###### Abstract  
The failed dental implant associated with maxillary sinusitis is a multifactorial phenomenon and should be investigated thoroughly. The inflammatory process induced by accumulated biofilm and wear debris may increase mucous secretion and mucous thickening, which finally may lead to severe complications such as maxillary sinusitis. The inflammatory cytokines might compromise the long-term osseointegration of the related implant. In this study, implants retrieved from three patients who experienced implant failure relating to maxillary sinusitis were investigated using scanning electron microscopy (SEM) and energy-dispersive X-ray spectroscopy. SEM analysis of the implant apical region revealed a less-compact bone structure, indicating the high bone turnover due to an inflammatory process. The ratio of calcium (Ca) and phosphorus (P) was negligible in all specimens. Detection of fluorine (F), sodium (Na), silicon (Si), gold (Au), aluminum (Al), and magnesium (Mg) confirmed the contamination. The selected cases presented different biological aspects that might play the central role in the failed dental implants associated with maxillary sinusitis: the contamination of potentially toxic elements, microorganism infection, and long perforation of implant apex into the sinus. Each of the above phenomena needs to be confirmed with further clinical study with a larger number of failed implants and accompanying tissue samples. dental implant; maxillary sinusitis; maxillary sinus floor augmentation; scanning electron microscopy (SEM); energy dispersive X-ray spectroscopy (EDS) 25 March 2021 16 April 2021 1  
with the lateral window technique varied between 61.7% and 100%, with an average survival rate of 91.8% [4]. However, during the implantation process in the maxillary posterior region, with or without the sinus lifting procedure, several complications may develop. Perforation of the Schneiderian sinus membrane during the implant installation tends to heal spontaneously [5; 6]; however, cases of odontogenic maxillary sinusitis (OMS) due to implant penetration into the maxillary sinus have been reported [7]. The incidence of OMS after maxillary sinus lifting is 0% to 20% [7; 8; 9]. The etiology of implant failure related to OMS has been rarely reported in the literature. In a previous study, [PERSON] et al. [10] reported that titanium (Ti) particles can activate the macrophages to interleukin 1 beta (IL-18). In orthopedic research, aseptic loosening of an orthopedic Ti implant is a well-established complication. A complex process of inflammation and osteolysis is supposed to be the pathogenesis of the implant-associated osteolytic phenomenon, which is dependent on innate and adaptive immune reactions [11]. Wear debris and particle phagocytosis by macrophages, fibroblasts, and osteoblasts represent a key role in the innate immune response, which provokes the elevation in the level of proinflammatory cytokines [for example, IL-18, interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-\(\alpha\)), and prostaglandin E2 (PGE2)] [11]. In addition to the phagocytosis of wear debris, the interaction between the particle and cell surface is believed to be a component of this biological response [12]. These inflammatory cytokines stimulate osteolysis by their regulation on osteoclasts and their monocytic precursors. The receptor activator of NF-kB (RANK)/the receptor activator of nuclear factor (NF)-kB-ligand (RANKL) is the central signaling pathway for the activation of osteoclasts that regulates the osteolytic process [13]. Unlike an orthopedic implant, a dental implant is exposed to a complex oral cavity environment with species-rich heterogeneous microorganisms and chemical compositions. The extraosseous surface of the implants and abutments will develop a biofilm within the oral cavity environment, which will trigger infection and cause inflammatory destruction of peri-implant tissue [14].