Haller (1763) injected a clear fluid into the periosteum demonstrating that "the origin of the bone is the artery that transports the blood and in it the mineral elements" advancing the idea that the cardiovascular system was responsible for bone formation. This was supported by earlier work by Hunter (1754) and Pritchard (1946) who studied what triggers osteogenesis: the same stimulus that causes inflammation or mechanical stress. How was the study conducted? Pritchard (1946) suggested that osteogenesis was the result of a nonmechanical humoral stimulus in relation to the cranial vault. Two groups of black- and white-capped Norway rats of the Lister strain were used. Young rats, aged between six and eighteen months, were used due to their rapid and vigorous cellular response. They each had incisions made through the pericranium, skull and dura mater to study bone repair with reduced blood supply to the fracture site. The fracture was created in the cranial vault as cartilage is rare at this site and minimal mechanical factors are involved. By examining rats at different intervals during the repair phase Girigs & Pritchard (1958) were able to support Pritchard's (1948) study that cartilage is produced in a healing fracture due to the reduced blood supply. They found that because the cartilage requires less oxygen, it acts as a temporary bridge between the fracture gap until the blood supply is restored. Thiimidine was used on forty-two five-week-old female rats to conduct an autradiographic study of cellular response in fracture repair. Periosteal index observations were conducted at various intervals between the one-hour and fourteen-day period. The results show that cell proliferation in the periosteum and adjacent soft tissues is the initiation… half of the article… the effect of the lack of lymphocytes on fracture repair. They used eight-week-old male recombination activator gene 1 knockout (RAG -/-) mice to model the absence of lymphocytes and wilt-type mice. Closed unilateral fractures were induced in all rats and the progression of fracture healing was assessed on days three, seven, fourteen, twenty-one and twenty-eight. The results of the experiment show that during fracture healing the biochemical properties, mineralization and remodeling were all improved in RAG-/- mice. Therefore there must be a regulatory role of lymphocytes during fracture repair. It can be assumed that a strong inflammatory response may have evolved to fight pathogens to prevent infection during injury. Anti-inflammatory cytokines present in the absence of lymphocytes increased both mechanical properties and bone formation in a fracture