after fracture)

= inflammatory reaction involves PMN

leukocytes, lymphocytes, macrophages, monocytes = hematoma also contains platelets produce PDGF mitogenic for fibroblasts

2. Callus formation stage (4 40

days after fracture)

= periosteal & endosteal mesenchymal

cells fibrocartilaginuos callus = chondroblast produce cartilage growth factor cartilage-sp type2 collagen & hyaluronic acid cell proliferation

3. Remodeling phase ( 25-50 days

after fracture)
= T lymphocyte produce lymphokine,

OAF (osteoclast activating factor) stimulate osteoclasts resorption = BMP proliferation & differentiation of mecenchymal cell chondrocyte calcification of cartilage matrix , vascular invasion & bone differentiation

1. Growth factors:
-

TGF = transforming growth factor BMP = bone morphogenetic protein FGF = fibroblast growth factor PDGF = platelet-derived growth factor IGF = insulin-like growth factor

2. Cytokine
Spesific factors stimulation of osteoblast & osteoclast Cytokine Bone formation Bone resorption IL-1 + +++ TNF + +++ TNF + +++ TGF -+++ TGF ++ ++ PDGF ++ ++ IGF-1; IGF-2 +++ 0 FGF +++ 0

3. Prostaglandine/leukotrient : stimulate osteoblastic bone formation 4. Hormone: - Estrogen : stimulate fracture healing - Glucocorticoid : stimulate osteoclastic bone resorption - Parathyroid GH: bone formation callus formation 5. Growth factor antagonist

Wound Healing