The Quebec Task Force defined whiplash as “an acceleration–deceleration mechanism of energy transfer to the neck”. It is logical that the lower the velocity change following impact, the lower the risk of injury. The accepted velocity change (delta-v) for whiplash injuries following rear impact has been quoted as 5 mph. There is some debate as whether this is valid in the clinical setting. We aimed to investigate this further.

A series of low speed controlled crash simulations were undertaken. There were a total of 27 runs on 23 individuals. Accelerometers were placed on the head and chest of the volunteers. Video recordings were analysed to assess relative displacement of the head and chest. The presence of symptoms was documented over a period of 7 days. The volunteers consisted of 23 males and 1 female with an average age of 38 (range 20–56). The average delta-v achieved was 2.3 mph (range 1.8–3.1 mph). The average maximum accelerations recorded were 3.46g at the chest and 2.93g at the head. The average difference was 0.53g. There was no significant displacement between the head and body. No symptoms were reported beyond 1 hour.

Whiplash is triggered if the disparity between movements of the head and neck is of sufficient magnitude. It seems logical that there is a threshold below which whiplash will not occur. Our results have shown that below a delta-v of 3 mph there is little difference in the magnitude and timing of the movements of the head and chest.

Therefore the whiplash mechanism of injury does not occur at these changes of velocity.

Osteomyelitis commonly causes bone destruction and is most frequently due to infection by Staphylococcus aureus. S. aureus is known to secrete a number of surface-associated proteins which are extremely potent stimulators of bone resorption in the mouse calvarial assay system. The precise cellular and humoral mechanisms whereby this stimulatory effect is mediated, in particular whether osteoclast formation or activity is directly promoted by these factors, have not been determined by this study. Surface-associated material (SAM)(0.001ug/ml)obtained from 24 hour cultures of S. aureus was added to cultures of mouse and human osteoclast precursors (RAW 264.7 cells and human peripheral blood mononuclear cells respectively). These cultures were incubated in the presence and absence of receptor activator of nuclear factor kappa B ligand (RANKL) and macrophage colony stimulating factor (M-CSF). It was found that independent of RANKL, SAM was capable of inducing osteoclast formation in cultures of RAW cells and human monocytes. This was evidenced by the generation of tartrate-resistant acid phosphatase-positive multinucleated cells, which formed lacunar resorption pits when these cells were cultured on dentine slices. In cultures where M-CSF, RANKL and SAM were added, osteoclast formation was increased, but did not exceed the osteoclast formation in cultures with M-CSF and RANKL. These findings indicate that S. aureus produces a soluble factor which can promote osteoclast formation. Identification of this factor may help to develop therapeutic strategies for treating bone destruction due to Staphylococcal osteomyelitis.