IL1B and diabetes mellitus: SASP response reinforces the senescent phenotypes by acting in an autocrine and paracrine manner.7 The majority of SASP is released into tissue and circulation by macrophages.33 These factors triggered the upregulation of primary periodontal tissue destruction mediators in diabetes, even altered oral bacterium.31 The latest literature9 pointed that early SASP response, characterized by the upregulation of IL-1β, is the main feature of cellular senescence.