History and Physical Examination Findings
A 7-month-old male 3.0-kg (6.6-lb) mixed breed dog was evaluated because of persistent deciduous teeth. Oral examination of the conscious patient confirmed multiple persistent deciduous teeth and suspicion of abnormally developed right and left mandibular first molar teeth on the basis of appearance of the clinical crowns. No other evidence of health problems were noted on physical examination. Results of a CBC and serum biochemical analysis were within the respective reference ranges. The dog was anesthetized, and dental charting and full-mouth intraoral dental radiography were performed. Inspection of the clinical crowns of both mandibular first molar teeth and evaluation with a dental explorer verified the presence of small indentations at the level of the gingival margin in the region of the furcation (Figure 1). Intraoral dental radiographs of affected teeth were obtained with indirect digital radiography and a size 2 phosphor-coated plate by use of a parallel technique (Figure 2).
Determine whether additional studies are required, or make your diagnosis, then turn the page →
Diagnostic Imaging Findings and Interpretation
Examination of intraoral radiographs confirmed abnormal root morphology of the right and left mandibular first molar teeth in the form of convergence and revealed radiopacities in the middle and mesial pulp horns with a density similar to that of dentin (Figure 3). A radiographic image of the left mandibular first molar tooth in a dog of similar age was obtained from 1 author's (LAH) case files and used for comparative purposes; the normal radiographic appearance of the tooth in this dog included slightly divergent mesial and distal roots without opacities in the pulp cavity (Figure 4). The abnormal crown indentations in the patient of this report were detectable in the radiographs as radiolucent fissure lines that extended down into the furcation. The apical third of the mesial root of the right mandibular first molar tooth had an excessively widened periodontal ligament space. This finding is considered characteristic for a lesion of endodontic origin.1
Treatment and Outcome
A recommendation was made to extract the mandibular first molar teeth because of susceptibility to periodontal and endodontic disease,2 but this treatment was declined by the client. Restoration of the invagination would have been a consideration but would have been technically challenging and would have required multiple radiographic reevaluations to assess tooth vitality with the patient under anesthesia.
The patient underwent a routine physical examination 10 months after the initial evaluation. All examination findings were considered normal with the exception of moderate gingivitis associated with the right mandibular first molar tooth (Figure 5). The left mandibular first molar tooth appeared to be less affected. Periodontal treatment and reevaluation of the previously detected abnormalities were recommended.
The patient was anesthetized, and a complete intraoral dental examination was performed. A 6-mm periodontal pocket, associated with the right mandibular first molar tooth, was found midbuccally (Figure 5; normal sulcular depth in dogs3 is 1 to 3 mm). Follow-up intraoral radiographs of the mandibular first molar teeth were obtained (Figure 6). The abnormalities observed on the initial radiographs were unchanged. However, assessment of the right mandibular first molar tooth revealed severe periodontal and endodontic disease as evidenced by the deep periodontal pocket identified by probing and periapical lucencies on radiographs. The loss of bone extended coronally along the distal aspect of the distal root to the alveolar margin, and substantial furcation exposure was present. The left mandibular first molar tooth had similar but less extensive periapical lesions affecting both roots and early lesion progression along the periodontal structures of the mesial root. The presence of a thickened dentin layer in both affected teeth, compared with that in the initial radiographs (Figures 2 and 3), indicated that both teeth remained vital for a period but subsequently became nonvital owing to pulpal infection. The ventral margin of the right mandible was thickened and its convex shape was more pronounced directly beneath the right mandibular first molar tooth. This finding was interpreted as reactive bone.
Given the extent of the lesions with concomitant bone loss and periodontal inflammation, the right and left mandibular first molar teeth were surgically extracted. A mucoperiosteal flap was raised, and each tooth was sectioned so that each crown-root segment could be elevated independently. The surgical site was flushed with sterile saline (0.9% NaCl) solution, and the flap was closed with 4–0 synthetic absorbable monofilament suture (poliglecaprone 25) in a simple interrupted pattern. The patient recovered uneventfully and was discharged from the hospital; the client was instructed to administer meloxicam (0.1 mg/kg [0.045 mg/lb], PO, q 24 h) and tramadol hydrochloride (1.0 mg/kg [0.45 mg/lb], PO, q 12 h) for 5 days and was recommended to feed the dog soft food until a recheck examination was performed. Two weeks after the procedure, results of the recheck examination revealed that the extraction sites had healed. A recommendation was made to return to feeding the dog its normal diet and to follow up with annual periodontal cleaning and evaluation under general anesthesia.
Comments
Dens invaginatus is a developmental tooth malformation for which the underlying cause remains unknown. Anatomically, the developing tooth consists of the enamel organ, dental papilla, and dental follicle. It is speculated that an abnormal infolding of the papilla or of the enamel organ during tooth development results in dens invaginatus.2 This condition predisposes human patients to dental caries and pulpal infection.2,4 It has been found in the permanent teeth of humans and can easily be missed on routine oral examination owing to a lack of clinical signs.2 Because pathological changes associated with dens invaginatus include caries, pulp disease, and periodontal inflammation, early identification is important.2 Surface irregularities of the clinical crown associated with dens invaginatus contribute to increased bacterial plaque retention and gingivitis. Depending on the host-specific response to plaque, progression to periodontitis can result. Periodontitis is an inflammatory disease of the tooth-supporting structures (gingiva, alveolar bone, periodontal ligament, and cementum).5 The changes in clinical crowns of affected teeth in the patient of this report were at the level of the gingiva and in the region of the furcation. Exposure of the furcation results in additional plaque retention, which exacerbates the clinical problem. The dog of this report developed gingivitis with periodontitis as evidenced by the inflamed gingiva and deep periodontal pocket.
More than 1 classification system for dens invaginatus lesions exists; however, radiographic evaluation, with lesions categorized on the basis of the degree to which they extend from the crown into the root, can be easily understood and applied.2 Type 1 lesions are those with a minimal enamel-lined invagination confined to the crown and not extending beyond the level of the external cementoenamel junction. In type II lesions, the invagination is also enamel-lined; it extends into the pulp chamber but remains within the pulp cavity with no communication with the periodontal ligament. A type IIIA lesion extends through the root and communicates laterally with the periodontal ligament through a pseudoforamen without direct communication with the pulp, and a type IIIB lesion passes through the root and communicates with the periodontal ligament at the apical foramen (usually with no communication with pulp). The lesion in humans is most commonly found in permanent teeth, and the indentations in the clinical crown are consistently located on the palatal aspect.6 Speculated causes of dens invaginatus include trauma and developmental or genetic abnormalities, with the evidence in favor of an underlying genetic cause.2 It has been postulated that the enamel layer in areas of invagination may be incomplete, resulting in dentin exposure and likely bacterial contamination from the oral environment, with subsequent pulpal infection and endodontic disease.4,6
A lesion that includes pulpal and periodontal tissues may represent 2 distinct diseases affecting each tissue individually and simultaneously or may represent a progression from one disease to the other. These lesions can be classified into primary endodontic with secondary periodontal involvement (class I; endodontic-periodontic), primary periodontal with secondary endodontic involvement (class II; periodontic-endodontic), or truly combined lesions (class III).7,8 In this instance, given the predisposition to both periodontal and pulp infection, a class III lesion category would be reasonable. However, it is not possible to be completely certain that the periodontal infection did not precipitate or at least accelerate the pulpal infection. Periapical disease was considered to be directly responsible for the reactive bone observed radiographically. Chronic, low-intensity inflammation irritates the periosteum, which responds by producing new bone on the cortical surface known as periostitis ossificans.9 The periodontal ligament space narrows with age. It is therefore important to remember that radiographic evaluation of the developing root apices will reveal a widened periodontal ligament space. Radiographic comparison with a normal tooth in a similarly aged patient can aid interpretation.10 One reference found in the veterinary literature describes the crown surface indentations as crinkling and suggests they are directly attributable to root convergence.11 In our opinion, the clinical and radiographic appearance of affected teeth in the dog of this report were consistent with type I dens invaginatus. These abnormalities were suspect for underlying pathological changes, and radiography was essential for further elaboration of the changes and for determination of appropriate treatment recommendations.
References
1. Dupont GA, DeBowes LJ. Radiographic evidence of pathology. In: Dupont GA, DeBowes LJ, eds. Atlas of dental radiography in dogs and cats. St Louis: Saunders, 2009;134–228.
2. Alani A, Bishop K. Dens invaginatus. Part 1: classification, prevalence and etiology. Int Endod J 2008; 41: 1123–1136.
3. Wiggs RB, Lobprise HB. Oral examination and diagnosis. In: Wiggs RB, Lobprise HB, eds. Veterinary dentistry principles and practice. Philadelphia: Lippicott-Raven, 1997;87–103.
4. Hülsmann M. Dens invaginatus: aetiology, classification, prevalence, diagnosis, and treatment considerations. Int Endod J 1997; 30: 79–90.
5. Klaus H, Rateitschak EM, Wolf HF, et al. Initial therapy. In: Rateitschak KH, ed. Color atlas of dental medicine: periodontology. 2nd ed. Stuttgart, Germany: Thieme, 1989;145–206.
6. Bishop K, Alani A. Dens invaginatus. Part 2: clinical, radiographic features and management options. Int Endod J 2008; 41: 1137–1154.
7. Zehnder M, Gold SI, Hasselgren G, et al. Pathologic interactions in pulpal and periodontal tissues. J Clin Periodontol 2002; 29: 663–671.
8. Wiggs RB, Lobprise HB. Basic endodontic therapy. In: Wiggs RB, Lobprise HB, eds. Veterinary dentistry principles and practice. Philadelphia: Lippicott-Raven, 1997;280–324.
9. Consolaro A, Consolaro RB. Bone reaction capability and the names of inflammatory bone disorders in endodontic clinical practice. Dent Press Endod 2012; 2: 12–19.
10. Nanci A, Bosshardt DD. Structure of periodontal tissues in health and disease. Periodontol 2000 2006; 40: 11–28.
11. Bannon KM. Clinical canine dental radiography. Vet Clin North Am Small Anim Pract 2013; 43: 507–532.