6.3.1 Prevalence

Historically, the epidemiology of TDI has been poorly studied. As a result, very little data on the prevalence of TDI in dogs and cats are available. Only a few studies have fully investigated the topic [1, 3]. Most available studies have focused solely on dental fractures and have generally ignored luxation injuries [2, 14]. In addition, the few available studies have not utilized a standardized classification system. As a result the reported prevalence of TDI varies considerably. The prevalence of dental fractures in dogs has been reported between 2.6% and 27% [2, 14]. The prevalence of TDI in dogs and cats with concurrent maxillofacial fractures increases dramatically to just over 70% [3, 15]. A recent study in the United States has shown a high prevalence of TDI in dogs and cats that is consistent with the prevalence of human TDI. In the study, 26.2% of dogs and cats had at least one TDI with a mean of 1.45 TDI per patient [1]. The worldwide prevalence may vary due to socioeconomic, behavioral, and cultural diversity. Several injuries (e.g., concussion, subluxation, root fracture) are likely to go undiagnosed due to lack of acceptable diagnostic ability and/or skill, which varies between veterinarians and veterinary practices.

6.3.2 Distribution by Sex, Age, and Breed

Within the general population, there appears to be no obvious sex predilection as males and females have a similar frequency of TDI [1]. However, when TDI associated with concurrent maxillofacial fractures is considered, young male animals are overrepresented, which may be related to the stereotypical young male behaviors [3, 16]. Although juveniles tend to have more TDI associated with maxillofacial fractures, within the general population TDI prevalence tends to increase throughout adolescence and peaks between three and six years of age [1] (Figure 6.1). After six years of age, the prevalence tends to drop off [1]. This may be explained either by the more docile nature of older animals; by an increase in dentin thickness from continued dentinogenesis, which makes the tooth more fracture resistant; or by a combination of both (and possibly other) factors. No obvious breed predilection has been reported. However, in one study, German Shepherd Dogs were the second most common breed affected with TDI [1].

6.3.3 Teeth Involved

Studies have shown that the majority of TDI occur in the upper jaw and most affect the rostral oral cavity (incisors and canines) [1–3, 14]. The most commonly injured teeth are, in order of decreasing frequency, the canine teeth, the premolar teeth, the incisor teeth, and the molar teeth [1, 14]. Considering only luxation injuries, the teeth most commonly affected are the canine and incisor teeth and are most often concussion injuries [1, 3]. Of the fracture injuries the premolar teeth have the highest frequency followed by the canine teeth, incisor teeth, and, lastly, molar teeth [1, 14]. The majority of TDI occur in strategic (canine and carnassial) teeth. Of the carnassial teeth injured, the vast majority of TDI are sustained by the maxillary fourth premolar teeth [1, 14]. Most injuries affect single teeth. However, luxation injuries and alveolar fractures often involve several sequential teeth.

Some distinct patterns of TDI are seen with specific mechanisms. A very good example of a typical TDI pattern is that seen in cats, which have sustained trauma associated with high‐rise syndrome. In addition to typical soft tissue and maxillofacial fracture patterns, specific teeth are usually traumatized. The initial impact of the cat hitting the surface is to the ventral mandible. The energy is then distributed into the maxilla causing mandibular molar and maxillary fourth premolar fractures [15]. Additionally, after the chin makes contact, one or both maxillary canines will make contact with the substrate, leading to maxillary canine fractures [15]. These maxillary canine fractures are also seen in cats that have presumably jumped off elevations within the home and have hit the teeth on the ground. In addition, it has been shown that the direction from which the traumatic force comes has a significant influence on the fracture pattern of dog canine teeth [17]. This information may give the clinician and owner some clue as to possible mechanisms of injury.

6.3.4 Types of Injuries

TDI are broadly categorized as either dental fractures or luxation injuries. Dental fractures are the most common injury at 82.3% of all TDI [1]. Enamel‐dentin‐pulp fractures were reported to be the most common TDI in one study followed by concussion and enamel‐dentin fractures [1]. However, enamel‐dentin fractures may be much more common than reported as they often go undiagnosed and untreated. Luxation injuries are much less common than dental fractures. However, they may also be more prevalent than reported because many concussion and subluxation injuries ultimately go undiagnosed. Most of the luxation injuries reported in a recent study were concussion injuries [1]. Most (66.8%) TDI are considered severe injuries that result in significant consequences if not treated in a timely fashion [1, 3]. For the purposes of discussion in this chapter, we will group TDI into four major categories: crown fractures, crown‐root fractures, root fractures, and luxation injuries.

6.4.1 Mechanisms

TDI may be caused by any collision with sufficient force to overcome the natural resistance of the dentoalveolar apparatus, such as altercations with other animals, motor vehicle accidents, falls from height, contact with a moving object, or simply sustained during playful activity, collision with another animal or object, or even during chewing/mastication. However, as these injuries often occur during unsupervised activities, the mechanism of injury is often unknown [1–3, 14], which increases the challenge of conducting highly fruitful epidemiological studies. In one study, German Shepherd dogs were found to be the second most common breed affected by TDI [1]. The duties in which this breed and other similar military and working breeds are often engaged may be considered a predisposing mechanistic factor for TDI. Some teeth may be biomechanically compromised and more susceptible to fracture under normal oral loads. Many dogs, especially military and police dogs, sustain distal abrasion (AB) of the canine teeth (i.e., cage chewer syndrome) through oral parafunctional habits [18] (Figure 6.2). This particular abrasion pattern creates a stress concentration point that decreases the fracture resistance of the tooth [19, 20].

6.4.2 Behavior

Numerous studies have shown an association between age‐related behavior and trauma [3, 16]. Young animals are known to be more exuberant, curious, and playful, which increases the likelihood of roaming, engagement in risky activities, and engagement in altercations with other animals, which in turn increases the risk of sustaining TDI.

Innate behavioral traits may also put certain animals at risk for acquiring TDI. For example, curiosity is a behavior innate to most cats. This curiosity often puts them into situations (e.g., perching and walking on elevations) where the risk of obtaining TDI is increased.

A probable causative factor in cage chewer syndrome discussed above is hyperactive behavior and anxiety disorders. In some working dogs, hyperactive behavior may be selected as a desirable trait that aids in their job performance. Hyperactivity is known to be an etiologic factor in the prevalence of TDI in children [21]. However, these behavioral traits alone do not cause the abrasion pattern that makes the teeth biomechanically weak. In the previously described scenario, the animal must have an abrasive object, such as a metal bowl or cage, to chew on in order for the behavior to manifest in dental abrasion, which brings us to a discussion of the animal’s environment as an etiologic factor.

6.4.3 Environment

Often the animal’s surrounding environment may contribute to the risk of acquiring TDI. Some examples of how the environment influences the risk of TDI include: multipet households may increase the level of competition and, thus, altercations; clutter and the presence of unsafe objects in the area where animals are housed invite opportunities for collisions; homes with elevations such as balconies provide unsafe environments for cats that enjoy perching behaviors.

The pet owner can control some environmental factors, such as removal of metal bowls and cages and other unsafe objects. However, some environmental factors are beyond human control. Environmental and behavioral factors coalesce in regard to the influence of seasons and lunar phases on animal behavior. Studies have shown seasonal patterns of increased maxillofacial trauma in warmer seasons [22]. Additionally, a recent study has shown an increase in the frequency of maxillofacial trauma surrounding a full moon [22]. We also know that nearly three out of every four maxillofacial trauma patients have at least one TDI, which represents a nearly threefold increase in the prevalence of TDI over the general population [3]. Therefore, any etiologic factor contributing to maxillofacial trauma should be considered to have a similar impact on TDI.

Likewise, environmental factors are important when considering “high‐rise syndrome” in cats, which, concurrent with a typical pattern of maxillofacial fracture, presents with a typical TDI pattern [15]. Cats that are placed in a risky environment (e.g., access to elevated patio/balconies) are at an increased risk of elevated falls and are much more likely to sustain TDI than cats that do not have similar access to elevations.

6.5.1 History

While information related to the timing and nature of the injury is incredibly beneficial in determining the most appropriate treatment method, this information is typically absent in veterinary patients. TDI more often occur in the absence of a witness who can speak to the mechanism and the exact timing of the injury. As a result, TDI are often incidental findings of the owner or veterinarian, which can negatively impact the prognosis for endodontic therapy. However, an effort should still be made to gather as much information as possible from the owner. Historical information regarding when, where and how the injury occurred and any previous injury or treatment may be useful in determining the most appropriate diagnostic and/or treatment method as well as future prevention.

6.5.2 Clinical Examination

6.5.2.1 Oral Examination

A thorough oral and maxillofacial examination is the first step in the proper management of any trauma to the oral and maxillofacial region. Use of a standardized examination chart is recommended. All oral and extraoral soft tissue wounds should be noted as they may be telling as to the nature of the injury or the likely dental and maxillofacial manifestations. Additionally, soft tissue wounds may have foreign material and/or dental fragments imbedded within (Figure 6.3).

Prior to fully examining the dentition for possible TDI, the oral cavity should be gently cleansed of dried blood and debris as this material may make injuries undetectable. Evaluation of the full extent and direction of the dental injury, as well as the magnitude when dealing with a luxation injury, is important information for determining an injury classification. If possible the patient’s occlusion should be assessed prior to intubating as this may provide revealing information for subtle luxation injuries or jaw fractures.

The clinical examination of individual teeth makes up a substantial contribution to the clinical decision‐making process in TDI. Because of the lack of objective and consistent feedback from dogs and cats, evaluation is a challenge that is unique to the practice of veterinary dentistry.

6.5.3 Diagnostic Imaging

6.5.3.2 Computed Tomography

While computed tomography (CT) has shown to be a crucial tool in the accurate diagnosis of maxillofacial trauma, the spatial resolution is generally considered suboptimal when evaluating the dentition [41]. However, given the prevalence of this imaging modality in veterinary medicine, it may prove beneficial in the diagnosis of some specific TDI. This author has successfully utilized CT for the diagnosis of vertical root fractures where traditional intraoral radiography has proven ineffective. When utilizing CT for imaging the dentition, utilizing an optimal CT protocol is crucial. In a recent study the optimal CT conditions in which to image the canine dentition was shown to be a sequential mode with slice thickness and interval no larger than 1 mm with a high‐frequency image reconstruction algorithm and an additional moderate edge enhancement [42] (Figure 6.4).

6.6.1 Dentin–Pulp Complex Response

Dentin is a complex mineralized structure that makes up the bulk of the tooth structure of a mature tooth. Dentin is a permeable structure composed of tubules, which traverse the dentin from the dental pulp to the dentinoenamel junction. These dentinal tubules create a highly permeable tissue that serves as a potential pathway for bacterial contamination of the dental pulp. In the healthy tooth, the dentinal tubule contains an odontoblastic process (see below), collagen fibers, and nerve fibers.

The dental pulp consists of four organized and named layers. The outermost stratum of the healthy pulp is the odontoblast layer, which lies immediately subjacent to the dentin. The odontoblast is the cell responsible for dentin production and possesses a process that extends into the dentinal tubules. Disturbances to dentin result in pulpal consequences. In turn, disturbances in the dental pulp impact the quantity and quality of dentin produced. For this reason it is useful to consider the dentin and pulp as an integrated, dynamic unit known as the dentin–pulp complex.

In the event of a peripheral insult, such as an enamel–dentin fracture, the odontoblasts within the region of insult have the potential to respond in a reparative way. The earliest response of the pulp is to decrease dentin permeability. Through a process known as dentin sclerosis, mineral crystals are deposited within the dentinal tubules. In addition, the surviving primary odontoblasts can be stimulated to produce a type of tertiary dentin often referred to as reactionary dentin (Figure 6.5). If the primary odontoblasts do not survive, newly differentiated odontoblasts can be recruited to the site of injury and produce a second type of tertiary dentin called reparative dentin (Figure 6.5). Dentin sclerosis and tertiary dentin often give a clinical appearance to the tooth of a central brown spot, particularly in areas of abrasion/attrition (Figure 6.6). If the process is slowly progressive, the dentin–pulp complex may be able to effectively protect itself and prevent pulpitis via dentin sclerosis and/or tertiary dentin. However, if the insult is prolonged, more rapid, or more severe, the pulp undergoes an inflammatory/immune reaction, which can become irreversible and result in a non‐vital/necrotic pulp. In addition, if the insult is rapid enough, the pulp cannot respond quickly enough to effectively decrease dentin permeability, which can lead to direct pulp exposure.

6.6.2 Pulp Response to Full and Near Pulp Exposure

Pulpal exposure, if left untreated, will result in pulpal necrosis and apical periodontitis (Figure 6.7). Although the patient will be in pain, the process of pulpal inflammation resulting in pulpal death and necrosis may take weeks to months. Within the first 24–48 hours after pulp exposure the inflammation (pulpitis) is primarily proliferative and limited to the superficial 2–5 mm of the pulp [44–47]. During this time, the chance of bacterial contamination is relatively low. After 48 hours, the inflammation progresses apically, the chance of bacterial contamination increases, and the likelihood of maintaining a vital tooth decreases dramatically. As the zone of inflammation and bacterial contamination progress apically, the superficial pulp begins to become necrotic. This new zone of necrosis also rapidly advances apically.

Stay updated, free articles. Join our Telegram channel

Join