15.2 Endodontic Anatomy and Morphology

A thorough working knowledge of the morphology of the normal dental endodontic system is essential in order to assess abnormalities and to make a logical decision concerning endodontic procedures [2]. Details of the anatomy and physiology of the structures pertinent to endodontic therapy are covered in previous chapters. The most clinically relevant aspects are reviewed here.

The external shape or morphology of the tooth is divided into three areas. The crown is that portion of the tooth visible above the gingival margin and the root is that portion of the tooth apical to the crown, lying under the gingiva and enclosed in the bony socket. The third area is the neck or cervical area, the junctional point between the crown and the root. The external tooth shape gives the practitioner an approximate localization of the internal structure (see Chapter 1 – Oral Anatomy and Physiology). The interior tooth vault that the pulp occupies is known as the root canal system. The portion in the crown is referred to as the pulp chamber, with its most coronal aspect identified as the pulp horns and the potion located in the root referred to as the root canal. Humans typically have an apical foramen in which the pulp communicates with the periapical periodontal tissues via a single opening, while dogs and cats have multiple microscopic foramina known as an apical delta [3–5]. There are typically between 5 and 20 of these small delta openings that penetrate the root within several millimeters of the root apex [3]. While it is impossible to clean and fill all the minute openings of this delta, sealing the canal in the apical one‐third generally produces an effective treatment [6]. The internal root canal apex or apical terminus is located 1–3 mm from the actual external root apex. The apex of the tooth is the tip of the root and it may be considered to be open or closed. Human teeth are considered to have an open apex due to a large foramen opening but mature dogs and cats are considered to have a closed apex because the multiple foraminal openings are microscopic openings that are not detected on radiographs. Immature, developing teeth of dogs and cats have a large open apex that closes as the tooth matures. As the tooth develops, dentin and cementum are produced at the apex of the root and the root closes. Although the tooth physically appears to have a solid root apex microscopic foramina provide a pathway to connect the pulp to the periodontal tissue. This is customarily called a closed apex. Standard veterinary endodontics typically deals with mature permanent teeth with adequate root apex closure. Immature teeth require alternative procedures to deal with their extremely wide canals (blunderbuss) and possibly open apices that may require additional development prior to endodontic therapy [6].

Lateral or accessory canals may provide passage between the pulp cavity and periodontal tissues in locations other than at the apex. While these are fairly common in human teeth they are less common in dog and cat teeth [7].

The pulp emerges from the tooth and connects with the periodontal ligament at the apical foramen or delta foramina. It is composed of soft connective, vascular, lymphatic, and nervous tissue. It contains odontoblasts, fibroblasts, fibrocytes, collagen fibers, elastic fibers, blood vessels, lymph tissue, and nerves [8]. Dentin, a pale yellow, ivory‐like substance comprised of collagen fibers and hydroxyapatite crystals, surrounds the pulp. The pulpal odontoblasts produce dentin. The odontoblasts function to produce dentin throughout the vital life of the tooth, resulting in thicker dentinal walls and narrower pulp cavities as the teeth mature. This maturing process is sometimes referred to as canal calcification [8]. Dentinal tubules perforate the dentin at right angles to the pulp and contain fluid, nerve fibers and cytoplasmic extensions or processes from the odontoblasts, called Tome’s fibers. In addition to normal aging, attrition, bruxism, pulpal irritation, and some injuries may cause increased dentin production [3, 9]. This increased dentin and calcified canals can result in narrowed canals or constrictions that can be a problem during cleaning and shaping with endodontic instruments [10, 11].

It must be emphasized that there are a formidable number of variations in dental anatomy, not only between species but within as well. Even within the same individual, great variations occur in the degree of calcification, dilaceration, and apical status. One of the most reliable guides for the veterinary dentist on most individuals is multiple radiographic views [2, 12].

15.3 Etiology of Pulpal and Periapical Pathology

The fact that the tooth is a vital structure makes it important to understand the changes that may occur in response to various stimuli. Inflammation, infective or sterile, of the pulp is termed pulpitis, and can be reversible or irreversible. Reversible pulpitis is generally a symptom of pulpal inflammation caused by some form of short‐term irritation such as caries, dental treatment, or trauma [8, 13]. If the cause can be removed or treated the pulp can return to a normal state, but if not and the irritation progresses or is long term then it can lead to irreversible pulpitis [8, 13]. Treatment for reversible pulpitis is generally of a restorative nature. Irreversible pulpitis and chronic inflammation is a pronouncement of impending pulpal death, termed pulpal necrosis, requiring root canal therapy or extraction. Chronic pulpal irritation and trauma‐related pulpitis can result in pulp necrosis, but in the absence of bacterial contamination this necrosis does not cause periapical periodontitis [14]. In contrast, there is a large body of evidence indicating bacterial infection as the cause of pulpal necrosis as well as periapical pathology [8, 14, 15]. Tooth fracture with pulp exposure, severe blunt trauma, advanced caries, tooth resorption (TR) and exposed root dentin that communicates with the pulp can result in irreversible pulpitis. Pupal injury causing pulpitis or even periapical periodontitis could possibly expose these tissues to the anachoretic effect. Anachoresis is thought to occur when bacteria are attracted to an area of inflammation and cause a local infectious process [16]. Bacteria may be carried to the periodontal periradicular tissues by the bloodstream during transient bacteremia or by way of regional gingival lymphatics that extend from the sulcus and periodontal lesions. Although some doubt the validity of this effect, it may explain the sudden onset of acute or chronic periapical involvement of teeth that appear to be apparently sound [16]. Only those conditions that allow bacterial access to pulp tissue result in irreversible pulpitis, necrosis, and periapical periodontitis.

A tooth can be damaged and the pulp injured by blunt or concussive trauma, resulting in inflammation or rupture of pulp vasculature with intrapulpal hemorrhage. Intrapupal hemorrhage may cause the collapse of venules, stopping blood flow and strangling the pulp (pulp strangulation theory) [14]. Because the pulp is in a low compliance environment, enclosed in dentin, pulp inflammation causing vascular permeability and vasodilation increases pulpal interstitial fluid pressure. This pressure increase may compress blood vessels and prevent beneficial blood circulation [9]. Although trauma‐induced pulpitis can potentially lead to pulpal necrosis, pulp is a resilient connective tissue and the inflammatory response usually resolves without necrosis [8, 14]. Some dental traumatic injuries may first present as a pink or blue tinged tooth due to rupture and vascular bleeding inside the pulp cavity. Once the blood or its breakdown components penetrate to near the dentinoenamel junction (DEJ) it becomes visible. If the pulpitis is reversible, the color may eventually diminish and the appearance of the tooth return to normal. If irreversible destruction has occurred, the color changes to a purple or gray as the pulp dies and the blood cell components are degenerated. Initial pain and discomfort during the period when the pulp is acutely inflamed tends to dissipate as the innervation undergoes necrosis. The necrotic pulp breaks down into noxious tissue substances that may escape the apical foramina and cause inflammation of the periodontal ligament and periradicular tissues [14].

Tooth avulsion or luxation interrupts the apical pulpal blood supply with a resultant inflammatory pulp response. With complete severance of the pulpal periapical blood supply an irreversible pulpitis will result in pulpal necrosis. However, with luxation the apical vascular supply may only undergo partial interruption, causing reversible pulpitis and then pulpal repair. Pulp hemorrhage and tooth discoloration may result from tooth luxation or avulsion [14].

Dental treatment has the potential to cause pulpitis due to frictional heat and vibration from motorized instruments, ultrasonic shock waves from ultrasonic instruments, chemicals, and medicaments used to treat exposed pulp and dentinal desiccation from using forced air to dry the tissue [13, 17]. Prevention of pulpitis during dental treatment is directed at using water‐cooled rotary instruments and limiting the use of water‐cooled ultrasonic dental scalers for no more than 30 continuous seconds per tooth [18]. Teeth with exposed dentin should not be completely air dried but remain moist during preparation and treatment. Some chemicals and medicaments used to treat pulp tissue can cause pulpitis but they usually are associated with reversible pulpitis [17]. Iatrogenic electrical shock from pets chewing an electrical cord can result in pulpitis and may be reversible or irreversible.

Another condition occasionally seen with an exposed pulp chamber or canal is hyperplastic pulpitis [19] (Figure 15.1). This condition exhibits itself in one of two forms, hyperplastic granulation and hyperplastic swelling pulpitis. Granulation tissue is usually a reddish rough overgrowth that partially or completely occludes the exposure opening. This results from the pulp attempting to construct a barrier between it and the source of inflammation. In primates, it is seen most commonly in carious lesions of the young. With carnivores, it is more commonly associated with pulp exposures due to fractures. This hyperplastic activity is an indication of the local immune system’s effort to maintain pulp vitality. With simple pulpal swelling the tissue will appear either reddish to blue and have a smooth tight surface. Pulp tissue demonstrating this condition is usually in a terminal change of vital to non‐vital and standard root canal treatment is indicated.

15.3.1 Periapical Pathology

In veterinary dentistry, periapical pathology is diagnosed from dental radiographs and appears as widening of the apical periodontal ligament space or periapical lucency and periradicular bone loss. Radiographic periapical lucencies do not all represent the same and their appearance can vary from tooth to tooth within a patient and among patients. Some will appear as diffuse and faint radiopacities in periapical tissue while others may be obvious circumscribed radiolucent halos surrounding the root apex (Figure 15.2). It should be noted that a definitive diagnosis of periapical pathology can only be made from histopathological evaluation of periapical lesions. Further determination of radicular or periapical cysts can only be made after complete sectioning and histopathological evaluation of all of the affected periradicular tissue [15]. Epithelial tissue reported on histopathology is not sufficient to diagnose apical cysts because it is found in apical granulomas as well as apical cysts, the difference being that cysts are sack‐like structures with a complete epithelial lining whereas granulomas only contain a mixed cell population including epithelial tissue. Therefore, cyst diagnosis can only be made after complete evaluation of a periapical soft tissue lesion. Cysts have only been reported a few times in veterinary patients and are considered rare. Infected pulp tissue is the primary cause of apical periodontitis. After the pulpal tissue becomes infected, bacterial toxins and metabolic byproducts escape from the root canal system through apical foramina to cause an immunoinflammatory response in the periradicular periodontal tissues. Over instrumentation, endodontic materials, medicaments, chemical irrigants, and trauma can cause periapical periodontitis. It is unlikely that sterile necrotic pulp can stimulate periapical periodontitis [14]. Periapical tissues have good collateral circulation, which allows for the building of a defensive barrier in an attempt to confine the pathogens and their toxins within the root canal system. Whether an acute or chronic process develops is dependent upon virulence of the organism, degree of organism challenge, and host immunoinflammatory response. Since bacterial infection in the pulp is the inciting factor, status of the pulp has to be considered together with periapical disease.

In human dentistry, several systems of categorization of apical periodontitis have been proposed that include clinical and histological findings in periapical pathology. These systems have included patient evaluation of pain perception and normal tissue parameters [14]. The World Health Organization (WHO) categorizes human apical periodontitis into five groups: acute apical periodontitis of pulpal origin, chronic apical periodontitis, periapical abscess with sinus, periapical abscess without sinus, and radicular cysts [14, 20]. The WHO categories will be used to define periapical pathology in this text as they are more suited to a discussion of veterinary periapical pathology [15].

Acute apical periodontitis of pulpal origin is the first line of defense initiated by the innate immune system in response to an extension of apical pulpitis into the apical periodontal tissues [3]. Acute apical periodontitis results in few periapical signs other than tenderness or pain on palpation or percussion, and this can be difficult to assess in the veterinary patient. Radiographs generally appear normal, although slight widening of the periapical periodontal ligament space may be seen. It may be associated with either vital or non‐vital teeth. If left untreated, acute apical periodontitis may progress into one of the following: chronic apical periodontitis, periapical abscess, with or without sinus, or radicular cyst.

Chronic apical periodontitis is a long‐term immunoinflammatory reaction involving the innate and adaptive immune systems in response to pulpitis [21]. With the advancing pulpal infection and inflammation, the inflammatory mediators stimulate osteoclast differentiation with resultant dissolution or resorption of periapical bone [14, 15]. This resulting disease produces the classical periapical lucency seen on radiographs [12, 15]. Although the immune systems are unable to eliminate the irritants they maintain an active defense response and there appears to be a balance between the pupal infection and the host immune response. Chronic apical periodontitis may establish itself as a chronic periapical granuloma. Granulomas have the same radiographic appearing lucencies as periapical cysts and they can only be differentiated histologically [14, 15]. Even though cysts and granulomas cannot be differentiated radiographically, they are caused by bacterial pulp infection and endodontic treatment is indicated.

Periapical abscess implies a painful collection of purulent exudate of sudden onset at the apex [14]. Technically, a periapical abscess cannot be diagnosed without histologic confirmation [14]. In man, signs are slight to severe swelling and pain, with some patients being febrile. The stoic nature of animals makes recognition of these signs difficult unless there is gross or obvious tissue swelling. Radiographically, as with acute apical periodontitis, no signs may be apparent, due to a lack of duration to cause dissolution or resorption of the periapical lamina dura. When radiographic changes are present, it may indicate the abscess is a flare‐up of a previous asymptomatic chronic lesion, sometimes called a phoenix abscess. In some cases, development of a sinus tract allows for the escape of toxins and the suppression of symptoms, which is identified as a periapical abscess with sinus. These sinus tracts may be seen facially or suborbital, ventral‐mandibular, or within the oral mucosa, either gingival or at the mucogingival line (Figures 15.3 and 15.4).

Radicular cysts may form as a result of stimulation of the epithelial cell rests of Malassez by inflammatory mediators [14, 15]. If the epithelial lined cyst communicates with the apical foramen or foramina it is a pocket cyst. If epithelium completely surrounds the cyst without communication with the pulp it is known as a true cyst. Radiographically cysts appear as periapical lucencies associated with the root apex. Periapical cysts have been rarely reported in veterinary literature [15, 22, 23]. While radicular cysts are recognized in humans, they are seldom diagnosed in dogs.

Condensing osteitis is a radiographic sign associated with chronic periapical periodontitis, causing reactive bone formation and increased radiodensity of periradicular alveolar bone. In this condition, pulpal inflammation may stimulate osteoblastic activity, causing reactive bone formation with resultant focal periapical radiodensity [12, 15]. It is the osseous response observed in teeth with previous endodontic treatment or low‐grade pulpal infection with corresponding strong immune defense and local tissue resistance. Idiopathic or focal osteosclerosis is a similarly described radiodensity of the periapical alveolar bone seen on dental radiographs. Osteosclerosis is ascribed to teeth having no endodontic disease and it is most commonly seen as a benign condition in dogs with excessive chewing habits. This is relatively asymptomatic in most cases. Low‐grade chronic pulpal inflammation of vital teeth, such as seen in occlusal stress (bruxing, excessive chewing, etc.) can induce this excessive periapical mineralization [15, 21]. Condensing osteitis and osteosclerosis are relatively asymptomatic and may be associated with some radiographic widening of the periapical periodontal ligament space [24].

Radicular ankylosis and external root resorption can eventually occur in some chronically infected endodontic cases [24]. Radiographically this presents as the loss of the periodontal ligament space and root tissue, giving the appearance of tooth root merging with adjacent bone and resulting in the loss of a distinctive root image.

Periradicular osteomyelitis radiographically appears as an osteopenia and expansion effects of the alveolus seen in some cases of chronic pulpal inflammation [24]. This appears most commonly around the cuspids of the cat involved with tooth resorptive activity. It is not uncommon in these cases for a degree of osteosclerosis to be present.

The osseous radiographic conditions most commonly reported are condensing osteitis or chronic focal sclerosing osteomyelitis [24]. Condensing osteitis and periapical osteosclerosis are indistinguishable radiographic signs seen as increased bone density involving periapical and periradicular alveolar bone.

If endodontic disease remains undiagnosed and intraradicular infection persists, the periapical tissues can be in flux between the different types of apical periodontitis. Additionally, the patient may experience asymptomatic periods as well as intense pain dependent on the type and severity of apical periodontitis present. In order for the veterinarians to fulfill their advocacy role for animals, they must be able to perform and interpret dental radiographs and then couple those findings with presenting history and physical findings to properly assess endodontic dental disease. Inadequate training and facilities for dental diagnosis and treatment should not be an excuse because trained veterinary dentists are available to help with diagnosis and treatment. If endodontic infection is certain and endodontic treatment is not an option then extraction is required.

15.4 The Endodontic/Periodontic Relationship

The stable function of a tooth is determined by its structural integrity, periodontal attachment, and support component. Endodontic and periodontic soft tissues are intimately related through accessory or lateral canals, furcation canals, apical foramen or delta, periodontal ligament, and exposed root dentinal tubules [26]. Therefore, it would seem logical that infection in either the endodontic system or the periodontal apparatus may cross‐contaminate or infect the other system. This is generally true; however, there is lack of a large body of evidence and research to implicate periodontal infection as a frequent cause of endodontic infection [27]. Although it seems likely that periodontal disease can spread to the endodontic system through exposed dentinal tubules, lateral or accessory canals, and the apical foramen or delta, some research in animals indicates that it may not happen unless dentinal tubules are exposed [27]. Cementum protects the root dentin and prevents bacterial entrance from the periodontium to the dentinal tubules while a rich pupal blood supply protects the pulp from periodontal inflammatory mediators and bacterial toxins. When open dentinal tubules of the root surface are exposed to periodontal infection (bacteria) ensuing pulpitis may be either reversible or irreversible. With either reversible or irreversible pulpitis, sclerotic dentin can be produced on the adjacent pulp canal wall and effectively seal the dentinal tubules from further bacterial irritation. Chronic periodontal disease can also cause mineralization of the pulp canal, resulting in a narrowed pulp canal [27].

Because pulpal disease can be primarily endodontic in origin, or even possibly secondary to periodontal disease, classification of the lesions as to the primary and secondary elements can provide a speculative prognostic guide for treatment [26, 27]. The relationship can be classified as primary endodontic disease, primarily endodontic with secondary periodontal involvement, primary periodontal disease, primarily periodontal lesions with secondary endodontic involvement, true combined lesions, or concomitant lesions. True combined lesions are found in teeth that have both endodontic and periodontal disease in the same tooth. Another classification is concomitant endodontic and periodontal lesions where there are two separate lesions in the same tooth but with different causes. In multirooted teeth, an endodontic lesion may be found in one root and a separate periodontal lesion found in another root. True combined or concomitant lesions may be hard to differentiate once they coalesce.

In veterinary dentistry, classification of endodontic and periodontal lesions and their relationship to each other is largely dependent upon physical and radiographic findings. Physical findings are typically those related to external facial signs, oral cavity examination, dental evaluation, and periodontal probing [3]. Pulp testing, used in evaluating human teeth, is of little or limited value in veterinary dentistry because it requires cooperation and a positive or negative response from the patient [28].

Teeth showing primary endodontic disease usually have crown fractures with or without pulp exposure and typical radiographic periapical lucency or a “halo” at the root apex. They do not have any radiographic periodontal signs. Physical signs can include facial or mucosal swelling over the root, and sometimes a draining sinus or fistula can be found in the mucosa around the tooth or externally on the face or ventral to the jaws.

Teeth with primary endodontic and secondary periodontal disease have a radiographic periapical lucency or halo that continues into a wide periodontal ligament space that follows the root architecture to the gingival margin. These lesions are known as “J” lesions. A periodontal pocket may be found when probing these teeth.

Primary periodontal lesions have a “wedge”‐shaped widened periodontal ligament space where the wide part of the wedge is coronal and the point of the wedge is apical. There can also be furcation bone loss noted on radiographs. Periodontal probing will reveal a periodontal pocket.

Primary periodontal lesions with secondary endodontic involvement have deep periodontal pockets and furcation bone loss from long‐standing periodontal disease that exposes the endodontic tissues to infection through exposed dentinal tubules, accessory canals, or the apical delta. There may not be any clear radiographic signs that distinguish this condition from primary endodontic with secondary periodontal disease.

In the early stages of true combined or concomitant endodontic and periodontal lesions the radiographic and physical signs may be distinguishable as separate lesions in the same tooth; however, once the two lesions coalesce, they become indistinguishable from primary endodontic and secondary periodontal lesions. If endodontic and periodontal lesions occur in different roots of the same tooth they are readily distinguishable.

Because each classification carries a different prognosis it is important for the practitioner to be able to adequately evaluate the endodontic and periodontic disease relationship for proper treatment planning [26]. With regards to endodontics, when the crown still has good integrity and the roots have not been fractured, a tooth with a primary endodontic lesion has a very good to excellent prognosis while a tooth with primary endodontic lesion and secondary periodontal lesion has a good prognosis. Teeth with combined or concomitant lesions have a more questionable prognosis and treatment outcome depends upon the correct identification of pathology and tissue destruction. In veterinary dentistry these teeth have a fair to poor prognosis; however, a combination of endodontic and periodontic treatment can be successful. An alternate treatment for teeth with concomitant lesions would be endodontics and hemi‐section or root resection to salvage part of a tooth and preserve some function [29] (Figures 15.5 and 15.6).

Generally, a tooth needs the periodontium to be in good health with its independent vasculature and nerve supply to maintain a healthy attachment. Therefore, extensive periodontal disease can give a tooth a poor prognosis, so the endodontic procedure may be unwise.