BONE REPAIR 1

Stress Fractures
• Repetitive cyclical low magnitude loading below the ultimate tensile strength of bone
over a long period = Micro-damage = Stress fracture
• Bone is living tissue & constantly remodelling = When micro-damage exceeds bone’s
intrinsic ability to repair itself = Fracture = Crack propagation = Failure
Classification Of Fractures
• Caused by singe application or injury (monotonic)
• Determined by magnitude, rate, area of distribution of force on bone
• Direct trauma = Soft tissue & fracture injury related to loading rate
• Compression, Tension, Shear … combination = Basic principles for determining fracture
patterns
•Fracture
HealingHealing
ability determined by the force inflicted
• Fracture healing = Complex, Highly ordered, Physiologic process
• In fracture healing = Bone regenerated & Properties of pre-existing are restored
• Growth & Differentiation factors, Hormones, Cytokines, Extracellular matrix interact with several cell types (bone,
cartilage) = Form primary cells or muscle mesenchymal cells recruited at the fracture injury site or from the circulation
DISTINT RESPONSES STAGES
• In bone marrow,
1. INFLAMMATION: Influx of cells and protein
cortex, periosteum, 2. REPAIR: Fibrosis, Osteogenesis, Chronogenesis,
external soft Angiogenesis
tissues 3. REMODELLING: According to stress and strain applied &
• Depends on type of
According to Wolff’s law
fracture, location, • 3 discrete and simultaneous processes are interdependent
method of • Intervention of any or all = Affect bone formation = Fracture
treatment will not heal
• 1 or several can
occur together
BONE REPAIR 2
Mechanism For Bone Healing
DIRECT (PRIMARY) INDIRECT (SECONDARY)
• No interfragmentary motion = Rigid internal fixation • Fractures that are not rigidly fixed
• Compression of fragments • Response in periosteum and external tissues
• No periosteal callus formation • Hard callus & External tissue form soft tissue
• Osteonal remodelling at interfragmentary contact points • Response in cortex and bone marrow
• Gap healing with woven bone • Cells from periosteum contribute in intramembranous & endochondral ossification
• Rapid repair pattern, influenced by biology and mechanics – enhanced by motion &
inhibited by rigid fixation
• Treated using slings, cast, intradermally fixation = Most heal this way
Haematoma, Inflammation, Angiogenesis, Cartilage formation, Bone
remodelling
BONE REPAIR 3
Decreasing Fracture Healing
SYSTEMIC FACTORS LOCAL FACTORS
• Malnutrition • Extensive injury to bone or surrounding soft tissue = Interruption of local blood supply
• Smoking • Imposition of soft tissue between the fracture fragments
• Diabetes mellitus • Inadequate reduction and/or immobilisation
• Bone death caused by avascularity, radiation, thermal or chemical burns or infection
Motion At Fracture Site
• Callus = Motion at fracture site
• Larger stress = Larger callus
• Excessive motion = Excessive strain = Vascular damage = DELAYED (3~6 months) & NON-UNIONS (6 months &
fracture interposed with soft tissue)
• Gap tissue characteristics (cartilage and/or fibrous tissue) reflect the local mechanical and nutritional factors that dominated in
• *soft tissues between 2 ends, relatively creatine = healing process is switched off = healing cascade/process needs to be triggered
NON-UNION TREATMENT
• NON-UNION = Bone ends have rounded off ATROPHIC
• In absence of infection… non-union treatment to stimulate bone • Poor blood supply
regeneration • Deficient biological processes
HYPERTROPHIC • Stabilisation & Repair enhancement
• Good blood supply • Autologous & allogenic bone graft
• Abundant callus BUT Insufficient stabilisation for fracture • Autologous bone marrow
repair • Ceramics
• Stabilisation ONLY – rods, pins, compression plates • Bioactive glasses
• Synthetic polymers
• Growth promoting proteins
• BMP’s, TGF-β, IGF, FGF, PDGF
• Mesenchymal stem cells
• Pulsed electromagnetic fields (PEMF)
• Ultrasound
• Pathophysiology, diagnosis, management of foot stress fractures: https://pubmed.ncbi.nlm.nih.gov/25419892/
• High risk stress fractures – pathogenesis, evaluation, treatment: https://pubmed.ncbi.nlm.nih.gov/16785578/
• The cell and molecular biology of fracture healing: https://pubmed.ncbi.nlm.nih.gov/9917622/
• The biology of fracture healing: https://pubmed.ncbi.nlm.nih.gov/21489527/
• Bone remodelling during fracture repair – cellular picture: https://pubmed.ncbi.nlm.nih.gov/18692584/
• Overview of fracture healing cascade: https://pubmed.ncbi.nlm.nih.gov/16188551/
• Fracture healing under healthy and inflammatory conditions: https://pubmed.ncbi.nlm.nih.gov/22293759/
• Delayed union and nonunions – epidemiology, clinical issues, financial aspects: https://pubmed.ncbi.nlm.nih.gov/24857025/
• Bone fracture healing – cell therapy in delayed unions and nonunions: https://pubmed.ncbi.nlm.nih.gov/25093266/
• Pulsed electromagnetic fields for treatment of tibial delayed unions and nonunions – prospective clinical study and review of literature:
https://pubmed.ncbi.nlm.nih.gov/22681718/
• Bone regeneration – current concepts and future directions: https://pubmed.ncbi.nlm.nih.gov/21627784/
TENDON REPAIR 1
Flexor Tendon Injury
• Common (10000) POST-SURGICAL SCARRING IN REPAIRED FLEXOR TENDONS
• Due to TRAUMA or CHRONIC • Matrix laid down in disorganised fashion  In a prolonged way = Reduction in
DISEASE gliding motion, Stiff digit, Poor hand function, Potential loss of livelihood
• Surgical repair is only TREATMENT • Adhesions & Tendon Rerupture = Affect digital dexterity, Difficult to treat, Impact
• Common complications on healthcare resources
• SCARRING:
• Forces that are meant to be transmitted from muscle to skeleton inefficiently
• Structure & Space occupied increase = Tendon is not efficiently functioning
• *swell inside
• *surrounding matrix stuck where between sheet and tendon =
adhesion where gliding motion stuck to surrounding tissue =
prevent gliding = larger in size = stiff digit = poor hand
function
• • *surgical
*dense connective tissue with very
removal fewfurther
causes cells where tension
swelling is with
in next lack of vascularity and
healing
Tendon Healing matrix
CLASSICAL – EXTRINSIC CLASSICAL – INTRINSIC
• Tendon rely on surrounding tissue • THEORY: Potenza using dogs  • Tendon has ability to heal itself
• Tendons have lack of blood Total immobilization model, • Lundorg & Rank  Implanted lacerated flexor tendon devoid of
capillaries BUT As lots of repaired cut tendons within digital sheath in knee joint pouch  Continuous layer of tenocytes present 2
capillaries observed, from other sheath  Healing mode weeks post repair & highly developed at 6 weeks (peripherally but a
tissues dominated by adhesions  minimum degree centrally)
Granulation tissue (capillary buds,
fibroblasts) proliferated from
synovial sheath in first several
days into injury site  No
intrinsic evidence of tendon
healing
TENDON REPAIR 3
Procedure

Surgery
TENDON REPAIR 4
Cell Migration
• Early evidence of intrinsic and extrinsic
cellular involvement in tendon healingL
Sheath cells are aggressive migrators and
Demonstrate increased proligraration rate,
collagen lattice contraction between
endotenon and synovial fibroblast =
modulation of formation of adhesions
during healing of injured tendons