Interpreting dental radiographs is quite similar to interpreting standard radiographs except dental pathologies and radiographic changes may be subtle and some pathologies are unique to the oral cavity. Also, several normal anatomical structures may mimic pathologic changes.
Interpreting dental radiographs is quite similar to interpreting standard radiographs except dental pathologies and radiographic changes may be subtle and some pathologies are unique to the oral cavity. Also, several normal anatomical structures may mimic pathologic changes.
This article highlights the most common oral and dental pathologies, which are illustrated by classic examples. Note that in practice these lesions may often be less obvious. Continuing education meetings and consulting services can give you more confidence with difficult cases.
Determining which teeth have been imaged requires not only a firm knowledge of oral anatomy but also of dental film design. Digital systems with veterinary templates do not require the clinician to determine which teeth are imaged since they are placed into that position by the program, assuming the images were properly placed within the system. If your system does not support a veterinary template, there is a mark on the image in a consistent location. Review the system instructions regarding its use.
Determining which tooth or teeth have been imaged requires three steps. The key involves the embossed dot on one corner of the film.1-4 First, place the convex (raised) side of the dot toward you and do not flip the film over. (This step is automatically done for you when using digital dental film systems.) This is labial film mounting, which is the accepted standard of the American Veterinary Dental College for film viewing. This positioning orients the film as if you were looking at the patient from a few feet away, and your eyes are in the same position that the X-ray tube was in when the film was taken.
Next, determine whether the image is maxillary or mandibular. Then rotate the film so the roots of the maxillary teeth point up, as if you were outside the patient's mouth looking in. Rotate mandibular films so that the roots point down.
Finally, determine whether the film shows the right or left side. Identify which end of the radiograph is toward the front of the patient and which is toward the back. Then imagine that the patient is standing in front of you with its nose pointing toward the front end of the radiograph and facing that direction. If the patient's nose is pointed to the right, you are looking at the right side of the patient's mouth. If the patient's nose is pointed left, you are looking at the left side. When positioned as described above, views of the incisors have right and left swapped, similar to looking at ventrodorsal abdominal films. So the left side of the correctly positioned film is actually the right side of the patient.
Numerous structures within the oral cavity mimic pathologic states depending on the placement of the tube head and film.1,5-8 Knowledge of normal radiographic anatomy will help avoid overinterpretation.
Normal alveolar bone (Figure 1) will appear gray and relatively uniform throughout the arcade unless it is near a tooth root or another anatomical landmark such as a mental foramen. It is slightly more radiolucent (darker) than tooth roots are. It also appears slightly but regularly mottled (uniform throughout the arcade as opposed to mottled in a single area such as with neoplasia). Alveolar bone should completely fill the area between the roots and extend coronally to the cementoenamel junction. The root canals should all be of the same diameter, allowing for root canal width differences in relation to the size of the tooth.
Other than normal anatomical variations, there should be no radiolucent areas in teeth or bone. Normal variations include
Figures 1, 2, 3, 4, 5, 6
Evaluate a suspicious periapical lucency, especially in the area of the mandibular premolars, with an additional film exposed at a slightly different angle (in the horizontal or vertical plane). If the radiolucency is still centered on the apex, it is likely a periapical lesion. If the lesion moves off the apex or disappears, it may be an artifact, normal radiographic anatomy (i.e. mental foramen), or some other pathologic process.
Compare any suspect changes in the width of the root canal of a tooth against the surrounding teeth as well as the contralateral teeth. Evaluate surrounding teeth on the same film as the suspect tooth. The contralateral view should preferably be taken at the same angle as the original. It is important to note that root canals are not exact cylinders, especially those in canines. A lateral view may have a much different canal width than a more vertical one (Figures 7A & 7B).9
Figures 7A, 7B, 8, 9, 10, 11
Finally, a thin white line will be seen over the maxillary canines and premolars (Figure 8), which is the confluence of bones between the palate and maxilla.5
Periodontal (alveolar) bone loss results from a combination of a bacterial infection and an inflammatory host response creating osteoclastic bone resorption.10 Alveolar bone resorption causes the loss of the tooth-supporting structures, which appears radiographically as crestal bone loss to a level below the cementoenamel junction.1,11,12 This decrease in bone height may also expose the furcation. Horizontal bone loss is the most common pattern in veterinary patients.10 This pattern appears as generalized bone loss of a similar level across all or part of an arcade (Figure 9).13 The other pattern is vertical (angular) bone loss, which appears as a single area of recession below the surrounding bone (Figure 10).13 The surrounding bone may be normal or may be undergoing horizontal bone loss. Thus, it is common to have a combination of the two types in the same arcade.
Bone loss does not become radiographically evident until 30% to 50% of the mineralization is lost.13 Thus, radiographic findings will always underestimate bone loss. In addition, bone loss on only one surface (i.e. lingual, palatal, or facial) may be hidden by the superimposition of bone or tooth, which may result in an undiagnosed bony pocket. Always interpret radiographs in light of the complete oral examination findings.
Possible differential diagnoses for bone loss due to periodontal disease include neoplasia, trauma, a foreign body, endodontic disease, bacterial or fungal bone inflammation or infection (osteomyelitis), or a systemic disease such as hyperparathyroidism.
Endodontic disease is defined either as tooth nonvitality or inflammation of the root canal system (root canal, pulp chamber, and dentinal tubules).1,14,15 Vital teeth rarely have radiographic signs of endodontic disease. The classic radiographic signs are created by pulp death and secondary infection of the periapical tissues (periodontal ligament and alveolar bone).
On radiographs, an individual tooth with endodontic disease may have one, some, or all of the changes listed below.1,8,16-18 However, only one needs to be present to establish a presumptive diagnosis of endodontic disease. Radiographic changes can be classified as either changes in the surrounding bone or within the tooth itself.
The classic finding, periradicular rarefaction, appears as a radiolucent area surrounding the apex of a root (Figure 11). On rare occasions, these areas may also be seen midroot, but they will virtually always be associated with periapical disease. Other, more subtle changes include a widened periodontal space, a thickened or discontinuous lamina dura, or even periradicular opacities.
Some superimposed radiolucencies are artifactual. These structures (i.e. mental foramina) can be imaged over an apex and falsely appear as osseous rarefaction. Two clues indicate that superimposed radiolucencies are artifactual. First, superimposed artifacts are typically seen on only one root. In contrast, it is rare to find a true periapical lesion on only one root of a multirooted tooth. In addition, artifacts tend to be regular in appearance, whereas true periapical lesions typically have irregular margins (but can be regular as well).
If any area is in question, it is best to expose an additional film with a slightly different angle. If a periradicular lucency is still centered over the apex, it is likely real and not an artifact.
As a tooth matures, secondary dentin production will cause a decrease in canal width.19 When a tooth becomes nonvital, this development stops secondary to the death of the dentin-producing odontoblasts. Consequently, nonvital teeth have a wider root canal width than the surrounding vital teeth (Figure 12).19 Conversely, on rare occasions, pulpitis may result in increased dentin production and create an endodontically diseased tooth with a narrower root canal width (Figures 13A & 13B). This situation is especially common in teeth that are also periodontally diseased19 and could lead to a misdiagnosis of the endodontically diseased tooth as healthy and vice versa with the contralateral tooth. Hence, it is important to evaluate adjacent and contralateral teeth.
Figures 12, 13A & 13B
Width discrepancy can be compared with any tooth (taking the size of tooth into consideration), but it is most accurate to compare the contralateral tooth. It is important to expose the comparison view at the same angle, as root canals (especially those in the canines in dogs) are not perfect cylinders. A change in the beam angle may affect the canal width on the radiograph.16
Endodontic disease may also be manifested radiographically as internal resorption16 because of odontoclastic activity within the root canal system due to pulpitis. These changes create an irregularly enlarged region within an area of the root canal system (Figure 14).
Finally, external root resorption can be seen with endodontic disease. It will appear as a defect of the root's external surface, generally accompanied by bone loss in the area (Figure 15). External resorption most commonly occurs at the apex in companion animals and is common in cats with chronic endodontic disease.
Differential diagnoses for endodontic disease include normal anatomy, superimposed structures, neoplasia, and cysts.
Several disorders are commonly encountered on dental radiographs of dogs and cats.
Feline odontoclastic resorptive lesions (FORLs)1,12,20-22 are the result of odontoclastic destruction of feline teeth and are classified as either type 1 (no bone replacement) or type 2 (bone replacement occurs).21,23 Odontoclastic resorption will occur at some point on the root surface and progress at varying rates until, in some cases, no identifiable tooth remains.
Studies have reported up to a 65% incidence of FORLs in cats more than 6 years of age.24 Numerous theories on etiology exist, but none have been proven. FORLs are not bacterial in nature, although in some cases the inflammation that activated the odontoclasts may have been caused by bacteria.23,25
Type 1 FORLs (Figure 16) are typically associated with inflammation such as gingivostomatitis or periodontal disease.23,25 Thus, they are commonly associated with periodontal bone loss on dental radiographs. The teeth will have normal root density in some areas and a well-defined periodontal space in areas not affected by the lesion. In addition, a definable root canal in the intact part of the tooth is often present. Type 1 FORLs exhibit resorption of the teeth and tooth roots without bone replacement (absence of dentoalveolar ankylosis).
Figures 14, 15, 16, 17, 18, 19
Type 2 FORLs (Figure 17) are usually associated with localized gingivitis (which can be severe in some cases) on oral examination, in contrast to the more widespread inflammation due to periodontal disease or gingivostomatitis seen with type 1 lesions.23,25 In these cases, the gingival inflammation is secondary to the FORL. These teeth have a different radiographic density as compared with normal teeth, as they have undergone marked replacement resorption. Findings will include areas with no discernable periodontal space (dentoalveolar ankylosis) or root canal. In the late stages, little to no discernable root structure (ghost roots) will be present. In these cases, the lost root structure will be replaced by bone.
Differential diagnoses for FORLs include caries (rare in cats), neoplasia, metabolic disease, or trauma.
The importance of dental radiography in FORL cases cannot be overstated.22 Type 1 lesions typically retain a viable root canal system and will result in pain and endodontic infection if the roots are not completely extracted. However, the concurrent presence of a normal periodontal ligament makes these extractions routine. With type 2 lesions, areas lacking a normal periodontal ligament (ankylosis) also demonstrate varying degrees of root resorption. In these cases, extraction by conventional elevation is difficult to impossible. If there is marked dentoalveolar ankylosis, a tooth with a type 2 FORL may be treated with crown amputation therapy.26 It is my opinion that teeth with an identifiable root canal on dental radiographs must be extracted completely, while teeth with no discernable root canal may be treated with crown amputation. If there is any question, always err on the side of complete extraction.
Carious lesions are the result of acidic degradation of the mineralized dental tissues (enamel and dentin).27 They appear radiographically as radiolucent areas in the crown or root of the tooth (Figure 18). They most commonly occur in domestic dogs on the occlusal surfaces of the molar teeth. However, they can also be seen in interproximal areas, particularly in areas of close tooth proximity. In most cases, an obvious lesion is noted on oral examination. The extent of tooth structure loss will be clinically evident to a certain extent and, thus, help with treatment planning.
As in periodontal disease, remember that about 40% of the mineral in the tooth must be lost before radiographic changes will be noticeable. So radiographs underestimate carious loss as well. Since the owner may elect extraction as opposed to root canal therapy on an endodontically diseased tooth, endodontic involvement must be evaluated before initiation of cavity preparation.
Neoplasia is defined as a growth of abnormal cells that is not responsive to normal growth control.1,28-30 Neoplasms can be further classified as benign or malignant.
Cysts. A cyst is a closed sac lined with epithelium that contains fluid and may become infected or neoplastic or damage surrounding structures. Cystic structures will appear as radiolucent areas with smooth bony edges. Similar to other benign growths, they grow by expansion and, thus, displace the other structures (e.g. teeth). A dentigerous cyst is typically seen as a radiolucent structure centered on the crown of an unerupted tooth (Figure 19).
Benign neoplasia. Most benign neoplastic growths have no bone involvement on dental radiographs. If bone involvement does occur, it will typically be expansive (Figure 20) because benign oral soft tissue neoplasms do not generally directly invade or infiltrate bone. This pattern of growth will result in the bone pulling away from the advancing tumor, leaving a decalcified soft tissue-filled space in the tumor site.28 Bone margins are usually distinct. This expansive growth will typically result in tooth movement.
Malignant neoplasia. Malignant oral neoplasms invade bone early in the course of disease and result in irregular, ragged bone destruction.27 Initially, the bone will have an irregularly mottled, moth-eaten appearance (Figure 21), but radiographs late in the disease course will reveal a complete loss of bone in the area (the teeth will appear to float in space) (Figure 22). If the cortex is involved, an irregular appearance will be seen because of the cortical bone spicules being forced outward. In advanced cases, the root apices may develop a spiked appearance because of root resorption.
Differential diagnoses for neoplastic diseases include osteomyelitis (bacterial or fungal) and periodontal, endodontic, and metabolic bone disease (Figure 23).
Histologic testing is always necessary to accurately diagnose oral masses since a variety of benign and malignant tumors appear radiographically similar. In addition, osteomyelitis can create similar radiographic findings as malignant tumors. Finally, malignant or invasive tumors may show no bone involvement early in the course of disease. Be sure to note the type and extent of any bone involvement on the histologic examination request form (and possibly include copies of the radiographs and pictures) to aid the pathologist. Always interpret the histologic examination results in light of the radiographic findings. Question a diagnosis of a malignancy without bone involvement before initiating definitive therapy such as aggressive surgery, radiation therapy, or chemotherapy. Conversely, a benign tumor diagnosis with marked bone reaction should be further investigated before assuming that the patient is safe.
On dental radiographs, oral traumatic injuries (fractures) appear similar to comparable injuries in the appendicular skeleton. Resolution is the major difference. A postoperative dental radiograph of a case with proper surgical reduction will still reveal a fracture line disturbance (Figure 24). This must be considered when evaluating fracture displacement and fixation quality.
Root fractures and roots in fracture lines (Figures 25A & 25B) must be evaluated in these cases, as they may alter the treatment plan, fixation options, or future therapy. Proper radiographic interpretation is critical in the area of the mandibular first molar in older small- and toy-breed dogs, as pathologic fractures are quite common. These fractures occur when the mandible has been severely weakened by endodontic or more commonly periodontal disease. Standard radiographic resolution is often inadequate for diagnosing small periapical or periodontal lesions that contributed to the fracture. The increased detail of dental radiographs is required for proper diagnosis. Finally, if a mandibular fracture is not responding to what is considered proper therapy, dental radiographs may elucidate the cause of the nonunion (Figure 26).
Figures 20, 21, 22, 23, 24, 25A, 25B
Retained tooth roots after extraction attempts are common in veterinary medicine (Figures 27A & 27B). In most cases, no clinical signs are obvious, but the patient may suffer silently. In rare cases, the retained root may lead to abscess formation, resulting in marked morbidity to the patient and possible legal action from the client.
Figures 26, 27A, 27B
Regardless of the appearance of complete extraction, retained roots or other pathologies are still possible. Thus, postoperative radiographs are critical and must be obtained after all extractions. In addition, they will serve as a legal document in cases with complications. Finally, the AAHA Dental Care Guidelines for Dogs and Cats mandate postoperative radiographs on all extraction cases to ensure complete removal.31
It is impossible to perform proper dental therapy without dental radiography. Appropriate exposure technique and interpretation will greatly improve the quality of dental care within your practice.
Editors' Note: Dr. Niemiec is a co-founder of the dental radiography consultation service VetDentalRad.com.
Brook A. Niemiec, DVM, DAVDC, FAVD
Southern California Veterinary Dental Specialists
5610 Kearny Mesa Road, Suite B1
San Diego, CA 92111
1. Niemiec BA. Dental radiographic interpretation. J Vet Dent 2005;22:53-59.
2. Mulligan TW, Aller MS, Williams CA. Principles of image interpretation. In: Atlas of canine and feline dental radiography. Trenton, NJ: Veterinary Learning Systems, 1998;65-67.
3. Holmstrom SE, Frost P, Eisner ER. Dental radiology. In: Veterinary dental techniques. 2nd ed. Philadelphia, Pa: WB Saunders Co, 1998;107-131.
4. Verstraete FJ. Self-assessment color review of veterinary dentistry. Ames: Iowa State University Press, 1999;101-102.
5. Mulligan TW, Aller MS, Williams CA. Normal radiographic anatomy. In: Atlas of canine and feline dental radiography. Trenton, NJ: Veterinary Learning Systems, 1998;68-90.
6. DeBowes LJ, Deforge DH, Kesel L, et al. Normal canine intraoral radiographic anatomy. In: Deforge DH, Colmery BH, eds. An atlas of veterinary dental radiology. Ames: Iowa State University Press, 2000;3-14.
7. Aller MS. Normal feline intraoral radiographic anatomy. In: Deforge DH, Colmery BH, eds. An atlas of veterinary dental radiology. Ames: Iowa State University Press, 2000;117-135.
8. Glickman GN, Pileggi R. Preparation for treatment. In: Cohen S, Burns RC, eds. Pathways of the pulp. 8th ed. St. Louis, Mo: Mosby, 2002;103-144.
9. Niemiec BA. Fundamentals of endodontics. Vet Clin North Am Small Anim Pract 2005;35:837-868.
10. Wiggs RB, Lobprise HB. Periodontology. In: Veterinary dentistry—principles and practice. Philadelphia, Pa: Lippincott-Raven, 1997;18-231.
11. Hennet PR, Bellows J. Canine periodontics. In: Deforge DH, Colmery BH, eds. An atlas of veterinary dental radiology. Ames: Iowa State University Press, 2000;59-70.
12. Lyon KF, Visser CJ, Okuda A, et al. Feline stomatitis syndrome, periodontal disease, and feline odontoclastic resorptive lesions. In: Deforge DH, Colmery BH, eds. An atlas of veterinary dental radiology. Ames: Iowa State University Press, 2000;159-170.
13. Mulligan TW, Aller MS, Williams CA. Interpretation of periodontal disease. In: Atlas of canine and feline dental radiography. Trenton, NJ: Veterinary Learning Systems, 1998;104-123.
14. Cohen AS, Brown DC. Orofacial dental pain emergencies: endodontic diagnosis and management. In: Cohen S, Burns RC, eds. Pathways of the pulp. 8th ed. St. Louis, Mo: Mosby, 2002;31-76.
15. Wiggs RB, Lobprise HB. Basic endodontic therapy. In: Veterinary dentistry—principles and practice. Philadelphia, Pa: Lippincott-Raven, 1997;280-324.
16. Mulligan TW, Aller MS, Williams CA. Endodontic disease. In: Atlas of canine and feline dental radiography. Trenton, NJ: Veterinary Learning Systems, 1998;124-152.
17. Marretta SM, Anthony JMG. Canine endodontics. In: Deforge DH, Colmery BH, eds. An atlas of veterinary dental radiology. Ames: Iowa State University Press, 2000;35-58.
18. Anthony JMG, Marretta SM, Okuda A. Feline endodontics. In: Deforge DH, Colmery BH, eds. An atlas of veterinary dental radiology. Ames: Iowa State University Press, 2000;149-158.
19. Trowbridge H, Kim S, Suda H. Structure and functions of the dentin and pulp complex. In: Cohen S, Burns RC, eds. Pathways of the pulp. 8th ed. St. Louis, Mo: Mosby, 2002;441-456.
20. Mulligan TW, Aller MS, Williams CA. Acquired defects: caries and regressive changes. In: Atlas of canine and feline dental radiography. Trenton, NJ: Veterinary Learning Systems, 1998;153-169.
21. DuPont GA, DeBowes LJ. Comparison of periodontitis and root replacement in cat teeth with resorptive lesions. J Vet Dent 2002;19:71-75.
22. DuPont GA. Radiographic evaluation and treatment of feline dental resorptive lesions. Vet Clin North Am Small Anim Pract 2005;35:943-962.
23. Reiter AM, Mendoza KA. Feline odontoclastic resorptive lesions: an unsolved enigma in veterinary dentistry. Vet Clin North Am Small Anim Pract 2002;32:791-837.
24. van Wessum R, Harvey CE, Hennet P. Feline dental resorptive lesions. Prevalence patterns. Vet Clin North Am Small Anim Pract 1992;22:1405-1416.
25. Wiggs RB, Lobprise HB. Domestic feline oral and dental disease. In: Veterinary dentistry—principles and practice. Philadelphia, Pa: Lippincott-Raven, 1997;482-517.
26. DuPont GA. Crown amputation with intentional root retention for dental resorptive lesions in cats. J Vet Dent 2002;19:107-110.
27. Wiggs RB, Lobprise HB. Clinical oral pathology. In: Veterinary dentistry—principles and practice. Philadelphia, Pa: Lippincott-Raven, 1997;104-139.
28. Mulligan TW, Aller MS, Williams CA. Osseous lesions. In: Atlas of canine and feline dental radiography. Trenton, NJ: Veterinary Learning Systems, 1998;184-203.
29. Anderson JG, Revenaugh AF. Feline oral neoplasia. In: Deforge DH, Colmery BH, eds. An atlas of veterinary dental radiology. Ames: Iowa State University Press, 2000;159-170.
30. Ogilvie GK, Moore AS. Managing the canine cancer patient—a practical guide to compassionate care. Yardley, Pa: Veterinary Learning Systems, 2006;37.
31. Holmstrom SE, Bellows J, Colmery B. AAHA Dental Care Guidelines for Dogs and Cats. J Am Anim Hosp Assoc 2005;41:277-283.