## 1 Introduction  
This study aims to investigate the prevalence and anatomical variations of Atlas Posterior Arch Deficiency (APAD) using CBCT imaging. The objective is to enhance the understanding of this rare anatomical variant and to provide insights into its implications for both clinical practice and future research. Atlas Posterior Arch Deficiency (APAD) is a congenital anomaly characterized by the partial or complete absence of the posterior arch of the atlas vertebra (C1), the first cervical vertebra of the spine [1]. This condition results from a failure of the posterior ossification centers to fuse during embryonic development, leading to a structural defect in the atlas. Consequently, the posterior arch, which normally forms a protective ring around the spinal cord and vertebral arteries, may be deficient, predisposing the individual to cervical spine instability and potential neurological compromise [1, 2, 3]. The cervical region contains several vital structures, including the cervical vertebrae, muscles, blood vessels, nerves, and various glands. Each cervical vertebra is numbered C1 through C7, with C1 being the first cervical verteb, also known as the atlas [1; 3]. The term \"atlas\" is derived from Greek mythology, reflecting its function in supporting the weight of the head, akin to the mythical role of Atlas. The ring-like structure of the atlas (C1) is unique among the cervical vertebrae as it lacks a vertebral body and spinous process. Instead, it consists of anterior and posterior arches and two lateral masses. In contrast, the other cervical vertebrae (C2-C7) have a more typical vertebral structure with a vertebral body, spinous process, and transverse processes. C1 supports the weight of the skull and allows for the nodding or \"yes\" motion of the head, articulating with the occipital condyles of the skull to form the atlanto-occipital joint [1; 3; 4]. The articulation of the atlas is unique and plays a crucial role in supporting the weight of the head and facilitating its movement. Dysfunction or injury to these articulations can lead to a range of clinical conditions and symptoms, emphasizing their importance in maintaining overall spinal health and function [2; 3]. During embryonic development, the vertebrae form from segments of mesodermal tissue called somites. The atlas specifically arises from the first occipital sclerotome, a specialized region of the mesoderm located at the base of the skull. The mesenchymal cells within the first occipital sclerotome undergo chondrification, differentiating into cartilage. ossification, the process of bone formation, begins around the seventh week of gestation. The atlas ossifies from multiple centers, including separate centers for the anterior and posterior arches, as well as for the lateral masses [3; 4; 5]. These ossification centers gradually fuse during childhood and adolescence to form the mature atlas. All synchondroses of the C1 fuse slightly earlier in females, as reported by [PERSON] et al. (2022) [5]. The etiology of APAD involves disturbances in embryonic development during the formation of the atlas. Various hypotheses have been proposed, including that disruptions in chondrogenesis, vascular insufficiency, or genetic factors influence skeletal development. The exact pathogenesis remains incompletely understood, and further research is needed to elucidate the underlying mechanisms contributing to APAD [3; 4; 5]. APAD is frequently asymptomatic and may remain undiagnosed unless discovered incidentally on imaging studies. Symptomatic cases may present with a range of clinical manifestations, including neck pain, stiffness, headaches, or neurologic symptoms such as sensory disturbances, motor weakness, or gait abnormalities. Symptomatic presentation may occur secondary to associated conditions such as spinal cord compression, instability, or traumatic injuries [1; 2; 4; 6]. The precise incidence of APAD is not well established, as it is often asymptomatic and underreported.