Titanium is considered a biocompatible biomaterial of dental titanium alloys (Ti-6Al-4V). However, patients with certain dental metals (Hg++, Al, Ti, etc.), including dental Ti implants, can provoke a chronic silent inflammatory state.

On the other hand, periodontitis favours the adherence of biofilms on the surface of teeth, increasing the local recruitment of innate immune cells (neutrophils, macrophages, and dendritic cells). Thus, a chornic proinflammaotry cytokine release of cytokine/chemokines, including CX3CL1, can amplify the local inflammatory resposnes and also promote oral disbiosis. In fact, recent studies link Alzheimer's disease (AD) with periodontitis. However, systemic CX3CL1 and MCP-1 elevations can be also detected in patients with long-term dental Ti implants without periodontisis. The periodontisis favours the teeth destruction and also enhances the accumulation of oral biofilm. In fact, porphyromonas gingivalis has been associated with AD, and high systemic CX3CL1 levels have been found to contribute to p-Tau accumulation in the brain of AD transgenic mices.

Thus, this CX3CR1 overexpression as a chronic silent proinflammatory response can predispose patients with periodontal disease and poor bucal higiene to AD. Collectivelly, CX3CR1 overproduction affects the normal control of the inhate inmune system and favours the destruction of the supporting tissues of the teeth in patients with periodontal disease. Thus, the link between AD and periodontitis via CX3CL1 opens up a new therapeutic role of delta chemokine blockers against periodontitis and AD pathology.