Periodontal disease is considered one of the main pathologic diseases occurring in humans. Its pathologic process involves inflammatory reactions producing periodontal bone resorption and the tooth loss. But some patients do not present an evident clinical inflammation with bone resorption, and in others, the inflammation is prominent without bone resorption. A key question could be to investigate a different way of responding to aggression. Inflammation requires a complex intracellular metabolic process, starting with the harmful recognition and activation of the inflammasome, continues the energy supply with the alteration of oxidative stress conditions, and finishes with the elimination of the aggression with autophagy/apoptosis mechanisms, then concludes with recovery. Peroxisome proliferator-activated receptors (PPARs) are essential molecules produced in inflammation, and its genes and its activation have been related to periodontal disease. Also, an important aspect is the influence of PPARs in bone metabolism; the main periodontitis symptom is bone loss and PPARγ activation that can downregulate the bone resorption in experimental periodontitis, PPARγ-coated titanium dental implant surfaces could carry the antiinflammatory gene and restrain inflammation. PPARs could be one of the meeting background points with atherosclerosis/cardiovascular disease, diabetes and metabolic syndrome showing a modified proinflammatory statement such as it is described in periodontitis.
Keywords: atherosclerosis; autophagy; diabetes; inflammasome; metabolic syndrome; mitochondria; periodontitis.