## 1 Introduction  
The incidence of cancer is increasing year by year. There is a need in the scientific community for early detection methods because by the time a clinical diagnosis is made, for the majority of patients, it is in a late stage, and thus the mortality rate is high. Research on markers related to prognosis of tumours is also increasing [1; 2; 3]. Human Dickkopf-related protein 1 (Dkk-1), composed of 266 amino acids, has a predicted molecular weight of 25.8 kDa, being a secretory protein from the _Dickkopf_ gene family that comprises five evolutionarily conservative members [4]. Dkk-1 is a secretory antagonist of the classical Wnt signalling pathway. Dkk-1 was found to be abnormally expressed in tumour cells, inhibit cell proliferation and induce apoptosis through proapoptotic factors [5]. However, due to the differences in the tumour environment and the complex regulatory mechanisms in different tumours, Dkk-1 expresses differently in various types of tumours, such as lung, gastric, colorectal, pancreatic, bladder urothelial, breast, ovarian and cervical cancer, multiple myeloma, hepatocellular, oesophageal and oral squamous cell carcinoma [3; 6; 7; 8]. Most of the reported studies point out that Dkk-1 plays a complex and different role in tumour occurrence, development and metastasis stimulation of various types of cancers or it is related to the late stage, all through a variety of complex regulatory mechanisms. More and more evidence has shown that Dkk-1 may not only be a useful biomarker of metastasis, but also a biological marker with the potential to evaluate tumour diagnosis and prognosis [6]. In oral-cavity-related diseases and conditions, Dkk-1 suppresses osteoblast differentiation but increases the expression of the osteoclast differentiation factor receptor activator of nuclear factor kappa B ligand (RANKL) and decreases the expression of osteoprotegerin (OPG), which induces osteoclastogenesis [9; 10; 11]. Dkk-1 is a key regulator of bone remodelling in physiological and pathological conditions, and blocking this factor may stimulate osteoblastgenesis and inhibit osteoclastogenesis [12; 13; 14]. Dkk-1 upregulation is associated with alveolar bone loss in humans with periodontal disease [15], but its inhibition is also related to the TNF-\(\alpha\) inhibitor and an interleukin (IL)-1 receptor antagonist treatment in rheumatoid arthritis patients [16; 17; 18; 19]. Therefore, a change in the level of Dkk-1 may serve as a biomarker of disease activity and bone erosion [20]. The above-mentioned OPG/ligand system, which is involved in osteoclast differentiation and activation, along with the Wnt pathway, also implicated in the regulation of bone homeostasis, can be considered the key routes regulating bone loss in several bone disorders, including osteoporosis, rheumatoid arthritis and periodontitis [21]. Periodontitis is chronic inflammation of the supportive apparatus of the tooth, and it is characterized by progressive loss of alveolar bone [22; 23; 24]. The defence mechanisms of the periodontal tissues lead to the initiation and progression of the inflammatory cascade that leads to bone resorption, which appears as radiolucency on radiographs around the root [25; 26; 27; 28]. Apical periodontitis caused by endo-periodontal lesions can be symptomatic or asymptomatic and is generally observed through incidental findings during routine radiographic examinations using an orthopantomography (OPT) [29; 30]. Although useful as a preliminary paraclinical examination, these techniques have significant limitations because of the inherent two-dimensional imaging of three-dimensional structures. In order to solve this drawback, cone beam computed tomography (CBCT) was developed [31]. Even though it offers superior clarity and details, due to the increased radiation exposure, the routine use of CBCT imaging in dental practices is not justified [31].