## 1 Introduction  
Facial asymmetry is defined as the presence of a clinically significant variation in the size, shape and position of bilateral structures on opposite sides of the mid-sagittal plane (MSP) of the craniofacial complex [1]. Facial asymmetry, in particular mandibular asymmetry, has been related to morphological and functional changes in the temporomandibular joint (TMJ) [2], especially dimensional [1], volume [3] and condylar position asymmetry [3; 4] but also with the position and morphology of the mandibular fossa [5], unilateral disc displacement [6; 7] and joint hypermobility [8; 9]. In the same way, condylar growth alterations, such as condylar hyperplasia, which is characterized by an increased metabolic activity of one of the two condyles, can lead to asymmetrical mandibular development and therefore to facial asymmetry [10; 11; 12]. Unilateral condylar hyperplasia most frequently occurs in patients aged between 11 and 30 years, mainly affecting females [13], without a predominance for the left or the right side. Despite being described many years ago, the etiopathogenesis still remains unclear; in the literature, various theories have been suggested, which include, trauma, hormonal imbalance, infection, arthrosis, vascular disorders and a genetic role [14]. Common features include enlargement of the mandibular condyle and condylar neck and excessive growth of the mandibular body [15]. Additionally, condylar hyperplasia has been described as self-limiting, meaning that its progression can occur at any time [16]. Moreover, it can be active, which means it is characterized by un ongoing growth, or unactive, in which growth has stopped [17]. One of the most challenging features of unilateral condylar hyperplasia is identifying whether the abnormal growth of the condyle is still active [18]. In fact, therapeutic options for patients with active condylar hyperplasia are different from the ones that can be applied to patients with asymmetrical mandible but without active condylar growth [19]. The diagnosis is based on a combination of anamnesis, clinical exam, 2D and 3D radiographic images and bone scintigraphy. Bone scintigraphy represents an effective tool to identify if condylar growth is active or not with a pooled sensitivity of 0.71 (95% CI: 0.57-0.82) [18]. In the last years, single-photon emission computed tomography (SPECT) has been performed since it was defined to be more accurate and reliable compared to bone planar scintigraphy to evaluate condylar growth with a pooled sensitivity value of 0.90 (95% CI: 0.79-0.97) and a pooled specificity value of 0.95 (95% CI: 0.82-0.99) [18]. SPECT uses a radionuclide, technetium-99m (99 mTc), to quantify its absorption within the bones [18]. In suspected condylar hyperplasia, the absorption of the radionuclide in the hyperplastic condyle is compared with the contralateral one; differences of more than 10% in absorption are interpreted as active condylar growth [20]. Although SPECT can identify condylar growth, its specificity can be questioned [21]. Indeed, it is difficult to determine what changed bone metabolism. For example, bone healing, inflammatory responses, tumors and metabolic diseases such as hyperparathyroidism can all lead to an augmented bone turnover [22; 23]. The range of SPECT's sensitivity and specificity described in the literature is very wide [18; 21], so it is necessary to perform other additional exams for the diagnosis of condylar hyperplasia. Different characteristics of the hyperplastic condyles of asymmetric patients with abnormal SPECT were identified by means of micro-CT scans, particularly a higher cortical porosity, a higher bone volume fraction, a considerably higher trabecular thickness and separation, a higher number of trabeculae and a lower degree of mineralization compared to the architecture of mandibular condyles not affected by active condylar hyperplasia [20].