Chronic alcohol consumption significantly affects vital organs such as the liver and kidneys, leading to impaired function that disrupts bone metabolism [27]. AP is associated with elevated systemic inflammatory markers, resulting in the destruction of periradicular tissues, including pathological bone resorption.

This systematic review evaluated studies examining the inflammatory response and periapical bone resorption in in vivo animal models, simulating chronic alcohol consumption alongside AP development. Key findings from the seven included studies revealed that animals exposed to both chronic alcohol consumption and AP exhibited heightened levels of inflammatory markers and altered bone structure, characterized by increased resorption and reduced density, compared to controls (AP without alcohol). These effects were dose-dependent, with higher alcohol concentrations (15% or 20% v/v) producing more severe outcomes than lower concentrations (5% or 10% v/v) [26].

Animal studies on light alcohol consumption are scarce. While Yamamoto et al. [28] observed no detrimental effects on liver function with a 5% ethanol consumption, Maurel et al. [29] reported that prolonged moderate alcohol intake (8%–20%) adversely impacted bone remodeling in rats, in contrast to the negligible effects of short-term low-concentration exposure. Dal-Fabbro et al. [26] demonstrated a dose-dependent relationship, where 15% and 20% alcohol concentrations caused marked inflammatory reactions and bone resorption compared to lower doses.

In humans, chronic alcohol consumption is classified as light (1–10 g of ethanol/day), moderate (11–30 g/day), or heavy (> 30 g/day) [30]. Differentiating between these levels is crucial, as such light consumption may enhance bone density, while a heavy intake is linked to secondary osteoporosis and other organ damage [31]. In addition, a binge drinking pattern among adolescents and young adults is an emerging concern. Simulating that pattern in rats with 20% alcohol has been shown to cause damage to the alveolar bone, reducing the ratio of bone-to-tissue volume ratio in the alcohol-exposed group, with further intensification in the alcohol protocol associated with AP [23].

Variations in the effects of different alcoholic beverages on bone metabolism have also been highlighted, likely due to their unique constituents, such as polyphenols in wine or silicon in beer. In addition, factors like age and sex may further influence these effects [22, 32].

Findings from Pinto et al. [20] in which rats were exposed to successive increases in alcohol concentration up to 25%, corroborated earlier results [21]. These studies demonstrated that chronic alcohol consumption led to larger periapical lesions, greater inflammatory infiltrates, and systemic changes that exacerbated bone loss in AP models. The associated mechanisms involved altered cytokine levels, biochemical markers, and metabolites.

To model chronic alcohol intake in rats, alcohol concentrations of at least 20% were considered sufficient [26, 33]. Most studies included in this review employed spontaneous alcohol consumption, a wide accepted method for simulating addiction [34], with some protocols reaching concentrations of up to 25%.

Rats exposed to chronic alcohol consumption exhibited elevated biomarkers of liver damage, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase [25], as well as increased bilirubin levels [20]. Elevated uric acid levels were also noted [20], likely due to alcohol’s purine content impairing renal excretion [35, 36]. Metabolomic analysis revealed reduced serum glycine and phosphocholine levels, further implicating systemic disruptions in bone formation pathways [37].

Bone homeostasis depends on a dynamic balance between osteoblasts, which form bone, and osteoclasts, which resorb it. Chronic inflammation promotes osteoclastogenesis via cytokines such as IL-1β, IL-6, IL-7, and TNF-α which disrupt bone remodeling by increasing RANKL expression and reducing OPG levels. RANKL binds to RANK on osteoclast precursors, stimulating their activation and promoting bone resorption. OPG, acting as a decoy receptor for RANKL, modulates this process, preserving bone integrity [38, 39]. Excessive alcohol intake exacerbates these pathways, as demonstrated by increased RANKL [21, 24] and TRAP expression, reduced OPG levels [26], and elevated inflammatory cytokines [20] in alcohol-consuming groups. These effects correlate with greater periapical bone loss and larger lesion volume, as observed in Dal-Fabbro’s studies [24, 26].

The studies herein included showed the association of alcohol groups to a lower bone density with larger volume and area of periapical lesions [21, 22], as assessed either by micro-CT [20,21,22] or digital radiographic images [25].

Animal studies offer advantages, including enhanced control over the study population and the ability to conduct histological analyses. Despite their limitations, most of the research involving laboratory animals has employed an alcohol-feeding protocol lasting at least 4 to 6 weeks, aiming to replicate the harmful effects associated with chronic alcohol consumption in humans. Thus, it is widely accepted that alcohol administration for a period of 1 month or longer can be classified as chronic exposure [40]. Moreover, in the selected studies, the lack of significant variation in rat strains, weights, or ages helps to minimize potential bias associated with these factors.

The impact of alcohol consumption on oral health has long been recognized, with particular emphasis on its role in the development of oral cancer. Maserejian et al. [41] demonstrated that alcohol intake, regardless of beverage type or drinking pattern, is associated with an increased risk of oral premalignant lesions, reinforcing the recommendation to reduce alcohol consumption for oral cancer prevention. Beyond oncological concerns, alcohol consumption has also been linked to oral trauma, halitosis, periodontal disease, and caries. Grocock [42] highlighted the importance of assessing alcohol use in dental settings, recommending that dental professionals incorporate alcohol risk assessment and reduction advice into routine care. The authors emphasized that taking a thorough alcohol history from all patients and using dental visits as opportunities to deliver preventive messages could contribute significantly to public health. Despite this, barriers to implementing such strategies in practice remain, and further efforts are needed to promote alcohol prevention advice, including enhanced education, training, and structural support.

In this context, our findings provide additional evidence of the clinical relevance of alcohol consumption in dentistry. Chronic alcohol exposure also appears to exacerbate the inflammatory response associated with AP, potentially resulting in more severe or persistent periapical lesions and decreasing the predictability of endodontic treatment outcomes. Clinically, this highlights the importance of considering alcohol intake during diagnosis and treatment planning, including a thorough medical and social history and clear communication with patients regarding prognosis and tailored management strategies.

Although the seven included studies presented a moderate risk of bias, an important limitation is that most of them were conducted by only two research groups. This may limit the generalizability of the findings. On the other hand, the use of samples collected from the same animals across studies may reduce variability related to animal, caging, and experimental conditions, thereby minimizing certain sources of bias. Another limitation is that it remains uncertain whether similar findings would be observed if the AP was previously established, or which pattern of ethanol exposure poses the greatest harm. In addition, questions persist regarding the impact of ethanol consumption, combined with individual characteristics, on the progression of periapical lesions.

sTo strengthen the evidence base and enhance the clinical relevance of future findings, we highlight the need for well-designed studies using standardized methodologies and conducted across multiple research centers. Such approaches would improve the transparency, reproducibility, and applicability of results to clinical practice. In this context, systematic reviews play a crucial role in summarizing scientific evidence, identifying the limitations and biases of included studies, and avoiding unnecessary duplication of research. They also provide a solid foundation for developing well-designed studies with standardized methodologies. To better understand the relationship between alcohol consumption and AP, further research is essential.