The short answer is NO – Bone pressure necrosis is not a concern with the high insertion torque values achieved by osseodensification using the MOD® Burs. In fact, the literature supports that higher insertion torque values and more dense surrounding bone are a combination that enhances primary stability and healing, and minimizes micro-motion of the implant. [02] The term Pressure Osseonecrosis (bone pressure necrosis), although used frequently, has never been clearly defined in the literature other than generally viewed as excessive compression (pressure) of bone created during implant insertion and it is limited to cortical dense bone. [03] The theory is that high insertion torque values for implant placement above 40-45 Ncm may create pressure ischemia and microcirculation disturbances to osteocytes leading to bone resorption. Compression of bone beyond its physiologic limits may result in ischemia leading to osseous necrosis. [04-05] However, no scientific data exists to support these opinions and this phenomenon has never been scientifically proven. On the other hand, both animal histological and human controlled clinical studies have shown that high insertion torque does not induce bone necrosis. Trisi et al, demonstrated that high IT in dense bone does not induce bone necrosis or implant failure. In fact, histologically, high IT increased initial BIC (bone to implant contact) and promoted primary healing and remodeling for weeks 1-6 when compared to low IT placed implants. Implant placed with 110 Ncm showed primary bone healing with no dip at 3 weeks and 40% bone remodeling at 6 weeks. [06] Clinical study by Ottoni et al, has correlated High IT with increased survival rate of single tooth implants under functional loading. He concluded that for every 9.8 Ncm of torque added; the risk of implant failure was reduced by 20%. [07] Khayat et al, concluded that the use of high IT up to 176 Ncm did not prevent or inhibit osseointegration. [08] Perren et al inserted compression plates in the tibia of sheep and observed that pressure at the screw sites of about 40 MPa did not result in pressure necrosis but rather a gradual decrease in pressure due to bone viscoelasticity. [09] Transient ischemia may be an important factor in initiating fracture healing. Ischemia in the rat tibia for 4.5 h was found to cause periosteal proliferation instead of bone death. [10] In Summery, there is a slow gradual decline in bone stress produced at implant insertion. This decline is a result of : 1.    Viscoelastic relaxation of bone. 2.     Normal remodeling by basic multicellular units whereby pre-stressed bone is replaced by new bone through internal remodeling rather than surface resorption. [11-12] Higher insertion torque combined with the enhanced osseodensification of the implant site is highly desired.