Pain and disability following wrist trauma are highly prevalent, however the mechanisms underlying painare highly unknown. Recent studies in the knee have demonstrated that altered joint contact may induce changes to the subchondral bone density and associated pain following trauma, due to the vascularity of the subchondral bone. In order to examine these changes, a depth-specific imaging technique using quantitative computed tomography (QCT) has been used. We've demonstrated the utility of QCT in measuring vBMD according to static jointcontact and found differences invBMD between healthy and previously injured wrists. However, analyzing a static joint in a neutral position is not necessarily indicative of higher or lower vBMD. Therefore, the purposeof this study is to explore the relationship between subchondral vBMDand kinematic joint contact using the same imaging technique. To demonstrate the relationship between kinematic joint contact and subchondral vBMDusing QCT, we analyzed the wrists of n = 10 participants (n = 5 healthy and n = 5 with previous wrist trauma). Participantsunderwent 4DCT scans while performing flexion to extension to estimate radiocarpal (specifically the radiolunate (RL) and radioscaphoid (RS)) joint contact area (JCa) between the articulating surfaces. The participantsalso underwent a static CT scan accompanied by a calibration phantom with known material densities that was used to estimate subchondral vBMDof the distal radius. Joint contact is measured by calculatinginter-bone distances (mm2) using a previously validated algorithm. Subchondral vBMD is presented using mean vBMD (mg/K2HPO4) at three normalized depths from the subchondral surface (0 to 2.5, 2.5 to 5 and 5 to 7.5 mm) of the distal radius. The participants in the healthy cohort demonstrated a larger JCa in the RS joint during both extension and flexion, while the trauma cohort demonstrated a larger JCa in the RL during extension and flexion. With regards to vBMD, the healthy cohort demonstrated a higher vBMD for all three normalized depths from the subchondral surface when compared to the trauma cohort. Results from our preliminary analysis demonstrate that in the RL joint specifically, a larger JCa throughout flexion and extension was associated with an overall lower vBMD across all three normalized layers. Potential reasoning behind this association could be that following wrist trauma, altered joint contact mechanics due to pathological changes (for example, musculoskeletal trauma), has led to overloading in the RL region. The overloading on this specific region may have led to a decrease in the underlying vBMD when compared to a healthy wrist. However, we are unable to conclude if this is a momentary decrease in vBMD that could be associated with the acute healing phase following trauma given that our analysis is cross-sectional. Therefore, future work should aim to analyze kinematic JCa and vBMD longitudinally to better understand how changes in kinematic JCa over time, and how the healing process following wrist trauma, impacts the underlying subchondral bone in the acute and longitudinal phases of recovery