Development anomaly and non-vitality: Two case reports

Abstract

Anatomic aberrations are seen in human dentition. The maxillary incisor region of the permanent dentition where these anatomical aberrations are commonly seen is considered an area of embryonic hazard. Aberrations affecting the internal and external morphology can at times be the cause of complex pathological conditions involving the pulpal and periodontal tissues and can pose a challenge to the clinician for the diagnosis and clinical management. Detecting and treating the anomalies at an early phase is essential as it poses a threat for the loss of vitality of the concerned teeth. The aim of this paper is to highlight the fact two different developmental anomalies of maxillary incisors, namely palatoradicular groove and Turner's hypoplasia, led to the loss of vitality of the same.

Palatoradicular groove is a developmental groove involving the crown and extends up to a variable distance onto the root.[1,2] This may result from an infolding of the enamel organ and the epithelial sheath of Hertwig.[3] Peixoff et al. have suggested that the anomaly results from an attempt to form another root.[4] The groove can occur on the mesial or distal surface as well as on the facial surfaces of the central incisors,[5] termed as facial radicular groove.[6,7] The anomaly might be unilateral or bilateral.[8,9] A single tooth can have two grooves, one on the facial surface and the other on the palatal surface.[10] In addition, the palate gingival groove has been observed in maxillary second molars.[11] These grooves act as a nidus for plaque accumulation which finally results in the formation of a severe localized periodontal lesion. Hypoplasia is defined as a quantitative defect of enamel visually and is histomorphologically identified as an external defect involving the surface of enamel and associated with reduced thickness of enamel.[12] Unlike other abnormalities which affect a vast number of teeth, Turner's hypoplasia usually affects only one tooth in the mouth and it is referred to as a Turner's tooth. If Turner's hypoplasia is found on a permanent canine or a premolar, the most likely cause is an infection from the primary tooth. If Turner's hypoplasia is found in anterior teeth, the most likely cause is traumatic injury to the primary tooth. The traumatized tooth is pushed onto the developing tooth underneath it and consequently affects the formation of enamel. Because of the location of permanent tooth's developing tooth bud in relation to the primary tooth, the most likely affected area on permanent tooth is facial surface.[13] Hypoplasia was catergorized into the following types by Silberman et al.[14]

Type 1: Enamel discoloration due to hypoplasia

Type 2: Abnormal coalescence due to hypoplasia

Type 3: Some parts of enamel missing due to hypoplasia

Type 4: A combination of previous three types of hypoplasia

This article presents two case reports of maxillary incisors that turned non-vital due to developmental anomalies.

Case Reports

Case 1

A 33-year-old patient with good health presented to the outpatient department with the complaints of pain and salty discharge in the left upper anterior quadrant of the jaw for the past 6 years. History revealed that pain was mild and intermittent. During clinical examination, the left maxillary lateral incisor (#22) [Figure 1] had an intact crown without caries/fracture, with negative vitality testing and positive to percussion. The mobility of tooth was grade II; on examination, there was a 9-mm pocket and purulent exudate from the gingival sulcus of the palatal aspect. On probing, a deep groove extending from the cingulum to mid-root area was noted on distopalatal aspect of the tooth [Figure 2]. Oral hygiene was poor, with calculus present all around the tooth.

Figure 1.

Lateral incisor showing palatoradicular groove and its management

Figure 2.

Lateral incisor showing palatoradicular groove and its management

Radiographic examination [Figure 3] revealed a radiolucent parapulpal line superimposed over the root canal and a pear-shaped radiolucency in the coronal aspect was present. A circumscribed radiolucent area with irregular borders having crestal bone loss was found in the region of #22. A diagnosis of endodontic periodontal lesion with palatoradicular groove and periapical abscess was inferred. An interdisciplinary treatment plan was formulated for the patient.

Figure 3.

Preoperative radiograph

After oral prophylaxis, endodontic treatment [Figure 4] was done under rubber dam isolation. Full thickness mucoperiosteal flap was elevated; granulation tissue was curetted in periradicular area [Figure 5]. Since the root apex was infected for a long duration, apicectomy was performed [Figure 6]. Root end filling was done with glass ionomer cement. The palatoradicular groove was isolated to its most apical extent. Thorough scaling and root planing were performed over the groove and the diseased granulation tissue was curetted out to leave the soft tissue more conducive to regeneration. Radicular groove was eliminated by means of radiculoplasty using round bur [Figure 7]. A chemical conditioning of the groove was performed by using 10% polyacrylic acid, and glass ionomer cement type 1 was applied into the defect. The area was kept isolated of blood and tissue fluids during the setting of the cement by using local hemostatic gelatin sponge. Platelet-rich plasma was packed in the defect [Figure 8]. The flap was approximated and supported with sling sutures [Figure 9]. Patient was instructed on post-surgery precautions and maintenance protocol, which included rinsing with 0.12% solution of chlorhexidine twice a day for 5 weeks. During this period, the patient was recalled once a week for professional oral prophylaxis. Sutures were removed 14 days after the surgery. At this time, complete soft tissue closure was still demonstrable. Probing depth reduced to 4mm after 2 months [Figure 10]. Six-month [Figure 11a] and 1-year follow-up radiographs [Figure 11b] revealed the complete disappearance of radiolucency in relation to the lateral incisor.

Figure 4.

Post-obturation radiograph

Figure 5.

Elevation of mucoperiosteal flap

Figure 6.

Apicectomy and root end filling

Figure 7.

Radiculoplasty done with round bur

Figure 8.

Platelet-rich plasma to be packed

Figure 9.

Flap approximated with sling sutures

Figure 10.

Follow-up periodontal probing (2 months)

Figure 11.

(a) Follow-up radiograph (6 months) (b) Follow-up radiograph (1 year)

Case 2

A 20-year-old male patient reported with a complaint of painful, discolored left upper front tooth (#21) with deposits on it. Patient had a history of trauma to his upper front primary teeth at the age of 2 years. On clinical examination, a horizontal groove with brown discoloration around the cervical region of #21 was observed, resembling circular enamel hypoplasia [Figure 12a]. Intraoral periapical radiograph showed loss of enamel around the cervical region of the tooth [Figure 12b] with no other abnormalities. Thermal vitality test showed no response. A test cavity was prepared in #21 and the tooth had no response, indicating non-vitality. The treatment plan included root canal therapy [Figure 13] followed by jacket crown.

Figure 12.

(a) Clinical picture showing Turner's hypoplasia (b) Preoperative radiograph

Figure 13.

Postoperative radiograph

Discussion

Presence of palatoradicular groove (case 1) is considered to be an important contributing factor for the development of localized periodontitis. It acts as a “plaque trap”, facilitating the development of a combined periodontic–endodontic lesion.[15] This might even lead to it being misdiagnosed as a primary endodontic lesion.

The endo–perio lesion in the present case seems to be a primary periodontic lesion with secondary endodontic involvement. It was because of the fact that there was no history of trauma and/or discoloration of the tooth. Though the lesion was principally periodontal, the manifestation of the pathology is diagnosed by the vitality tests.

The groove had a funnel-like shape and irregularities on the external surface that promoted the accumulation of bacterial plaque and calculus, resulting in the onset and progression of periodontal disease.[16] As a result of this breach in the epithelial attachment, the progression of bacterial products through dentinal tubules could secondarily compromise the pulp tissue, causing a primary periodontic/secondary endodontic lesion which necessitated both pulpal and periodontal therapy.[17]

The treatment of palatoradicular groove presents a clinical challenge. A favorable outcome can be achieved only with the comprehensive treatment approach that effectively manages all local factors contributing to the disease process.

The rationale[18] behind the selected treatment plan was the following:

1. Removal or saucerization of the radicular portion of the groove (radiculoplasty) to eliminate bacterial plaque, calculus, and to prevent bacterial recolonization.

2. Cleaning and sealing of the coronal portion of the groove to prevent bacterial recolonization.

Materials such as composite and amalgam have been used to fill the palatoradicular groove.[19,20] Although mineral trioxide aggregate sets in the presence of moisture, it might get washed off from the transgingival defect. Instead, glass ionomer cement was chosen because it does not have this limitation. The technique of conditioning and sealing the groove with glass ionomer cement is a very conservative approach for eliminating deep palatoradicular grooves. Conditioning of the groove removes the surface debris, increases the wettability, and increases the bond strength of glass ionomer cement.[21] Glass ionomer cement was used since it has an antibacterial effect, chemical adhesion to the tooth structure, and good sealing ability.[22,23] Clinical and histological studies have reported that there is an epithelial and connective tissue adherence to glass ionomer cement during the healing process.[24] The same clinical observation was also found in this case. In the present case, since the groove was extended onto the root surface with substantial periodontal destruction, a flap procedure, including curettage of granulation tissue and root planing, was undertaken.

In the present case, there was an option to extract the tooth and do a replacement appliance. Although the palatal surgical approach is difficult to access, saving the tooth is a more conservative treatment plan. Moreover, the tooth was in the esthetic zone and the papillary reconstruction would have been difficult after extraction and implant placement. Therefore, an approach for saving the tooth was chosen instead of the more complex and costlier implant procedure.

Case 2 had type 4 enamel hypoplasia. The brown discoloration occurs due to disturbances in ameloblastic layer, leading to defective matrix formation caused by traumatic injuries, but the stretched inner enamel epithelium continues to induce the differentiation of new odontoblasts, and hence the dentin formation is not affected.[25] Severe pulpal infection of primary teeth results in excessive osteolysis of inter-radicular bone and early exposure of the succedaneous tooth before adequate root length formation.[26]

These structurally defective teeth are not only weak but also provide favorable area for colonization of bacteria. The hypoplastic permanent teeth are seven times more sensitive to carious attack compared to those without hypoplasia. Hypoplastic primary teeth are two times prone to caries than normal teeth.[14]

The hypoplastic tooth had turned non-vital without any history of trauma or any carious insult. The tooth would have turned non-vital because of the defective enamel and open dentinal tubules which act as a nidus for bacterial entry into the pulp space, thereby leading to pulp necrosis.[27] Delayed treatment on affected deciduous and permanent teeth can lead to pulp pathosis and its sequelae.

Conclusion

The need for a careful examination and early detection of all possible developmental defects in the permanent dentition and the importance of preventive measures should be stressed for maintaining the vitality of the tooth.

Key Learning Points

• The key to achieving favorable results in these types of developmental anomalies is accurate diagnosis and treatment planning.

• Deep radicular grooves can predispose to pulp necrosis and the establishment of combined periodontic–endodontic lesions.

• It is advisable to detect enamel hypoplasia as early as possible to prevent the teeth from turning non-vital.