History and Physical Examination Findings
A 7-month-old 2.72-kg (6-lb) sexually intact female Chihuahua was referred to a veterinary dental practice because of multiple persistent deciduous teeth and missing teeth. The referring veterinarian had noted the problem 1 month earlier during a routine presurgical examination for a scheduled ovariohysterectomy. The owner had not noticed any oral problems and stated that the dog had reached normal developmental milestones. There were no current medical concerns, and the dog was up-to-date for vaccinations and parasite prevention. The owner had not performed any oral care at home. At the referral visit, the dog was found to be bright, alert, and responsive, with rectal temperature and respirations within expected ranges. The cardiac rhythm and rate were deemed normal, with synchronous femoral pulses. No abnormalities were found on general physical examination. Oral examination in the awake patient revealed calculus and gingival indices of 0 with normal occlusion. The deciduous right maxillary canine tooth, right maxillary second and third premolar teeth, left maxillary canine tooth, left maxillary second premolar tooth, right mandibular canine tooth, and left mandibular third incisor tooth were persistent. The permanent right and left maxillary first and second premolar teeth, right mandibular first premolar and third molar teeth, and left mandibular third incisor tooth, first premolar tooth, and third molar tooth were missing. A retained distal root of the deciduous left maxillary third premolar tooth was noted. The permanent dentition that had erupted appeared normal on visual examination. Blood samples were obtained prior to the referral examination, with CBC and serum biochemical analysis results within the respective reference ranges. Oral radiography with a comprehensive oral health assessment and treatment planning was recommended.
The dog was premedicated with dexmedetomidine hydrochloridea (0.01 mg/kg [0.005 mg/lb], IM) and hydromorphone hydrochlorideb (0.05 mg/kg [0.023 mg/lb], IM). General anesthesia was induced with propofolc (4.5 mg/kg [2 mg/lb], IV) and maintained with isofluraned delivered at a variable rate in oxygen with a nonrebreathing circuit anesthetic machine. Intraoperative fluid therapy consisted of a balanced isotonic fluid delivered at 5 mL/kg/h (2.3 mL/lb/h) via IV catheter. Heart rate, blood pressure, ECG data, oxygen saturation with hemoglobin (measured by pulse oximetry), and end-tidal partial pressure of CO2 were monitored throughout the procedure with a multiparameter monitor. With the dog fully anesthetized, complete oral examination that included periodontal probing and charting and oral radiography was performed. Selected radiographic images are provided (Figure 1).
Diagnostic Imaging Findings and Interpretation
Oral radiographs obtained with parallel and bisecting angle techniques revealed that the previously noted missing teeth were all absent. Previously noted persistent deciduous teeth were present, with the deciduous right maxillary canine tooth and second and third premolar teeth and the deciduous left maxillary second premolar tooth showing evidence of resorption. The distal root of the deciduous left maxillary third premolar tooth was retained. Additionally, the permanent right and left mandibular second molar teeth were single rooted as indicated by the presence of a single root canal, and interesting developmental abnormalities of the permanent right and left maxillary fourth premolar teeth and right and left mandibular first molar teeth were noted. A round to oblong inclusion with an opacity similar to that of enamel appeared to be located centrally in the pulp chambers of both the maxillary fourth premolar and mandibular first molar teeth (Figure 2). The roots of the right mandibular first molar tooth were convergent, and the roots of the left mandibular first molar tooth had a parallel conformation, indicating a degree of convergence. The roots of the right and left mandibular first molar teeth should normally be divergent. The changes in root morphology and the pulpal opacities were likely due to the same developmental abnormality.
In the maxillary fourth premolar teeth, the radiopacities appeared as oblong opacities associated with the furcation between the mesial and distal roots and extended distally through the caudal aspect of the pulp chamber. In the mandibular first molar teeth, the radiopacities were also associated with the furcation between the mesial and distal roots but extended mesially through the rostral aspect of the pulp chamber. The distal root of the left mandibular first molar tooth appeared dilated, and the mesial root dentin was heterogenous and comparatively radiolucent. Despite the described changes to tooth morphology, no signs of endodontal disease associated with the teeth1 were seen.
Periodontal probing and charting were performed, and where appropriate, a dental explorer was used to further evaluate the furcation for affected teeth. Rough areas with a discontinuous contour were noted in the cervical region of all 4 carnassial teeth at the level of the lingual entrance to the furcation. Further probing and examination revealed a defect of the enamel associated with each abnormality. On the basis of oral examination and radiographic findings, a diagnosis of carnassial tooth malformation (CTM) was made.2
Treatment and Outcome
Treatment options discussed with the owner centered on extraction or continued monitoring of affected teeth. If teeth were maintained, the owner was informed that annual complete oral examinations including oral radiography would be necessary to monitor for pathological changes owing to the risk of endodontal disease from bacterial infiltration through the enamel defects and the risk of periodontal disease from material becoming trapped by the rough surface of the enamel defects and forming plaque. Endodontic treatment (root canal therapy) was discussed but was not considered an option on the basis of the degree of root development present at that age, high risk of a toy-breed dog developing periodontal disease, extent of the pulpal lesions, and defects in the crowns and their likely interference with complete cleaning, shaping, and obturation of the root canal. The owner opted to have the teeth extracted.
The oral cavity was rinsed with 0.1% chlorhexidine acetate solutione to decrease bacterial load. Prior to surgery, ultrasonic scaling and polishing were performed on permanent teeth where plaque had accumulated owing to crowding with persistent deciduous teeth and in other areas where required. Right and left infraorbital and inferior alveolar nerve regional blocks were performed with 0.3 mL (1.5 mg) of bupivacainef (total amount). Full-thickness mucogingival flaps were created, and persistent deciduous teeth were surgically extracted. The permanent right and left maxillary fourth premolar teeth and the left mandibular first molar tooth were surgically sectioned and extracted. The right mandibular first molar tooth was removed by simple extraction. Rough alveolar bone was reduced with a medium-grit, tapered diamond burg on a water-cooled high-speed handpiece. Intraoral radiographs were obtained after the extractions to ensure complete removal of all tooth roots. Gross examination of the extracted right mandibular first molar tooth revealed the enamel defect previously identified at the lingual aspect was also present on the buccal aspect of the tooth (Figure 3). The defect had not been appreciated previously owing to the presence of normal furcational bone and attached gingiva. The mucogingival flaps were closed with 5-0 poliglecaprone 25 absorbable monofilament sutureh in a simple interrupted pattern. The dog was discharged from the hospital with tramadoli (2.2 mg/kg [1 mg/lb], PO, q 12 h) and meloxicamj (0.1 mg/kg [0.05 mg/lb], PO, q 24 h) for analgesia. Antimicrobials were not dispensed for the dog because the abnormalities were not infectious.
A recheck examination was performed 2 weeks after surgery. There had been no postoperative concerns, and the owner reported that the dog was eating and drinking normally. All surgical sites had healed well without complication. Oral care at home was discussed with the owner, and daily brushing of the teeth was recommended.
Comments
Developmental dental anomalies in dogs are uncommon. In the dog of the present report, the permanent maxillary fourth premolar teeth and the mandibular first molar teeth, also known as the carnassial teeth, were affected by CTM. This is a recent reclassification of an anomaly of the carnassial teeth in dogs previously considered to be dens invaginatus (DI),2 a developmental malformation caused by deepening or in-folding of the enamel organ into the dental papilla prior to calcification of the dental tissues. Dens invaginatus has also been referred to as invaginated odontoma, dilated gestant odontoma, dilated composite odontoma, tooth inclusion, dentoid in dente, and dens in dente3 owing to its radiographic appearance. Previous classification of what is now described as CTM in dogs was based on radiographic identification of a radiopaque density in affected teeth, which was thought to be similar to DI in people, and the gross presence of an enamel defect consistent with a pit or fissure.2,3 A recent investigation2 of 6 dogs with mandibular carnassial tooth anomalies previously attributed to DI found marked differences from reported features of DI in people and revealed that the condition in dogs has more similarities to molar-incisor malformation than to DI. The etiopathogenesis of DI in people involves invagination of the enamel organ or Hertwig epithelial root sheath during tooth development.2 Histologic and immunohistochemical testing of DI lesions has identified a thin layer of reduced enamel epithelium with decreased mineral density of enamel lining the invagination, compared with the outer enamel.4 Dens invaginatus anomalies communicate with the external enamel, and the physical appearance of lesions can range from a small pit on the tooth surface to a severe invagination causing the so-called tooth-within-a-tooth radiographic appearance.5 The cause of DI in people is thought to be genetic, with a reported prevalence between 0.3% and 10%.6 One large study7 of Turkish dental patients revealed that the teeth most commonly affected by DI are the maxillary second incisor teeth (80%), followed by the canine teeth (20%). The results of that study7 indicate that the condition occurs bilaterally in 25% of affected individuals.
The aforementioned investigation of CTM in dogs2 included clinical assessment, radiographic and CT imaging, and evaluation of histologic and immunohistochemical features of affected teeth. The anomalies were found to be bilateral, usually affecting the mandibular first molar teeth, but in some cases, similar changes were also found in maxillary fourth premolar teeth, maxillary and mandibular first premolar teeth, and a mandibular canine tooth. Oral examination findings included defects in the enamel of the crown that extended to involve the furcation in multirooted teeth. However, not all affected teeth had visibly noticeable defects. As found for the dog of the present report, oral radiographs were necessary to confirm physical findings.2
Diagnostic imaging findings associated with CTM in the previously described study2 included enamel defects; radiopaque structures within the crown; root convergence, parallelism, or dilaceration; and furcation defects. Periodontal bone loss and endodontal lesions were found where teeth were pathologically compromised. Whereas CTM lesions appeared radiographically as radiopaque structures within the crown similar to DI anomalies, they appeared as heterogenous solid tissue with attenuation between that of enamel and dentin on micro-CT, and histologic examination revealed this material was separated from the external enamel with a clear demarcation or a small layer of dentin-like material between tissues. The abnormal tissue was of unknown origin and lacked dentinal tubules but was surrounded by disorganized dentin and did not always contact the outer enamel, and enamel fissures were not consistently present. Interestingly, channels were found in the abnormal tissue of all teeth but did not consistently communicate with the oral cavity, pulp, or furcation of the affected tooth. Histologically, the abnormal tissue did not resemble enamel or dentin, and amelogenin, which confirms the presence of the components of enamel, was absent in all samples.2 Unlike human DI lesions, defects noted in CTM are solid and thought to arise from the dental papilla,2 but the etiopathogenesis is unknown.
Molar-incisor malformation in people is also characterized by abnormal hard tissue deposits within affected teeth, but it affects the deciduous and permanent maxillary and mandibular first molar, canine, and first incisor teeth and has a symmetric distribution.8 Other hallmarks of molar-incisor malformation include deviations of the pulp chamber, abnormal tissue at the cervical region of the tooth often associated with depressions or fissures in the enamel, and root malformations. The abnormal tissue in the teeth of people with this condition is osteodentin-like, arising from the dental papilla or dental follicle.9,10,11,12 The pathogenesis of molar-incisor malformation has been traced to antenatal and immediate postnatal adverse medical events; medications, congenital health problems, and neonatal infections have all been implicated.8 The dog of the present report and the small number of dogs in the study by Ng et al2 did not have a known history of exposure to infectious or inflammatory disease or adverse perinatal events. However, small-breed and toy-breed dogs are at increased risk for developmental abnormalities and problems with parturition including dystocia.2,13
Treatment for CTM depends on the extent of the lesion and associated radiographic findings. In dogs with lesions found early, with no evident enamel or gross external structural tooth defects and no radiographic signs of pathological changes, teeth can be managed conservatively with periodic oral examinations and radiographs.14 Unfortunately, lesions may go unnoticed, leading to periodontal and endodontal disease. Owing to the capacity of enamel and crown defects to accumulate debris, plaque, and calculus, the first signs of problems are often associated with periodontal disease.3 Defects in the enamel also increase the risk of bacterial translocation to the pulp cavity, leading to endodontal disease. In advanced stages, where severe pathological changes have occurred, the only treatment for CTM may be extraction. In 1 clinical report,14 a canine tooth that was identified as affected with DI in a dog was treated with standard endodontic therapy. Whether endodontic therapy can be a successful approach for the treatment of CTM anomalies is still relatively unknown, and its use may be hindered by the solid mass of tissue interfering with the ability to completely disinfect, clean, shape, and obturate the root canal system. In some cases, clinically and radiographically normal teeth in human patients are monitored long-term for endodontal and periodontal changes, with treatment planning at the right time to prevent infection, pain, and orthodontic problems.11 In 1 study8 of 38 patients affected by molar-incisor malformation, complications attributed to the condition included periodontal bone loss, endodontal lesions, and endodontal-periodontal lesions (53%, 50%, and 29% of patients, respectively); of 34 teeth with endodontal or endodontal-periodontal lesions, 18 were lost early, 10 underwent root canal therapy, and 6 were monitored with no treatment, but affected untreated teeth often required extraction after only a few years. Common treatments after extractions in people include orthodontic treatment to prevent or alleviate malocclusions and prosthetic implantation.8
Radiographs are an essential component for full evaluation of the oral cavity and as part of a complete medical record. In previous prospective studies of 226 dogs15 and 115 cats,16 clinically relevant abnormalities were identified by radiography in 28% and 42% of dogs and cats, respectively, that had no obvious clinical lesions of the teeth. In the same studies,14,15 radiography revealed additional information about affected teeth in 50% of dogs and 54% of cats that had lesions of the teeth identified clinically. In the dog of the present report, radiography was valuable for evaluation of apparently missing teeth and surgical planning for persistent deciduous teeth, but several teeth afflicted with the developmental condition of CTM were also unexpectedly identified by this method, which allowed for appropriate treatment to prevent complications related to the increased risks of periodontal and endodontal disease associated with this abnormality.
Acknowledgments
No financial support was received for the research, authorship, or publication of this report. The author declares there was no conflict of interest.
Footnotes
Dexdomitor, Pfizer Animal Health, Kirkland, QC, Canada.
Sandoz Canada Inc, Boucherville, QC, Canada.
Diprivan, AstraZeneca, Mississauga, ON, Canada.
Attane, Piramal Critical Care Inc, Bethlehem, Pa.
Nolvadent Oral Cleansing Solution, Fort Dodge Laboratories Inc, Fort Dodge, Iowa.
Vivicaine, Novocol Pharmaceutical of Canada Inc, Cambridge, ON, Canada.
Shipp's Dental and Specialty Products, Marana, Ariz.
Monocryl, Ethicon Endo Surgery, Guaynabo, Puerto Rico.
Standstone Pharmacies, Calgary, AB, Canada.
Metacam Oral Suspension, Boehringer Ingelheim, Burlington, ON, Canada.
References
- 1. ↑
DuPont GA, Debowes LJ. Endodontic disease. In: DuPont GA, Debowes LJ, eds. Atlas of dental radiography in dogs and cats. St Louis: Saunders Elsevier, 2009;142–152.
- 2. ↑
Ng KK, Rine S, Choi E, et al. Mandibular carnassial tooth malformations in 6 dogs—micro-computed tomography and histology findings. Front Vet Sci 2019;6:464.
- 3. ↑
Stein KE, Manfra Marretta S, Eurell JAC. Dens invaginatus of the mandibular first molars in a dog. J Vet Dent 2005;22:21–25.
- 4. ↑
Yamada M, Nagayama M, Katsumata A, et al. Hypomineralized enamel of dens invaginatus: its distinct images and pathogenesis of the type III invagination using micro-focusing computed tomography. J Hard Tissue Biol 2014;23:449–454.
- 5. ↑
Kallianpur S, Sudheendra U, Kasetty S, et al. Dens invaginatus (type III B). J Oral Maxillofac Pathol 2012;16:262–265.
- 6. ↑
Gallacher A, Ali R, Bhakta S. Dens invaginatus: diagnosis and management strategies. Br Dent J 2016;221:383–387.
- 7. ↑
Colak H, Tan E, Aylikçi BU, et al. Radiographic study of the prevalence of dens invaginatus in a sample set of Turkish dental patients. J Clin Imaging Sci 2012;2:34.
- 8. ↑
Kim JE, Hong JK, Yi WJ, et al. Clinico-radiologic features of molar-incisor malformation in a case series of 38 patients: a retrospective observational study. Medicine (Baltimore) 2019;98:e17356.
- 9. ↑
Amirtham Witt CV, Hirt T, Rutz G, et al. Root malformation associated with a cervical mineralized diaphragm—a distinct form of tooth abnormality? Oral Surg Oral Med Oral Pathol Oral Radiol 2014;117:e311–e319.
- 10. ↑
Lee H-S, Kim S-H, Kim S-O, et al. Microscopic analysis of molar-incisor malformation. Oral Surg Oral Med Oral Pathol Oral Radiol 2015;119:544–552.
- 11. ↑
Brusevold IJ, Granvoll Bie TM, Baumgartner CS, et al. Molar incisor malformation in six cases: description and diagnostic protocol. Oral Surg Oral Med Oral Pathol Oral Radiol 2017;124:52–61.
- 12. ↑
Choi S, Lee J, Song J. Molar-incisor malformation: three cases of a newly identified dental anomaly. J Korean Acad Pediatr Dent 2017;44:370–377.
- 13. ↑
Münnich A, Kuchenmeister U. Dystocia in numbers – evidence-based parameters for intervention in the dog: causes for dystocia and treatment recommendations. Reprod Domest Anim 2009;44:141–147.
- 14. ↑
Coffman CR, Visser CJ, Visser L. Endodontic treatment of dens invaginatus in a dog. J Vet Dent 2009;26:220–225.
- 15. ↑
Verstraete FJ, Kass PH, Terpak CH. Diagnostic value of full-mouth radiography in dogs. Am J Vet Res 1998;59:686–691.
- 16. ↑
Verstraete FJ, Kass PH, Terpak CH. Diagnostic value of full-mouth radiography in cats. Am J Vet Res 1998;59:692–695.