Endodontic treatment of calcified pulp systems is challenging. Pulp canal calcification (PCC) is reported to occur after various luxation injuries at rates of 15 – 40 % (1, 2). Chronic irritation (e.g. caries), cervical pulpotomy, or restorative therapies are known to promote the apposition of hard tissues within the root canal (3-5). It may also occur after orthodontic treatment (6) or in elderly patients with a high rate of physiological apposition of dentin (7). Specifically, dentin dysplasia (DD), a kind of dentin malformation, also causes accelerated dentinal apposition (8, 9).
DD, a rare disturbance of dentin formation (incidence: 1:100,000), is an autosomal dominant hereditary disease caused by a coding malfunction of the dentin sialophosphoprotein gene. The disorder is characterized by apparently normal enamel but atypical dentin formation and abnormal pulp morphology (10). Two types of DD are distinguished based on clinical, radiological and histological findings: type I (“radicular”) and type II (“coronal”), hereinafter referred to as DD-1 and DD-2 (11). In both DD-1 and DD-2, the crowns of primary and permanent teeth mostly have a clinically and morphologically normal appearance and colour (in DD-2, however, the primary teeth are bluish amber-coloured). The affected teeth may exhibit abnormal mobility, premature exfoliation and, particularly in the case of DD-1, undeveloped or absent roots (12).
Radiographically, the pulp spaces may be narrowed and thus reduced in size or completely calcified. In DD-2, teeth in both dentitions often have thin roots but normal root lengths. Common radiologic signs include early pulp obliteration and thistle-tube shaped pulp chambers with multiple pulp stones in the absence of periapical radiolucencies (13). Besides aberrant dentin deposition in the pulp chamber in both types (DD-1 and DD-2), most typically in DD-1 there is an increased incidence of periapical radiolucencies due to the infection of the root canal system (9, 13, 14). To date, it is presumed that these teeth are highly susceptible to bacterial invasion due to various factors, including the presence of atypical dentin formation within a highly irregular pulp chamber, the lack of dentinal fluid, which induces enamel brittleness and, occasionally, micro cracks as a potential pathway for microorganisms, and aberrant dentin formation, which might affect the formation and structure of the enamel as well (15). Alterations to the enamel, including micro cracks and increased dentin permeability in the case of DD-1, may facilitate bacterial invasion and lead to pulp necrosis and apical periodontitis. Such a crack was detected in a three-dimensional (3D) micro-computed tomographic study of a molar of a DD-1 patient, but the ability of this technology to detect fine cracks seems to be limited (15).
Dentine dysplasia, a rare autosomal dominant dentine anomaly, was ﬁrst classiﬁed by Shields et al. (1) into two main categories: dentine dysplasia type 1 (DD1) and dentine dysplasia type 2 (DD2). The classiﬁcation was based on clinical, radiologic and histologic examinations. Den dentin dysplasia affects both the primary and permanent dentitions, with DD1 regularly featuring periapical pathosis due to infected root canal systems (2). O Carroll et al. (3) proposed a subclassiﬁcation of DD1 into four categories: types 1a, b, c and d based on their clinical and radiologic features. This subclassiﬁcation is of particular signiﬁcance to the diagnosis of DD1, which had also been termed radicular dentine dysplasia (2). Affected teeth diagnosed as DD1 have often been described as rootless teeth (4), due to excessively shortened or absent radicular structure,
There is no available evidence on the occurrence of apical periodontitis in teeth with DD, but several case reports suggest that these teeth may be at risk of developing apical pathologies (10, 14-18).
In the present case report, DD-1 was identified based on its specific radiologic features, including the characteristic root morphology, obliteration of the pulp chambers and root canals, and the presence of several periapical lesions in sound teeth (Fig.1,3). Typically, the roots appear shortened, blunted, and partially malformed (14, 16, 19, 20).
Endodontic treatment of calcified pulp systems (due to dental trauma or DD) is associated with a high risk of complications, such as root perforation, extensive dentinal hard tissue loss, and missing the root canal (14, 17). Thus, straight-line access close to or through the incisal edge was emphasized as being a key to preventing technical endodontic failures in anterior teeth with PCC (21). Guided endodontic treatment (GET) was recently introduced as a novel method of performing operator-independent guided straight-line access (22, 23). Here, 3D data collected by cone-beam computed tomography (CBCT) were matched with surface scan data and used to fabricate a 3D drill guide. Once the drill paths were virtually planned, templates could be fabricated to safely locate the root canals. Other case reports and one case series have also shown the feasibility and reliability of GET in cases with apical periodontitis as a late complication of dental trauma (23-31). To our knowledge, there is currently only one guided endodontics case report, which describes a promising 18-month outcome of a dens invaginatus malformation case treated, followed by endodontic surgery and root-end filling with mineral trioxide aggregate (30).
In DD cases in need of endodontic therapy, conventional orthograde endodontic treatment was reported to be potentially substitutable with periapical curettage and retrofilling, especially if the roots display normal length and development (32, 33). In the case of DD-1, extraction of teeth with periapical radiolucencies might be favoured over endodontic therapy due to the above-mentioned technical challenges and anatomic limitations (34-36).
To date, only a few case reports of endodontic treatment attempts in patients with DD-1 have been published, and they have partially sobering outcomes (14, 37-39). This is the first case report of a successful outcome of root canal treatment of multiple teeth in a patient with DD-1. GET prevented technical complications and enabled tooth retention in our patient.