Endodontic Disease PDF

P Chapter 1 The causes and sequelae of endodontic disease ulpitis is the inflammation of the pulp, whereas apical periodontitis is the inflammation of the tissues surrounding the apex of the tooth, including the periodontal ligament and the alveolar bone. Inflammation can be acute or chronic. A...

P Chapter 1 The causes and sequelae of endodontic disease ulpitis is the inflammation of the pulp, whereas apical periodontitis is the inflammation of the tissues surrounding the apex of the tooth, including the periodontal ligament and the alveolar bone. Inflammation can be acute or chronic. Acute inflammation Acute inflammation is characterised by: Redness Heat Swelling Pain Loss of function. The redness and heat produced in an area of acute inflammation are the results of vessel dilatation and increased blood flow to that area. Swelling is caused by the accumulation of tissue exudates which contain neutrophils and inflammatory mediators (Table 1.1). The exudate aims to dilute the toxins whilst the neutrophils ingest the pathogens by phagocytosis. Pain is felt because of the swelling exerting pressure on nerve endings. Certain chemical mediators can also stimulate pain receptors. Swelling and pain can result in loss of function of the inflamed area. Chronic inflammation Acute inflammation can be reversible by removal of the damaging stimulus. However, if it persists, chronic inflammation ensues. Chronic inflammation is the result of a balance between continued tissue damage and attempts by the host to eradicate the disease to produce some tissue repair. Macrophages are among the main effector cells in chronic inflammation. They secrete various inflammatory mediators and have a role in phagocytosis and antigen presentation. Lymphocytes additionally recognise foreign antigens by binding to them before proliferating to mount an immune response by cell-mediated immunity (T lymphocytes) or by humoral immunity (B lymphocytes). Symptoms are usually limited at the chronic inflammation stage. Causes of apical periodontitis Apical periodontitis is caused by bacterial infection of the pulp. In a healthy tooth, the pulp dentine complex is protected from oral microorganisms by the overlying enamel and cementum. However, these layers can be damaged by caries, cracks or fractures, tooth wear, restorative procedures or periodontal procedures to produce portals of entry for microorganisms. As bacteria penetrate into dentine, they release toxins that pass through the dentine tubules. The pulp responds to this by producing a layer of tertiary dentine as an additional protective layer. Increased intratubular mineral deposition may also reduce the permeability of the dentine (Figure 1.1). However, once the microorganisms penetrate into the inner dentine layers, the toxins they produce cause significant pulpal inflammation. If no treatment is provided, the bacteria eventually invade and colonise the pulp. The pulp is encased in a hard dentine shell and can therefore not expand to accommodate large amounts of fluid exudate. It also lacks sufficient collateral circulation. These factors limit the ability of the pulp to respond effectively to the insult. Pulpal inflammation can initially be reversible, with removal of the irritants resulting in resolution of the inflammation. However, as the immune challenge increases, the pulpal damage will advance beyond repair, resulting in irreversible inflammation and progressive pulpal necrosis. Restorative procedures additionally may ‘push’ a tooth with pre-existing pulpal inflammation to irreversible pulpitis. This occurs by overheating, desiccation or chemical irritation to the dentino-pulp complex. If rubber dam is not used, or poor fitting temporary restorations are placed, microleakage can also occur. The risk of permanent damage is higher when the restorative work is close to the pulp and the dentine is permeable. A root canal with a necrotic pulp is the ideal environment for bacterial colonisation as it provides a warm, moist, nutritious and anaerobic environment. The reduced presence of oxygen can also select aggressive anaerobic pathogens. The microorganisms are protected from the host defences as there is no blood circulation in the necrotic tissue. They derive their nutrients from the necrotic pulp tissue, periradicular tissue fluids, saliva and metabolic by-products of other bacterial species. Over time, the bacteria progress apically down the root canal. Leakage of toxins and metabolic by-products through the apical foramen also stimulates the inflammatory response in the periapical tissues. Inflammatory mediators are released that stimulate osteoclast differentiation. This results in apical bone resorption and production of an apical lesion surrounded by chronic inflammatory cells. This stage of the disease is described as chronic apical periodontitis associated with an infected necrotic tooth (Figure 1.2). The aim of root canal treatment is to reduce the bacterial load and seal the canals to prevent further ingress of bacteria. However, chronic inflammation can persist if inadequate disinfection is performed, with microorganisms remaining at levels sufficient to stimulate an inflammatory response. If the root canal system and coronal aspect of the tooth are not adequately sealed after root canal treatment, bacteria can re-enter and cause recurrence of the apical inflammation. It can be difficult to identify if the cause of the inflammation is persistence of, or re-entry of bacteria (or both). This stage of the disease is described as chronic apical periodontitis associated with an infected root-filled tooth (Figure 1.3). Bacteria can egress through the apical foramen and, in some cases, cause suppuration that presents as an acute apical abscess or a chronic sinus tract Which methods of sampling are used for bacterial detection? Apical periodontitis is caused by the presence of microorganisms and their toxins in the root canals causing progressive inflammation and necrosis of the pulp, followed by inflammation of the periapical tissues. Root canal treatment aims to reduce the microbial load to a level that permits the body to amount an effective immune response and promote healing. It has therefore been considered important to ascertain which microorganisms are present in the root canals of teeth with apical periodontitis to understand how the disease progresses, as well as how to manage it. Methods for isolation and detection of endodontic microorganisms fall into culturing and molecular technology (Table 2.1). For each, a sample must be taken from the root canal. This is normally performed with paper points. This will normally only allow sampling of microorganisms that are present in the main canal lumen. Files assist in collecting ‘scrapings’ from the canal walls. Collection of bacteria from dentine tubules and isthmuses is very difficult. Culturing The sample is transported in a medium that preserves viability whilst not enhancing growth. The microbes are then distributed onto agar media or cultured in broths under aerobic or anaerobic conditions. Species can then be identified by assessing features including colony and cellular morphology, tolerance to oxygen, gram staining and metabolic end-product analysis. Other tests that can be performed on the microorganisms include susceptibility to certain antibiotics, oxygen tolerance and cell wall profile. Molecular technology Molecular technology enables identification of microorganisms without the need for culturing. It can more reliably identify bacteria, including those strains that show ambiguous phenotypes. Fungi can be identified by their 18S RNA gene. The clinical sample is solubilised, DNA extracted and specific nucleic acid probes (primers) are added that are complementary to the target species being investigated. If the target species is present, hybridisation will occur. The polymerase chain reaction will then amplify the DNA to a level at which it can be detected. If the target species are absent in the sample, no hybridisation will occur and no DNA will be amplified. Electrophoresis and fluorescent in situ hybridisation can be used to assist with separation and visual identification of the strains present. Which bacteria are responsible for causing apical periodontitis? The culturing and molecular biology techniques have revealed the presence of more than 400 microorganisms. Different bacteria dominate the canals in primary and persistent cases of apical periodontitis (Table 2.2). Where do the bacteria reside in the root canal system? Bacteria occur in the main canal as well as in accessory canals, isthmuses and deltas in the following habitats: 1 The lumen in planktonic form 2 The canals walls as part of a biofilm 3 The dentinal tubules. A biofilm is a bacterial population that is embedded in a polysaccharide matrix and adheres to surfaces of solid–liquid interfaces (Figure 2.1). Biofilms are present in the root canal system and occasionally are extraradicular. The biofilm is advantageous to the microorganism in the following ways: Broader habitat range for growth: early colonisers alter the local environment and can increase nutrient availability and remove waste products. This enables other bacterial species that would not have survived alone to attach to, and form part of the biofilm. Increased metabolic diversity and efficiency: bacteria cohabiting in biofilms develop food webs whereby the metabolic byproducts from one species become the main food source for another. Interactions between different species also allow more effective breakdown and utilisation of host-derived substrates compared with the actions of a single species alone. Protection from the host defences: the extracellular polysaccharide resists phagocytosis from the host inflammatory cells. In addition, various species can produce different enzymes to neutralise the host inflammatory mediators and also inactivate antibacterial solutions that can be used to remove them during root canal treatment. Antibiotics usually require a level of bacterial activity to be effective. However, bacteria in biofilms often grow more slowly and are at the stationary phase of growth for longer. This can result in enhanced antibiotic resistance. Genetic exchange: methods such as conjugation, transformation and transduction enable dissemination of virulence and antibiotic resistance genes within bacterial species of the biofilm. Enhances pathogenicity: bacteria which individually have a low virulence can still have a role in causing disease when they partake in a biofilm. Their role can be to assist the survival of more virulent bacteria by improving adherence of the biofilm to host surfaces, obtaining nutrients from the host and evading host defences. How does the knowledge of the bacterial species and habitats influence endodontic treatment? The complexity of intracanal infection requires treatment with a broad spectrum antibacterial such as sodium hypochlorite. Antimicrobial agents are far less effective at destroying bacteria in biofilms than planktonic bacteria. They will therefore need to be used in greater concentrations, or employed with techniques such as ultrasonic irrigation to disrupt the biofilms. Whilst microorganisms present in the main root canal can be directly accessed and ideally eliminated by instrumentation and irrigation, those microbes that are located in lateral canals and dentine tubules are more difficult to reach and can require other therapeutic strategies to eliminate them R Chapter 3 Resorption oot resorption is the loss of dental hard tissues as a result of clastic action. Physiological (primary dentition) root resorption allows permanent successors to erupt. However, any resorption of permanent teeth is pathological. Pathological resorption may be internal or external, depending on the location of the resorptive lesion (Figure 3.1). Internal root resorption Internal inflammatory and internal replacement resorption Pathogenesis and aetiology The odontoblast/predentine layers of the pulpo-dentine complex must be damaged resulting in exposure of mineralised dentine. The aetiology is poorly understood (Table 3.1). When coronal pulp tissue is inflamed because of bacterial ingress, inflammatory mediators stimulate recruitment of odontoclasts from the more apical pulpal blood supply. These bind to and resorb mineralised tissue. Internal resorption will only progress with bacterial stimulation and a vital blood supply to provide nutrients. Internal replacement resorption occurs when hard tissue resembling bone (osteoid) or cementum is deposited (reparative phase) within the resorptive cavity. Clinical and radiographic findings Internal inflammatory resorption can present with symptoms and/or signs of pulpal and/or periapical disease (Table 3.1). May be an incidental (asymptomatic) finding on radiography. Specific management considerations A cone beam computed tomography (CBCT) scan is recommended in teeth considered restorable to determine the nature and extent of the resorptive defect. Endodontic treatment is recommended in restorable cases. An interappointment calcium hydroxide medicament can be placed to exert an antibacterial effect on tissue inaccessible to instrumentation. Obturate with thermoplasticised gutta percha to ensure that the complex root canal system is encompassed. Microsurgery is additionally required if there is an existing perforation. External root resorption Transient apical breakdown Pathogenesis and aetiology Rare radiological phenomenon caused by the localised transient inflammatory response (i.e. repair) associated with removal of necrotic tissue from the apices of traumatized teeth. Clinical and radiographic findings Discoloration; A small periapical radiolucency develops soon after the initial dental trauma, but usually resolves (i.e. repair) within 3 months of the injury; There may initially be a negative response to pulp testing; Usually resolves within 12 months. External inflammatory resorption Pathogenesis and aetiology Injury to the tooth by various aetiological factors (Table 3.1) can damage the cementum externally, exposing the underlying mineralised dentine. The injury also results in pulpal necrosis and subsequent bacterial infection. Bacterial toxins pass through the dentine tubules, inducing an inflammatory response on the external aspect of the root. Osteoclasts migrate to the area and bind to and resorb the damaged exposed (mineralised) dentine. Clinical and radiographic findings Signs and symptoms of pulpal and/or periapical disease or be asymptomatic. The radiograph will show a loss of tooth structure and radiolucencies in the adjacent bone. The root canal outline is seen through the radiographic defect. Early to moderate signs of external inflammatory resorption, especially on the labial or lingual aspects of the tooth, can be missed because of the two-dimensional nature of radiographs. Management  Root canal treatment with inter-appointment calcium hydroxide dressing. Microsurgery is sometimes required if a perforation is present. External replacement resorption The root becomes mistakenly incorporated into the remodelling process of the alveolar bone. Pathogenesis and aetiology In severe intrusion or avulsion injuries where the PDL is crushed and desiccated. The irreversibly damaged periodontal ligament and adjacent root are resorbed by osteoclasts and ‘replaced’ with bone produced by osteoblasts from the adjacent alveolar bone. The pulp tissue does not have a role in the progression of the resorption. Clinical findings High pitched metallic sound to percussion and no mobility in advanced cases. There may be no other signs of endo/perio disease. Radiologically resorption will only be detected on the proximal surfaces, where portions of the root are replaced with bone. Management No effective treatment and the tooth will eventually be lost. External cervical resorption (ECR) Pathogenesis and aetiology Damage to cementum at the cervical margin below the epithelial attachment exposes mineralised dentine to osteoclasts which resorb the underlying dentine. Bone-like material may be deposited in an attempt to repair the resorbed dentine. The pulp has no role in stimulating ECR. There is no firm evidence for any of these aetiological factors (Table 3.1). Diagnosis  Usually asymptomatic and will respond to vitality testing, as the pulp is not involved until the advanced stages (Table 3.1). Defect usually identified by probing or scaling. It will have sharp borders and a hard scratchy base. Profuse bleeding on probing. Proximal resorptive lesions can be noticed as chance radiographic findings. There is no classic radiographic appearance. Radiolucent (early)-radiopaque/mottled (advanced). Root canal will be intact. Management Treatment depends on the location, restorability and accessibility. CBCT is advisable to assess the nature of ECR prior to management. Treatment options include: external repair +/− endodontic treatment internal repair and root canal treatment, intentional replantation, periodic review (untreatable teeth), extraction (untreatable teeth). D Chapter 4 History taking iagnosis of endodontic disease is the process of determining the cause of the patient’s signs and symptoms. In order to reach the correct diagnosis a thorough history must be taken. Extraoral and intraoral examinations are necessary prior to performing additional clinical tests. These are discussed in more detail in Chapters 5–7. The information compiled from the history and examination allows the dentist to develop a differential diagnosis. This is a list of all the possible diagnoses. Special tests then help the clinician to arrive at a definitive diagnosis, although sometimes this is not confirmed until treatment has been completed and the pain resolves, or histology samples have been reported. Completing a patient history Presenting symptoms The patient should be asked why he/she has attended the appointment and be allowed to describe the problem. The clinician can then ask more direct questions to gain additional specific information. A variety of open and closed questions should be used (Table 4.1). The open questions allow the patient to describe the problem without any input bias from the clinician whilst closed questioning allows the consultation to remain focused on the problem, especially when there is limited time. Questioning must establish specific details of the problem and includes the following. Location of the pain Can you point to the tooth that is painful? If the patient cannot localise the exact tooth or area, he/she should be asked to point to the quadrant or side that the pain originates from. When the pain is severe and generalised, the patient should be asked if he/she can remember the site at which the pain was felt at its onset. Commencement When did the symptoms first occur? The pain may coincide with recent dental treatment to a particular tooth. Alternatively, the patient may recollect biting hard onto something. However, care must be taken not to make incorrect conclusions based on this information alone. Intensity of the pain On a scale of 1 to 10, with 10 being the most severe, how would you rate your symptoms? The intensity may change at certain periods such as eating or at night-time and therefore detail should be sought as to any changes in the intensity during a 24-hour period. Provocation and relief of pain Does anything worsen or relieve your symptoms? Patients may describe either biting or temperature changes as being the main initiating factors. Pain on biting or touching a specific tooth suggests acute apical periodontitis or an acute apical abscess. However, the pain may also be caused by a crack. Prolonged pain in response to hot, cold and sweet suggests inflammation of the pulp. Relief of the pain may be by non-steroidal anti-inflammatory drugs (NSAIDs), suggesting an inflammatory cause. Cold water may also relieve the pain. Duration of the pain How long does the pain linger after it has been provoked? A pain that lasts for seconds indicates dentine hypersensitivity or a reversible pulpitis. A pain lasting for several minutes after thermal stimuli indicates an irreversible nature. Relevance of medical history Medical history questionnaires should be updated at each appointment. Whilst there are no absolute contraindications to provision of root canal treatment, modifications to treatment are sometimes necessary. Some patients have been advised to avoid dental extractions and it may therefore be necessary to attempt to root treat teeth, even when this has a limited prognosis. This may be necessary for patients undergoing intravenous bisphosphonate treatment or head/neck radiotheraphy. Patients with cardiovascular, respiratory and central nervous system disorders may be taking medications that interact with antibiotics, analgesics or anaesthetics used during dental treatment. An up to date list of medications should be taken and checked prior to treatment. Patients with reduced liver or renal function can have reduced ability to metabolise the administered drugs and the dosage may need to be modified. Pacemakers can interact with older electric pulp testers, electrosurgery equipment and some ultrasonics. A cardiologist’s advice would be wise prior to using such equipment. Patients may be taking anticoagulant or antiplatelet drugs. Whilst it is possible to take an international normalised ratio (INR) to assess the risk of bleeding for patients taking warfarin, this is not possible for the novel oral anticoagulants. Therefore, a risk assessment must be taken prior to the procedure (Table 4.2) and, if there is a high risk of bleeding, consultation with the patient’s medical practitioner would be advised as the patient’s drug schedule may require alteration (Table 4.3). Known allergies must be assessed; these commonly include various antibiotics and latex. However, anaphylaxis following chlorhexidine use is increasing and dentists must be able to recognise and manage anaphylactic shock. Patients who are on long-term steroids or who have diabetes have been shown to have a decreased prognosis after root canal treatment, although this is not a contraindication for treatment. Diabetic patients must have their appointment times planned around meals to maintain their correct blood glucose levels. Pregnant patients may wish to defer non-essential radiographs until after their first trimester for their own piece of mind. However, there is still justification for taking radiographs to assist in pain diagnosis. Endodontic treatment can still be performed but, as always, care must be taken to limit the radiation dose as much as possible. Some patients who are pain free may wish to delay treatment until the second trimester. Extraoral examination An extraoral examination is necessary to assess for asymmetry caused by swelling and extraoral fistulas. Lymph nodes should also be palpated. Firm tender nodes accompanied by an elevated temperature are indicators of infection. The temporalis and masseter should be assesed for hypertrophy and their origins and attachments should be palpated for tenderness. The patient’s smile line may require assessment as this can influence treatment decisions that involve the gingival margins including replacing anterior crowns or surgical procedures. Intraoral examination A complete intraoral soft tissue examination must be performed and any relevant lesions documented and followed up appropriately. Any intraoral swellings should be assessed by visualisation and palpation (Box 5.1). Sinus tracts feature in longstanding infections to provide a drainage pathway for pus. The surface opening (stoma) of the sinus tract can be in the attached gingiva, alveolar mucosa or gingival sulcus. The stoma is commonly, but not always, adjacent to the source of the infection and therefore the origin of the sinus tract should be determined radiographically using gutta percha (Figure 5.1). Palatal fistulae tend to be less visible than buccal ones. An overall assessment of the restorative state of the teeth is required, noting deficient fillings and caries, prior to assessing the side or quadrant of concern in more detail. The teeth of interest should be assessed visually for tooth wear, large and/or defective fillings, cracks and caries. An estimation of the amount of remaining healthy tooth structure is required. The integrity of any crown margins must also be assessed. Teeth should then undergo various tests to assess tenderness to percussion and palpation, periodontal status and vitality (see Chapter 6). If there is still uncertainty as to the diagnosis, additional tests such as selective anaesthesia may be performed. When assessing teeth it is important that the contralateral tooth (if asymptomatic and not root filled) is tested first to enable the patient to understand what to expect and what can be considered normal. The occlusion and status of adjacent teeth must also be assessed to determine the strategic importance of maintaining particular teeth. This can affect management decisions of whether to root treat or extract. Percussion testing When a patient reports pain on biting, percussion and bite tests are useful aids to localise the problem. Devices such as a tooth slooth (Figure 5.2) allow the clinician to apply pressure to a specific cusp or fossa with more accuracy. Pain on biting occurs either when the pulpal inflammation has extended apically to the periodontal ligament space (acute apical periodontitis) or when there is crack in the tooth. Pain as a result of acute apical periodontitis manifests when pressure is applied, independent of the direction of the percussion. However, a cracked tooth will only be painful when the tooth is percussed in a specific direction. In addition, it is common for pain to be felt when the pressure is released, instead of when it is applied. Palpation testing The buccal and, when indicated the lingual/palatal sulci in the area under investigation should be palpated to detect any soft tissue swellings or bony expansion. This should be compared with the contralateral side. The patient should be asked to indicate any areas that feel particularly tender when the pressure is applied. This is an indicator of periradicular inflammation. Periodontal assessment Tooth mobility can be assessed by placing the ends of two mirror handles on buccal and lingual aspects of a tooth and applying pressure in various horizontal directions, as well as vertically. Causes of increased mobility are shown in Box 5.2. Periodontal probing around the root surface may identify generalised and localised isolated areas of bone loss. Generalised bone loss is usually of periodontal origin. Localised deep probing depths occur as a result of endodontic infection with pus discharging through the periodontal ligament. A vertical root fracture may also cause a localised narrow periodontal pocket (Figure 5.3). A basic periodontal examination (BPE) probe is best suited to identifying localised periodontal pockets because of its small cross-sectional area (Figure 5.4). Assessment of cracks Staining and transillumination can be used to assess cracks. When methylene blue dye is painted on the tooth surface it will penetrate into and stain the cracks. The use of dental loupes or a dental operating microscope will enhance visualisation of the cracks. However, it is difficult to assess the depth of the crack by visualising its surface appearance only, and it may need further investigation. Test cavities A test cavity involves preparing a cavity without local anaesthetic to determine if the tooth has an intact pulp. If the bur reaches the dentine without the patient reporting any sensation, the pulp is likely to be necrotic. However, its use is largely historical as the procedure is irreversibly destructive and can be very unpleasant for the patient. It is not a reliable test. Selective local anaesthesia Patients with irreversible pulpitis may be unable to identify the offending tooth, or even if the symptoms originate from the maxillary or mandibular arch. Adminstration of local anaesthesia adjacent to the most posterior tooth in the maxillary arch will anaesthetise the upper teeth and, if one of these is the offending tooth, the pain will resolve. If the pain does not subside after a reasonable period of time, the mandibular arch should be anaesthetised. Resolution of the pain would then indicate that the problem is mandibular. This technique is effective in determining whether the problem is localised to the maxillary or mandibular arch but will not deter.