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Utilizing a variety of animal models of TMJ OA caused by unilateral anterior crossbite (UAC), occlusion disorder (OD), monosodium iodoacetate (MIA), and IL-1β, the study shows that ferroptosis, which is typified by elevated p53 and ACSL4 and decreased GPX4, is a major contributor to TMJ OA

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[56] demonstrated that mice injected with MPTP but also receiving β-HB exhibited a smaller reduction in substantia nigra neurons, indicating that β-HB can attenuate the neurotoxic effects of MPTP on dopaminergic cell bodies