OTA Paper 1998

Wheeless' Textbook of Orthopaedics Menu items include:- - stages of bone healing - radiographic determinants of healing - Age - negative influences on bone healing - Induction of Bone Healing

Orthoteers

Flinders South Australian Orthopaedic Resitrars' Notebook Fracture Healing Unique in that there is reconstruction of the original tissue rather than healing with scar formation as in other tissues. McKibbin B JBJS (1978) (from Cardiff Royal Infermary) Stages of Fracture Healing: Inflammatory Stage: Fracture ® soft tissue injury and ruptured vessels Formation of Fracture haematoma Osteocytes deprived of nutrition at the fracture ends die and play a passive role in the repair process Presence of necrotic material ® inflammatory response Increased cell division evident within the first 8 hours reaching a maximum in some 24 hours Activity first seen in the periosteum and extends along the entire bone to be localised at the fracture site in a few days Acute Inflammation subsides ® repair phase Repair Stage: Organisation of haematoma occurs ® primary callus formation Micro environment is acidic (moves towards neutrality during repair and becomes alkaline) Electro negativity is also found in the region of a fresh fracture Pluripotential mesenchymal cells ® fracture site (cells from cambian layer periosteum, endosteal cells, ? endothelial cells ? monocytes) Capillary buds grow into the fracture site Callus is formed made up of fibrous tissue, cartilage and immature fibre bone Cartilage forms particularly in the periphery of the callus in regions of low O2 tension Increased movement ® increased cartilage formation Cartilage is resorbed as enchondral bone formation occurs Osteoclastic resorption of dead bone occurs Gradual increase in concentration of collagen and hydroxyappatite ® mineralisation of the matrix as woven bone Remodelling phase begins Remodelling Stage: Once the fracture has been bridged ® functional modification which continues for a prolonged period (years) Resorption of poorly placed trabeculae and new bone struts are deposited corresponding to lines of force Cancellous bone ®resorption and replacement takes place on the surface of trabeculae (creeping substitution Cortical bone ® osteoclasts ream out a tunnel followed by vessels bringing osteoblasts ® lay down lamellar bone to form the new osteon (cutter head) Process thought to be mediated through electrical variation in zones of tension and compression Electopositivity (associated with osteoclastic activity) occurring on a convex surface and negativity (associated with osteoblastic activity) on a concave surface Source of osteogenic tissue: Osteoprogeniter cells. Cells with a predetermined commitment to bone formation and occur in close association to bone surfaces or the marrow. OR Metaplasia of previously uncommitted fibroblasts which develop the power of osteogenesis given appropriate environmental stimulus. Cells arise from surrounding soft tissue. Osteogenic induction. This theory is supported by the formation of bone by non specialised cells in extra skeletal sites Control of Fracture Healing: Bridging by external, medullary or 1o callus 1. External callus: Dependent on the existence of another fracture fragment (ie no response from an amputation stump) Continuity of periosteum ® bridging callus ® induction, if no contact is made within a certain time ® primary callus response Mechanical and humeral influences as attempts to bridge the fracture are not continued indefinitely 2. Medullary callus Cartilage formation is less prominent in medullary callus Controlled by similar process and in displaced fractures may unite with the external callus Develops independently of rigid fixation 3. 1o Bone healing: May only be possible where there is rigid fixation, evacuation of fracture haematoma and intimate contact of one bone end with the other Equates with the process of normal bone turnover Direct bone union occurs when rigid fixation prevents formation of fracture callus. Osteoclasts resorb the dead bone of the fracture ends and osteoblasts form new bone directly across the fracture. The fracture depends on the plate or means of fixation for stability for some time. Indirect bone union occurs in the absence of rigid fixation through callus formation. Factors affecting fracture healing: Soft tissue injury and local blood supply Radiation, chemical or thermal burns Infection, anaemia or hypoxia Excessive compression ( more than 30lbs) inhibits enchondral ossification but cyclic compression is beneficial Intermittent shear stresses promotes cartilage formation High shear stresses promotes fibrous tissue formation Corticosteroids inhibit osteoblast differentiation ® slow healing Growth hormone increases fracture healing (only if deficient) Denervation retards fracture healing Exercise increases fracture healing Head injury promotes fracture healing by a humoral mechanism Vitamin C is required for normal collagen matrix formation Union: Incomplete repair, the bone moves as one but clinically is still a little tender and attempted angulation is painful. The fracture is clearly visible on X-Ray with fluffy callus. Not safe to be unprotected. Consolidation: Complete repair, calcified callus is ossified and attempted angulation is painless. Repair is complete and further protection is unnecessary. Delayed union: A fracture that has not united in what is considered a reasonable amount of time for a fracture of that type in that location. Non-union: A fracture that will not unite without surgical intervention. A Non union is usually non tender. Incidence of non union said to be 5% in all long bone fractures Malunion: Consolidation of a fracture in a deformed position. Cell induction: Influence a certain cell, tissue or substance may have on another cell such that the second cell or descendants of that cell exhibit physiological processes that the original cell did not. Perkins timetable For normal fracture healing: (Pioneered delayed splintage) A spiral fracture in the upper limb unites in 3/52 double it for consolidation double it again for the lower limb double it again for a transverse fracture Blood supply of bone; Nutrient artery ® medullary arteries supplies the marrow and inner 2/3 of diaphysial cortex. In areas away from muscle or facial attachments ® supply full thickness of cortex Multiple metaphyseal arteries which anastomose with terminal branches of the medullary arteries at the junction of metaphysis and diaphysis Multiple periosteal arterioles supply the outer 1/3 of the cortex Periosteal vessels alone are sufficient to support normal fracture repair All veins drain to the periosteal surface Increased blood flow secondary to a fracture peaks at 2/52 at six times the normal base line ® 3.5 times the normal baseline at 3/52 which persists until 8-10/52 and returns to normal at about 12/52. Extra osseous blood supply to external callus develops rapidly after a fracture and perhaps replaces the damaged medullary supply, Indications for ORIF of fractures: Absolute: Unable to obtain an adequate reduction Displaced intra-articular fractures Certain types of displaced epiphyseal fractures Major avulsion fractures where there is loss of function of a joint or muscle group Non-unions Re- implantations of limbs or extremities Relative: Delayed unions Multiple fractures to assist in care and general management Unable to maintain a reduction Pathological fractures To assist in nursing care To reduce morbidity due to prolonged immobilisation For fractures in which closed methods are known to be ineffective Questionable: Fractures accompanying nerve of vessel injury Open fractures Cosmetic considerations Economic considerations Traction: Fixed traction Pull is exerted against a fixed point Balanced traction Pull against the weight of the body Combined traction Traction fixed to the splint and the splint is suspended against the weight of the body Skin traction (Buck's) can pull no more than 4 or 5 kg

Principles of Bone Healing from Neurosurgical Focus Iain H. Kalfas, M.D., F.A.C.S. Department of Neurosurgery, Section of Spinal Surgery, Cleveland Clinic Foundation, Cleveland, Ohio Abstract Our contemporary understanding of bone healing has evolved due to knowledge gleaned from a continuous interaction between basic laboratory investigations and clinical observations following procedures to augment healing of fractures, osseous defects, and unstable joints. The stages of bone healing parallel the early stages of bone development. The bone healing process is greatly influenced by a variety of systemic and local factors. A thorough understanding of the basic science of bone healing as well as the many factors that can affect it is critical to the management of a variety of musculoskeletal disorders. In particular, the evolving management of spinal disorders can greatly benefit from the advancement of our understanding of the principles of bone healing.

OTA paper 1998

OTA paper 1998