Obesity induced compressive stress on weight bearing joints is associated with osteoarthritis (OA) progression. However, the precise impact of obesity on the microarchitecture and pathology of subchondral bone remains unclear. We hypothesized that obesity increased bone remodeling of subchondral bone has resulted in accelerating the pathology of knee OA. We first investigate the relationship between body mass index (BMI) and age of OA patients. We collected total of 616,495 cases of OA with total knee replacement (TKR) from Australia Orthopaedic Association National Joint Replacement Registry (AOANJRR) and British Orthopedic Association National Joint Registry (NJR). Our result showed that obese patients with BMI higher 30 have TKR 7 years earlier than those with BMI less than 25. The mean age of patients with BMI greater than 30 for TKR is 67.23+9.17 as compared to 73.07+8.41 in those BMI less than 25. To examine if the compressive stress caused by increased BMI has an impact on the subchondral bone (STB) of OA, we next examined total of 125 cases of tibia plateaus from patients with OA with micro CT and histomorphometry. The result showed that higher bone formation in STB was detected in the obese patients as compared to patients with normal-weight. Statistically significant differences were seen between obese group and normal-weight group for the following parameters: OV/TV (0.0090±0.0148vs0.0017±0.0342, P=0.04), OS/BS (0.0791±0.1114vs0.0178±0.0301, P=0.023), OS/BV (0.9390±1.1950vs0.2714±0.5336, P=0.027), OS/ES (6.1345±7.1964vs1.0454±1.4486, P=0.003). However, no significant difference in bone remodeling was seen in the STB of medial compartment between two groups. There were no significance differences in microstructural changes in STB and subchondral bone plate between two groups. In conclusion, we showed that obesity predicted a younger age of TKR in OA patients. Induction of bone formation in STB and compromised joint structure may be the cause of early total knee replacement in patients with obesity.