OC19 DEFICIENCY OF THE SPECIFIC IMMUNE SYSTEM ENHANCES FRACTURE REPAIR IN-VIVO

An estimated 10% of patients have problems with fracture healing. Initial studies have revealed that it is likely that both the innate and specific immune systems play a role in fracture repair, but this has not been attributed to particular components, cells or their products. It is known that the functionality of the immune system is impaired with age and this may account for the higher rate of delayed union in elderly patients. We used a validated mouse model of a reproducible closed tibial fracture. In order to prevent any foreign body inflammatory/immune response no artificial internal fracture fixation was used and instead external support was provided using a Plaster of Paris cast. The role of the specific immune system was studied using an immunodeficient Balb/c SCID (Severe Combined Immuno Deficient) mutant mouse. The SCID mice were matched for age, sex (all males) and weight to the control, wild type Balb/c mice. Mechanical (4 point bending) and radiographic (Radiographs scanned and calculations of callus area, index and density made with image analysis software) measures were used to assess fracture repair at 21 days. Mechanical measurements revealed an enhancement of fracture healing in the SCID mouse strain compared to the control strain, with stress at yield and Young’s modulus higher in SCID mice than controls. (Stress at yield: 4.2 +/− 0.23MPa in Controls, 7.1 =/− 0.6MPa in SCIDs, P We conclude that an abnormality of the immune system due to either lack of the specific immune system (T and B cells) or an enhancement of the innate system results in increased mineralization, stiffness and strength of fracture healing, and that further investigation might result in novel therapies directed toward avoidance of non/delayed-union.