## 1 Introduction  
Impacted teeth are often encountered during the diagnosis and treatment of malocclusions in adolescent orthodontic patients [1]. Impaction occurs when a tooth does not erupt into its designated position in the dental arch within the expected developmental period. The upper canine is one of the teeth that mostly undergoes impaction, preceded only by third molars, with a prevalence range from 0.8% to 5.2% depending on the population examined. Canine impaction is more frequent on the palatal than labial side; it is twice as common in female than in male patients and it has a clear tendency toward being unilateral rather than bilateral [2, 3]. The etiology of maxillary canine impaction is multifactorial: as reported by [PERSON] and [PERSON] [4] in their review, different reasons concur to upper canine impaction such as local obstruction (e.g., odontoma, deciduous teeth, supernumerary teeth, etc. ), local pathology (e.g., cysts, granuloma, etc. ), the disturbance of normal development, malshaped or missing lateral incisors, crowded or delayed eruptive pathways, known as guidance theory, genetic factors, known as genetic theory, and environmental alterations. Several authors independently reported a higher prevalence of palatal displacement of maxillary canines in cases where lateral incisors were congenitally absent. They hypothesized that the absence of the lateral incisor disrupts the normal eruptive guidance pathway of the canine, thereby facilitating its palatal migration. However, these conclusions were primarily derived from clinical observations rather than from systematic investigations involving large, well-defined cohorts and appropriately matched control groups [5]. Supporting these initial impressions, a subsequent study conducted on a large sample of individuals with palatally displaced canines found that only about half of the subjects exhibited normally developed lateral incisors. The remaining half presented with lateral incisor anomalies, including agenesis, peg-shaped morphology, or microdontia. These findings are consistent with the earlier clinical observations and further suggest a strong association between lateral incisor abnormalities and the palatal displacement of maxillary canines [6]. In accordance with the guidance theory and based on the previously discussed evidence, if the lateral incisor is absent, delayed in development, peg-shaped, or significantly undersized with only the initial stage of root formation, the canine will lack the proper guidance to follow its normal eruptive path. Consequently, the canine may deviate downward along a more palatal trajectory within the alveolar ridge, converging apically toward the medial aspect of the alveolar process. In this scenario, the periosteum in this region may serve as a secondary guide, promoting further eruption of the canine over the following one to two years. In cases where the lateral incisor is completely absent, the canine may undergo a self-correcting eruption along the natural curvature of the dental arch around the ages of 11-12 years. However, when a late-developing, aberrant lateral incisor is present and has already erupted, this self-correction mechanism is no longer available. Instead, the malformed incisor may act as a physical barrier, impeding the eruption of the canine by obstructing its path on the palatal side [4]. The hypothesis that canine impaction is predominantly governed by genetic factors remains contentious and lacks widespread acceptance. If impaction were chiefly under genetic control, a symmetrical pattern of expression would be expected, resulting in a higher prevalence of bilateral impactions. Unilateral presentations would be anticipated only in a minority of cases, potentially attributable to differential gene expression or incomplete penetrance. Nonetheless, epidemiological data from a wide range of orthodontic studies consistently reveal a predominance of unilateral canine impaction, reported in approximately 60% to 75% of cases.