## 1 Introduction  
Aluminum (Al) is the most abundant metal in the Earth's crust, naturally occurring as Al\({}^{3+}\) in various compounds, such as silicates, oxides, and hydroxides. Despite its ubiquity, Al has no known physiological role in human metabolism and can be toxic at high levels. The potential negative effects of Al on human health have been studied extensively. Notably, [PERSON] et al. [1] and [PERSON] et al. [2] provided comprehensive reviews on the systemic toxicity of Al, highlighting its impact through various exposure routes, including environmental contamination and occupational hazards. Al contamination arises from both natural processes, such as the weathering of rocks, and anthropogenic activities, including mining, recycling, and manufacturing. High exposure levels are particularly concerning in industrial areas where Al is processed, leading to potential health risks for both humans and animals. Despite its widespread presence, Al ions can accumulate in the body, leading to conditions such as encephalopathy, especially in individuals with compromised renal function. Al toxicosis has been linked to numerous health issues, including reproductive toxicity, pulmonary lesions, bone abnormalities, immunotoxicity, and neurological disorders. Chronic exposure can lead to significant tissue accumulation, exacerbating these conditions. The primary sources of Al exposure include air, drinking water, food, pharmaceuticals, and agrochemicals [1]. However, the potential impact of Al particles from biomedical devices, particularly dental implants, remains underexplored. In the context of implantable devices, the concentration of aluminum particles and the rate of metabolism are critical factors influencing cytotoxicity. A critical threshold of aluminum concentration in tissues has not been defined, though it has been estimated that the level in healthy human bone tissue ranges from 5 to 10 mg/kg [1]. Higher concentrations of aluminum particles can lead to increased oxidative stress and inflammation around the implant site, potentially compromising the success of the implant. The metabolic rate of surrounding tissues, particularly in areas with high bone turnover, may exacerbate these effects, leading to greater cytotoxicity and potential implant failure. Safe concentrations of aluminum particles must be carefully controlled in dental materials to minimize adverse effects, ensuring biocompatibility and long-term stability of the implant. Dental implants, first introduced by [PERSON] in the late 1960s, initially featured machined surfaces [3]. The milling, turning, or polishing processes used to manufacture these surfaces frequently led to lengthy healing periods and significant failure rates, especially in regions with low bone density, such as the posterior maxilla. Subsequent research indicated that moderate surface roughness could enhance osseointegration [4; 5; 6; 7], leading to the development of techniques such as sandblasting and acid-etching (SAE). SAE involves blasting the implant surface with ceramic particles (e.g., Al\({}_{2}\)O\({}_{3}\)) to create micro-craters, followed by acid treatment to remove residual particles and further modify the surface [8]. It is difficult to completely remove blasting particles despite these efforts, which raises questions regarding the possibility of residual Al remaining on the implant surface. It has been widely demonstrated that with the use of a blasting material, such as Al\({}_{2}\)O\({}_{3}\), a potential risk of contamination by remnants of blasting particles with dissolution of aluminum ions into the host tissue cannot be excluded [9; 10]. It has also been reported that Al ions may inhibit normal differentiation of bone marrow stromal cells and normal bone deposition and mineralization [11; 12], and aluminum has been shown to induce net calcium efflux from cultured bone [13]. Moreover, aluminum may compete with calcium during the healing of the implant bed.