Pro-inflammatory cytokines, most notably TNF play a pivotal role in apoptosis, inflammation and tissue damage. However, the function and mechanisms of TNF in OA are inconsistent. For example, some studies have indicated that TNF causes apoptosis by binding to the ‘‘death receptor” TNF-receptor-1 (TNF-R1). This extrinsic apoptotic pathway involves ligand binding to the “death receptor”, followed by transmission of signals to the interior of the cell through Fas-associated death domain protein (FADD) and poly ADP-ribose polymerase (PARP), and finally recruitment of initiator caspases, such as caspase-8, which induce apoptosis. However, other studies have reported that TNF activates anti-apoptotic family proteins, such as bcl-2, without promoting apoptosis. TNF has also been reported to protect against apoptosis, maintaining the renewal of local inflammatory mediators by promoting increased expression of cytokines in chondrocytes. Material gain and linewidth of Quantum Dot ensemble are calculated assuming the Gaussian distribution of the density of states due to the size-deviation of dots. The effect of electric field is incorporated in the analysis through the mean and variance of TNF accelerated driven Death of Mandibular Condyle via interleukin-1β/nerve growth factor signaling.energy states. The results showing the enhancement of optical gain and linewidth with electric field indicate important applications in sub-cellular medical imaging of the mechanical cartilage modulation in the growth plate by sustained ex vivo effected high frequency electric field on quantum imaging enhancement of chondrogenesis in PGLA scaffolds loaded chondrocytes.