Apical periodontitis (AP) represents chronic inflammatory reaction of periradicular tissues of teeth with necrotic pulp. Although AP has been considered as a multifactorial disease, different microorganisms and their virulence factors from infected root canals are considered to be the primary cause of periradicular inflammatory process. The interplay between microbes and host leads to an inflammatory cascade of events that includes activation of innate and adaptive components of immunity. Activation of different immune cells in AP is intermediated by different molecules known as mediators of inflammation. These molecules establish various network interrelationships in the inflamed periapical area and induce alveolar bone resorption. This narrative review aimed to explore and present the current knowledge of selected inflammatory mediators, including cytokines, matrix metalloproteinases, bone resorption regulators and components of oxidative stress involved in the alveolar bone resorption in AP.