Periodontal and Endodontic Disease

Periodontal and endodontic diseases are common in small animal practice and are similar in several ways:

• The basic pathology is inflammation resulting in bone resorption.
• The cause is most commonly contamination by oral flora.
• The end result of the pathologic process is loss of the tooth, permitting the adjacent tissues to recover from the chronic infection.

The major difference between periodontal and endodontic diseases is the location of the primary lesion.

Periodontal disease is centered in the periodontium (gingiva, periodontal ligament, alveolar bone, cementum), spreading along the periodontal space toward the root apex and causing loss of alveolar bone as it progresses. If allowed to continue to develop, it will eventually affect the periapical region of the tooth root, leading to retrograde pulpal infection. Thus, endodontic disease can occur as a result of severe periodontal disease.

Endodontic disease is centered in the pulp cavity, as a result of inflammation or necrosis of the pulp inside the tooth. The pathology spreads outward through foramina at the root apex or other areas of the root surface to involve the periodontal ligament and alveolar bone. If allowed to continue to develop, it will eventually affect more coronal areas of the periodontium. Thus, periodontal disease can occur as a result of severe endodontic disease.

Periodontal and endodontic disease may co-exist in the same tooth. It is often possible to recognize radiographically which condition was first to appear. When the condition starts as periodontal disease, subsequently spreading to involve the periapical region of the tooth root, it is referred to as periodontal-endodontic lesion. When the condition is primarily centered at the periapical region of the tooth root, secondarily affecting the mid- or coronal tooth-supporting alveolar bone and causing a fistula through the gingival attachment into the oral cavity, it is referred to as endodontic-periodontal lesion. Regardless of what came first, treatment must include both aspects of the disease (although many teeth with "perio-endo" or "endo-perio" lesions are so severely affected that extraction often is the only practical treatment option).

Periodontal Disease

Periodontal disease is the most common disease occurring in domestic dogs and cats and is defined as plaque-induced pathology of any part of the tissues that hold the tooth in the mouth - the gingiva, periodontal ligament, alveolar bone, and cementum. When accumulation of plaque is prevented by effective oral hygiene, periodontal disease does not develop [1]. Local severity and systemic impact on the rest of the body are reasons that companion animals should receive an oral examination every time they are seen by a veterinarian. Periodontal disease is often separated into two clinical conditions.

Gingivitis is an inflammation of the gingiva, presenting clinically as reddening and edema initially at the gingival margin and progressing to visible ulceration and spontaneous bleeding. Gingivitis is reversible if dental plaque is removed by home or professional oral hygiene procedures.

Periodontitis is an inflammation and destruction of the non-gingival periodontal tissues and can be thought of as "alveolar bone osteomyelitis." It is diagnosed clinically as "loss of attachment" (i.e., the connective tissue attachment between the root and the alveolar bone no longer extends to the level of the cementoenamel junction [CEJ] of the tooth), which is recognized:

• Because gingival recession exposes part of the root.
• When a gently applied blunt-tipped probe can be passed between the tooth root and the gingiva into a periodontal pocket apical to the CEJ.
• Radiographically as horizontal or vertical alveolar bone loss.

Anatomy, Pathophysiology, and Oral Environment

The gingiva provides a thick protective cap to the alveolar margin (the tip of the alveolar bone closest to the crown). The marginal gingiva abuts the tooth crown and is not attached to bone but held in place by the hemidesmosomal attachment of the sulcular epithelium to the enamel surface. The periodontal ligament holds the tooth in the jaw by means of fibers and provides a shock-absorbing effect to prevent fracture of teeth during forceful occlusal action. The alveolar bone surrounding the roots has the most rapid turnover of any bone in the body. The alveolar margin is the critical area in development of periodontitis.

Evaporation causes the salivary fluid to become deposited as a glycoprotein layer (the pellicle) on the tooth crowns, entrapping bacteria. Plaque is the developing biofilm on the surface of the teeth. The salivary fluid in which the teeth are bathed has antibacterial properties (lysozyme, lactoferrins, IgA with specific antibodies), and the combination of this antibacterial activity and daily occlusal scrubbing works well to keep the plaque from getting out of hand under "normal" conditions. Excellent long-term oral health is easy to achieve if daily oral hygiene is impeccable [1]. When oral hygiene is less than optimal and plaque is allowed to accumulate, it becomes thicker and more complex, and the protective components in oral fluids have less effect on the microbial inhabitants in the deeper layers. Calculus forms when calcium carbonate and other calcium salts in salivary fluid crystallize on the tooth surface, mineralizing the soft plaque into a hard material. Following dental scaling, it takes 2 to 3 days for plaque to become sufficiently mineralized to form calculus that resists being readily wiped off by dental abrasion. Calcium salts are more likely to be deposited on plaque in an alkaline environment. The mouths of dogs and cats are slightly alkaline (oral fluid in humans is usually slightly acidic). Thus, dogs and cats are more prone to deposition of calculus than are humans [2].

Plaque Development and Periodontal Infection

When occlusal scrubbing is insufficient or infrequent, plaque thickens and matures. In the deeper part of plaque, the oxygen is strangled out of the fluid as a result of metabolism of aerobic organisms, and an anaerobic environment is established. This is unique to the plaque on teeth because of the lack of vascularity of the enamel surface on which plaque forms. Gingivitis and periodontitis are referred to as "bacterial infections," but several hundred bacterial species have been identified to date in normal and diseased mouths of dogs and cats [3]. Plaque development on a clean tooth surface following dental scaling follows a predictable pattern:

1. Colonization of the pellicle by aerobic cocci.
2. Adhesion of aerobic rods on the sticky and irregular surface provided by the growing coccal layer.
3. The aerobic cocci and rods multiply, and as they do so, the oxygen gradient in the thickening plaque changes so that at its deepest point oxygen is no longer available. The occasional obligate anaerobes caught deep in plaque can now grow. Plaque maturation to the point where it will support anaerobic organisms takes about 24 hours in the dog.
4. The biochemical environment changes, as plaque continues to mature, and is enriched by products of gingival inflammation. The mixture of microbial detritus and products of inflammation forms a physical and chemical environment that allows spirochetes and other organisms with complex growth requirements to thrive.
5. A “climax biofilm community” results - a semi-stable state in balance with available nutrients and oxygen, made more complex in the case of plaque by the presence of calculus, which provides protected spaces in an anoxic and nutrient- rich environment.

Periodontopathogens are bacteria that are the putative cause of gingivitis and periodontitis. They (a) are cultured more commonly from diseased individuals than from non diseased individuals and from diseased areas of the mouth than from healthy areas in the same individual; (b) produce toxins or tissue-destructive enzymes such as matrix metalloproteinases; (c) show cytotoxic effects on tissue culture; and (d) reveal other "virulent factors." DNA probe technology has allowed recognition of a group referred to as pathogen-related oral spirochetes (PROS) in dogs as well as in humans [4]. Carnivore and human oral floras have many similarities, but also some important differences. The gram-negative anaerobic rod Porphyromonas gingivalis is considered to be the key human periodontopathogen. A catalase-positive form of P. gingivalis is found commonly in canine and feline periodontal specimens and is recognized as a distinct species - Porphyromonas gulae [5]. Other recognized canine and feline Porphyromonas organisms include P. cangingivalis, P. canoris, P. cansulci, P. crevioricanis, and P. gingivicanis [6].

Progression of Periodontal Disease

As with bacterial infections in any other tissue, the initial effect is inflammation (gingivitis). Neutrophils are attracted to the site, move onto the epithelial surface through large intercellular spaces of the sulcular epithelium, and engulf, ingest, and digest the plaque bacteria. When a pathogenic plaque mixture is present, many neutrophils become over-full and burst, and some retire into the adjacent tissue before they burst; bursting neutrophils release bacterial toxins and destructive enzymes, including matrix metalloproteinases (e.g., collagenase) within tissue, causing breakdown of connective tissue integrity. The bursting neutrophils also release pro-inflammatory cytokines (e.g., IL-1β, IL-6, PGE2 and TNF-α) that propagate the inflammatory response. The sulcular epithelial layer ulcerates, exposing the more vulnerable connective tissue to direct bacterial invasion. As the destructive inflammatory-infective mixture descends deeper into the tissue, inflammation-induced resorption nibbles away the alveolar bone to produce periodontitis. Continuing bone loss causes instability of the attachment and mobility of the tooth, which is pushed against the remaining bone during chewing. This further enhances alveolar bone resorption by squeezing the blood vessels adjacent to the tooth. In an aging toy-breed dog with severe periodontitis, only a match-stick of mandibular bone may be present adjacent to the roots of the large first molar tooth, and pathologic fracture of the mandible is possible (Fig. 22-1). If the process continues for long enough, the eventual result is loss of the tooth. This is actually a defense mechanism - finally, the remaining tissues can recover because the presence of the constant overwhelming plaque bacterial burden has been removed.

Figure 22.1. Dog with severe periodontitis. (A) Excessive plaque and calculus accumulation at mandibular incisor, canine, and premolar teeth. (B) Dental radiograph of left mandibular premolars and molars showing advanced loss of alveolar bone; the mandible is at risk of pathologic fracture.

In the (usually long) period between the initial gingivitis and the final exfoliation of the tooth, bacteria adjacent to capillaries are squeezed into the vascular space, causing bacteremia. Bacteremia secondary to periodontal disease occurs daily in patients with gingivitis and active periodontitis, and it is normally rapidly cleared by the reticuloendothelial system in otherwise healthy patients [7]. Bacteremia is accompanied by chronic body-wide release of inflammatory mediators, immune complexes, and bacterial and cellular degradation by-products that may produce direct or immune-mediated distant organ pathology. The long-term consequences of these intravascular effects are the subject of ongoing investigations. It is known that an association exists between severity of periodontal disease and distant organ abnormalities in both humans (Table 22.1) [8] and dogs [9,10]. Circulatory markers of systemic inflammation are increased in dogs with more severe periodontal disease; they decrease following periodontal treatment [11]. Studies are underway to determine whether the cause (plaque → gingivitis/periodontitis → bacteremia/systemic inflammation) and effect (distant organ damage) hypothesis is correct.

Prevention and Therapy

Prevention is primarily directed at removing or reducing subsequent accumulation of plaque and calculus, or at suppressing the tissue-destructive effects of the inflammatory response. Professional supra- and subgingival scaling as needed, followed by daily tooth brushing, is the "gold standard" for prevention. Products that enhance dietary abrasion or chemically suppress plaque or calculus deposition are recognized by the Seal of Acceptance system of the Veterinary Oral Health Council. Systemic antibiotic treatment is not indicated for periodontal patients except in very limited circumstances [12]. A trivalent Porphyromonas bacterin for use as a periodontal disease preventive in dogs is under development [13]. Treatment with anti-inflammatory drugs has been shown experimentally to have a protective effect on alveolar bone in dogs [14]. Anti-osteoclastic drugs such as bisphosphonates also retard alveolar bone loss experimentally in dogs [15]. Use of these pharmacologic agents long-term in veterinary patients has not been investigated and thus cannot be recommended at this time.

In some patients, several different types of procedures may be indicated with the patient under anesthesia. It is useful to differentiate between preventive and treatment procedures, both of which fit under the term periodontal management [2]. Frequent home oral hygiene and professional dental scaling are the primary preventive procedures. Professional scaling under anesthesia is necessary when accumulation of calculus is moderate. Gingivitis and mild or moderate periodontitis (periodontal pockets of up to 5 mm) can be managed effectively by scaling followed by frequent (daily) oral hygiene in an otherwise healthy dog or cat.

When periodontitis is extensive, or when complicating factors exist such as systemic illness, preventive procedures alone are insufficient. The most commonly indicated periodontal treatment in dogs and cats is extraction - it is also the most reliable means of preventing further local deep-seated periodontal infection and its systemic consequences. Some severely affected teeth can be successfully retained in the mouth by a combination of scaling, periodontal surgery, and conscientiously applied oral home hygiene.

Endodontic Disease

Endodontics refers to the branch of dentistry concerned with the anatomy, physiology, and pathology of the dentin, dental pulp, and periapical region and with the treatment of endodontic disease [16]. The periapical region of the tooth root becomes involved when bacteria invade the pulp, rendering it partially to totally necrotic. Exposed pulp in germ-free rats remains vital and relatively uninflamed, and the exposed site is repaired with reparative dentin. Thus, without bacteria and their by-products, periapical disease of endodontic origin does not occur.

Endodontic Anatomy

The pulp is a soft tissue with highly differentiated odontoblasts arranged peripherally in direct contact with the dentin. Because of the close relationship between odontoblasts and dentin, they are considered a functional entity and referred to as the pulp-dentin complex[17]. The pulp also consists of loose connective tissue, intercellular substance, blood and lymph vessels, nerves, and fibers. The pulp connects with periapical tissues through the apex in each root. Root development in dogs and cats results in the formation of several apical foramina, in ground sections appearing as apical delta. Secondary, accessory, lateral, and furcation canals also may connect pulp tissue with periodontal ligament [18,19]. Endodontic success is influenced by obturation of all these canals. If bacteria from progressing periodontal disease reach and involve these canals, pulp involvement will result. Some epithelial cells persist within the periodontal ligament during tooth development, the epithelial rests of Malassez, forming a net-like structure around the tooth root [20].

Arterioles enter through the apical foramina and pass centrally through the pulp, giving off lateral branches that divide further into capillaries. Minor vessels may enter through secondary, accessory, lateral, and furcation canals but do not provide sufficient collateral circulation. Venous return is collected by a network of capillaries that unite to form venules coursing down the central portion of the pulp. The blood supply diminishes with age, rendering a pulp more susceptible to irreversible damage. Inflammation in a localized coronal zone does not cause immediate strangulation of apical vessels and death of the pulp, as it is confined by a combination of ground substance and a unique blood supply. Arteriovenous shunts redistribute the blood and prevent buildup of unsustainable pressure in the rigid environment [17,20]. Autonomic and sensory nerve fibers enter the pulp with the vessels through the apical foramina. Individual axons branch into many terminal filaments, which may enter the dentinal tubules. The autonomic nerve supply consists of sympathetic fibers that control microcirculation. The two types of sensory fibers are myelinated A fibers and unmyelinated C fibers. The faster-conducting A fibers are responsible for sharp, localized pain owing to rapid movement of fluid in dentinal tubules, resulting in mechanical distortion of tissue in the pulp-dentin border and stimulation of A fibers. Stimulation of the slower-conducting C fibers gives rise to the duller, throbbing, less-localized pain [17,20].

The primary role of the pulp is to produce dentin by mature odontoblasts, which are incapable of further division and, if damaged, may be replaced from undifferentiated mesenchymal cells. The odontoblast cell bodies are separated from mineralized dentin by an unmineralized predentin layer. Primary dentin is formed during tooth development. Secondary dentin is formed physiologically after the tooth is fully developed. Its formation continues throughout life, enabling the vital pulp to partially compensate for the loss of enamel or dentin caused by mechanical trauma or disease. Teeth of young adult animals have a fairly wide pulp cavity, whereas in old animals the pulp cavity is usually narrow. The narrower the pulp cavity, the thicker are the dentinal walls, and thus the stronger and more aged is the tooth. Comparing the radiographic appearance of the pulp cavity between ipsi- and contralateral teeth is an effective means of determining pulp vitality in teeth with suspected endodontic pathology. Tertiary dentin (reparative dentin) is formed in response to trauma or disease [17,20].

Dentin consists of thousands of dentinal tubules radiating outward from the dental pulp to the enamel in the crown and cementum in the root. The tubules contain the long, narrow odontoblastic processes and are filled with dentinal fluid. A pressure gradient between the pulp and oral cavity accounts for the outward flow of fluid. Exposure of tubules from tooth fracture or cavity preparation results in outward movement of fluid to the exposed dentin surface. Peritubular dentin lines the tubules and is laid down by the odontoblastic process; intertubular dentin is found between tubules. Partial or complete occlusion of tubules may occur as a result of aging or in response to stimuli such as mechanical wear or caries. When tubules become filled with mineral deposits, the dentin becomes sclerotic and less permeable, shielding the pulp from irritation. Dentinal sclerosis gives aged teeth a characteristic translucency, and clinically the dentin appears glassy [17,20].

Causes of Endodontic Disease

Rapid tooth wear removes enamel and dentin faster than odontoblasts can form dentin. The pulp may be exposed or eventually succumb to prolonged chronic inflammation. Causes of tooth wear include abrasion (tooth wear caused by contact of a tooth with a non-dental material), attrition (tooth wear caused by tooth-by-tooth contact in malocclusion), and erosion (demineralization of the tooth surface because of acids). Caries is the most common cause of endodontic disease in humans but is rather uncommon in dogs and has not yet been reported to occur in cats. It results from demineralization of the tooth surface by acids that are formed during fermentation of highly refined carbohydrates by cariogenic bacteria. Although the most common responses to caries are dentin sclerosis and formation of reparative dentin, the formation of a dead tract in dentin is not considered to be a defensive reaction. It is an area in dentin with tubules devoid of odontoblast processes, providing a channel for bacteria to reach the pulp [20].

Crown infraction is an incomplete fracture of enamel without loss of tooth structure. Though these fractures are weak points through which bacteria and by-products can challenge the pulp, rarely do they result in permanent pulp damage. An uncomplicated crown fracture is a fracture of enamel only or enamel and dentin without pulp exposure. If enamel is involved only, the consequences are minimal; if dentin is exposed, a pathway exists for stimuli to pass through dentinal tubules to the pulp, resulting in formation of sclerotic and reparative dentin, chronic pulpitis, or pulp necrosis. A complicated crown fracture is a fracture of enamel and dentin with pulp exposure. If left untreated, this always results in pulp necrosis. This fracture is common in canine teeth of dogs and cats owing to motor-vehicle trauma, falls from great heights, kicks, and hits. Military, police, and prison dogs are more prone to fracture of canine teeth if their distal tooth surfaces are weakened by wear from chewing on cage bars (cage biter teeth). Fractures of carnassial teeth in dogs are frequently caused by chewing on hard objects (e.g., nylon bones, cow hooves, large ice cubes). Resorption initiating on external root surfaces and progressing into root and/or crown dentin are often the cause of crown fracture in cats, with root fragments remaining in the alveoli. A crown-root fracture is a fracture of enamel, dentin, and cementum. The pulp may or may not be involved. If a crown-root fracture cannot be made into an uncomplicated crown fracture by periodontal surgery and/or orthodontic extrusion, the tooth should be extracted. A root fracture is a fracture of cementum and dentin, usually with pulp exposure. The coronal segment is displaced and pulp necrosis may result, but generally the apical segment is not displaced and has an intact blood supply. Apical root and midroot fractures have a good to fair prognosis (root canal therapy and splinting of the coronal segment), while coronal root fractures have a poor prognosis [20].

In concussion and subluxation, the tooth shows normal or slightly increased mobility and sensitivity to percussion, but no displacement. The tooth should be monitored radiographically to determine pulp vitality. Luxation refers to clinically or radiographically evident displacement of the tooth within its alveolus. Lateral and extrusive luxation occur most commonly and are often associated with fracture of the alveolus. Intrusive luxation is a rare complication associated with trauma that forced a tooth with periodontal disease into the nasal cavity, resulting in chronic rhinitis and nasal discharge. Surgical exposure through an intra-oral approach is required to remove the tooth. Avulsion (exarticulation) refers to complete extrusive luxation. The teeth most commonly avulsed in dogs are the incisors and canine teeth. The success of reimplantation of an avulsed tooth is greatly influenced by the length of time that the tooth is out of the alveolar socket. Luxated and avulsed teeth require repositioning, stabilization, and root canal therapy owing to the likely loss of blood supply to the pulp [20].

Thermal injury causing pulp hyperemia, pulpitis, or pulp necrosis is caused by poor dental scaling and polishing techniques (insufficient cooling water, too much pressure on the working tip, prolonged scaling/polishing at the same location), restorative cavity and crown margin preparations; and careless use of thermocautery, diathermy, electrosurgery and laser units near teeth, and electric cord injuries. Anachoresis refers to infection of pulp tissue in a state of hyperemia by hematogenic invasion of bacteria through apical and non-apical ramifications. Progression of pulp hyperemia to pulpitis in the presence of bacteria ultimately results in pulp necrosis. Other causes of endodontic disease include external tooth resorption, progressive internal tooth resorption, severe periodontitis, use of local anesthetics that contain a vasoconstrictor, excessive root planing, unbased restorations, and rapid orthodontic tooth movement. Tooth resorption is common in cats, but infrequent in dogs. Periodontally diseased teeth have narrower root canal widths compared with healthy teeth owing to deposition of reparative dentin along the dentinal walls. Bacterial infection of the pulp is possible in areas devoid of cementum and through lateral, accessory, secondary, and furcation canals if exposed to oral fluids [20].

Clinical Signs

Evaluation of the endodontic patient requires assessment of previous trauma and chewing history and inspection and palpation of intra- and extraoral tissues, focusing on tooth discoloration, crown defects, intra- and extraoral swellings, and sinus tract formation. Reduced biting pressure during play or aggression training and reluctance to eat hard or fibrous food may be noted. To relieve discomfort during late signs of abscess development, the animal may attempt to contact cool or cold surfaces and liquids. Regional lymphadenopathy and fever develop as the abscess reaches an acute stage. In cooperative patients, the occlusal surface of several healthy teeth and the suspect tooth can be percussed with a finger or the handle of a dental mirror. Hyperreaction indicates that the infection extended beyond the pulp into the periapical region. The pressure build-up in this small space from edema and inflammation will yield pain on percussion. Endodontic disease may result in crown discoloration (pink, red, purple, gray, or brown). Progressive tooth discoloration and/or radiographic changes can reasonably be interpreted as indicative of pulp necrosis. One study revealed that over 90% of teeth with crown discoloration are non vital [21]. Transillumination of normal and suspect teeth reveals vital teeth to be rather translucent, whereas nonvital teeth tend to appear more opaque. Crown integrity is evaluated with a fine dental explorer. The tip of the explorer will find irregularities in the crown surface or catch in an open pulp chamber. Recent pulp exposures reveal bleeding pulp, whereas old pulp exposures show black debris and necrotic pulp tissue. Tooth mobility is directly proportional to the integrity of the attachment of the root. The degree of depressibility of the tooth within its alveolus should also be tested by pressing the tooth into its alveolus and watching for any vertical movement. The pressure exerted by purulent exudate in the periapical region may cause some transient tooth mobility. Crown-root and root fractures often result in mobility of a crown segment. Before incipient swelling becomes clinically evident, it may be detected by gentle palpation with the index finger. Swelling and sinus tracts originating from endodontically diseased maxillary fourth premolar teeth in dogs and cats often are located ventral to the medial canthus of the eye. Intraoral sinus tracts are commonly draining at the mucogingival junction. Swellings and sinus tracts owing to endodontic disease often have a history of responsiveness to antibiotics and recurrence when antibiotic therapy is discontinued. Sinus tracts can be traced with a gutta-percha cone, and a radiograph is obtained to locate their source [16].

Pathophysiology and Radiographic Signs

A reversible pulpitis is pulp inflammation to the extent that thermal stimuli (usually cold) cause a quick, sharp, hypersensitive response that subsides as soon as the stimulus is removed. If the irritant is removed, the inflamed pulp will revert to an uninflamed state that is asymptomatic. An irreversible pulpitis may be acute, subacute, or chronic, partial or total, infected or sterile. The acutely inflamed pulp is symptomatic; the chronically inflamed pulp is usually asymptomatic. A symptomatic irreversible pulpitis elicits prolonged episodes of pain. A thickening of the apical periodontal ligament may become evident on radiographs in the advanced stage of disease. A reddish cauliflower-like growth of pulp tissue through an open pulp chamber is one variation of asymptomatic irreversible pulpitis and attributed to a low-grade chronic irritation of the pulp and the generous vascularity characteristically found in young animals. Pulp necrosis results from an untreated irreversible pulpitis, a traumatic injury, or any event that causes long-term interruption of the blood supply to the pulp, and may be partial or total. Total necrosis before it affects the periodontal ligament is asymptomatic. Protein breakdown products, bacteria and endotoxins will eventually spread beyond the apical foramina into the periapical region, leading to thickening of the periodontal ligament and manifesting as tenderness to percussion and chewing [20].

Acute apical periodontitis is a painful inflammation around the apex before the bone begins to resorb and results from an extension of pulpal disease into the periapical tissue, an overextension of endodontic instruments or materials, or occlusal trauma such as bruxism. It may occur around vital and nonvital teeth. The apical periodontal ligament may be within normal limits or only slightly widened on dental radiographs because of edema. An acute apical abscess is a painful, purulent exudate around the apex. The periodontal ligament may be within normal limits or only slightly thickened on dental radiographs with a relatively normal (or slightly thickened) lamina dura because the fulminating infection has rapidly spread beyond the confines of the cortical plate before bone demineralization can be detected radiographically. Presenting signs include rapid onset of slight to severe swelling (cellulitis spreading into fascial planes), moderate to severe pain, and slight increase in tooth mobility; fever and general malaise are present in more advanced cases. Chronic apical periodontitis (granuloma) is generally asymptomatic and manifests radiographically. Bacteria and endotoxins, cascading out into the periapical region from a necrotic pulp, cause extensive demineralization of cancellous and cortical bone and large or small, diffuse or circumscribed, radiographically evident lesions. Slight tenderness may be evident on percussion and/or palpation testing. A sinus tract may yield frank suppuration. As pressure from pus is relieved by drainage, the sinus tract may close temporarily; if pressure from pus builds up again, the sinus tract returns. Epithelial rests of Malassez may respond to the stimulus in the apical periodontal ligament by proliferating to wall off the irritants coming through the apical foramina, creating a periapical cyst. A phoenix abscess is an acute exacerbation of chronic apical periodontitis, and symptoms identical to those present with an acute apical abscess will appear (Fig. 22.2) [20].

Figure 22.2. Dog with an apical abscess originating from the left maxillary fourth premolar tooth. (A) Left infraorbital swelling. (B) Crown-root slab fracture. (C) Dental radiograph showing a large radiolucent halo around apex of the distal root.

Periapical osteosclerosis is excessive bone mineralization around the apex of a vital tooth caused by low-grade pulp irritation; this condition is asymptomatic and benign and does not require endodontic therapy. Condensing osteitis (focal sclerosing osteomyelitis) is excessive bone mineralization around the apex of a non-vital tooth caused by long-standing and low-toxic exudation from an infected pulp, resulting in mild irritation and circumscribed proliferation of the periapical bone. Acute osteomyelitis can arise directly from an endodontic infection. Live bacteria pass the apex and multiply in the marrow spaces and soft tissue of the bone, resulting in localized or widespread infection of the bone; if untreated, the acute form may progress to a chronic form, eventually leading to bone necrosis. Calcification of pulp tissue includes diffuse mineralization (often a pathologic process related to various forms of injury) or pulp stones (denticles) that form around epithelial cells remnants. Perhaps the greatest endodontic significance of pulp calcification is that it may hinder root canal shaping [20].

Endodontic Treatment

Vital pulp therapy is primarily utilized for "recent" tooth fractures or after intentional surgical crown reduction to preserve pulp vitality and increase strength of the tooth by allowing continued dentin formation. If the pulp is exposed for longer periods of time or has become necrotic, standard root canal therapy is performed and includes accessing the pulp cavity, debriding, shaping, disinfecting and obturating (filling) the root canal, and access restoration. An apexification procedure is a type of root canal therapy that is performed to stimulate the formation of a closed apex with hard tissue when a necrotic pulp is present in an incompletely developed permanent tooth in young animals or in teeth of adult animals that have "open" apices owing to apical root resorption. Surgical root canal therapy is performed when standard root canal therapy has failed or will likely fail in teeth with advanced periapical disease. This includes access through oral mucosa or skin, alveolectomy, apicoectomy and retrograde filling. Extraction is the treatment of choice for teeth fractured through the long axis of the tooth root(s) and teeth with advanced root resorption.