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DIAGNOSIS of PULPAL DISEASES Presenter: Dr. R.O. Kekere-Ekun Keywords: Diseases, Pulp, Diagnosis. OBJECTIVE Describe The

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DIAGNOSIS of PULPAL DISEASES Presenter: Dr. R.O. Kekere-Ekun Keywords: Diseases, Pulp, Diagnosis. OBJECTIVE Describe The DIAGNOSIS OF PULPAL DISEASES Presenter: Dr. R.O. Kekere-ekun Keywords: Diseases, Pulp, Diagnosis. OBJECTIVE ● Describe the pulp, its functions and response to irritants/injuries. ● List the clinical classification of the diseases of the pulp. ● List the various causative factors involved in pulp diseases. ● Describe the diseases of the pulp in terms of signs and symptoms. ● Identify the potential sequelae of the diseases of the pulp. ● Itemize the essentials of diagnosis of the diseases of the pulp. ● List the various clinical examinations and tests that can be used to make a diagnosis for the diseases of the pulp as well as describe what the results of each test indicate. ● Describe how to conduct pulp tests and identify materials that can be used to conduct pulp tests. ● Describe the different clinical pulpal conditions according to the following aspects: –Patient dental history; –Patient signs and symptoms; –Pulp test results; –Radiographic findings. ● Note the top differential diagnosis of the diseases of the pulp. INTRODUCTION The dental pulp is a unique tissue and its importance in the long-term prognosis of the tooth is often ignored by clinicians. It is unique in that it resides in a rigid chamber which provides strong mechanical support and protection from the microbial rich oral environment. If this rigid shell loses its structural integrity, the pulp is under the threat of the adverse stimuli from the mouth, such as 1 caries, cracks, fractures and open restoration margins, all of which provide pathways for micro-organisms and their toxins to enter the pulp. The pulp initially responds to irritation by becoming inflamed and, if left untreated, this will progress to pulp necrosis and infection. The inflammation will also spread to the surrounding alveolar bone and cause periapical pathosis. The magnitude of pulp-related problems should not be underestimated since their most serious consequence is oral sepsis, which can be life threatening, and hence correct diagnosis and management are essential. Clinicians must have a thorough understanding of the physiological and pathological features of the dental pulp as well as the biological consequences of treatment interventions. Whenever any disease is to be treated, there are several general principles that must be followed. The first, and perhaps the most important, is to identify the disease and its cause which can usually be achieved with a thorough history, clinical examination and appropriate diagnostic tests. Identification of the cause is essential since it must be removed as an integral part of the treatment of the disease. Then the other general principles of treatment can be followed and these include removing the effect of the disease, restoring the tissues to their normal function, monitoring the healing and stability over time, and preventing recurrence of the disease. The importance of correct diagnosis and treatment planning must not be underestimated. There are many causes of facial pain and the differential diagnosis can be both difficult and demanding. THE DENTAL PULP Pulp tissue is alive and functioning: ● Surrounded by the hard structures of teeth [enamel and dentine]. ● It, in fact, has produced much of that very hard structure [odontoblast secreting pre- dentine]. ● It can produce more hard structure as a defense system [part of inflammatory response]. ● It provides nourishment for the odontoblasts which lines its surface. ● These odontoblasts have long processes which extend approximately one-third as far as the amelodentinal junction. ● The tubules beyond the odontoblast processes are normally patent and filled with tissue fluid. 2 ● When irritants are applied to the distal ends of the dentinal tubules, the odontoblasts will form more dentine, within the pulp as secondary dentine, within tubules as peritubular dentine, or lead to occlusion of the tubules as mineralized deposits as tubulae sclerosis. ● The more the area of exposed dentine, the greater is the effect on the pulp. ● The pulp and dentine can thus be regarded as one interconnected tissue–the dentino- pulpal complex, protected from irritation by an intact layer of enamel. Pulp tissue is alive and functioning: ● Pulp has the potential to produce a robust inflammatory response to irritation/infection. ● By its inflammatory responses, it also produces pain for the patient. ● Pulp tissue can break down and become necrotic. ● Infection/inflammation can spread throughout the pulp tissue and out the tooth to the surrounding tissues. ● Therefore, the pulp tissue requires careful protection in all that we do in dentistry to avoid the negative responses and to encourage the positive ones. ● This affects diagnostic decisions, restorative decisions, prep and cavity designs, methods of preparation, and materials used. THE NORMAL TOOTH ● A tooth with a non-inflamed pulp; ● It is asymptomatic; ● It exhibits a mild to moderate transient response to thermal and electric pulpal stimuli; ● This +ve response subsides almost immediately after such stimuli are removed; ● The tooth and its attachment apparatus do not cause a painful response to percussion and palpation; ● Radiograph will reveal no pulpal or periradicular pathosis; 3 ● However, as a result of caries, restorative procedures, trauma, thermal, physical or chemical injury, etc. the normal pulp may become inflamed and present itself clinically as either a reversible or irreversible pulpitis. CLASSIFICATION OF THE DISEASES OF THE PULP Introduction It is widely accepted that the most common cause of pulp and periapical diseases is the presence of bacteria within the involved tooth, and the most common pathways of entry for these bacteria are via caries, cracks, fractures and open restorative margins. Other possible pathways for bacterial penetration are associated with periodontal disease and dental trauma. Pulpal inflammation and necrosis are also initiated by restorative procedures, trauma, chemical irritation and severe thermal stimulation. These inflammatory lesions cause localized oedema and a resulting increase in intra- pulpal pressure and cell death. Increased damage associated with an inflammatory exudate cause local collapse of the venous part of the local microvasculature. This causes local tissue hypoxia and anoxia resulting in localized necrosis, the chemical mediators of which cause further localized oedema, completing the cycle. EXPOSED SENSITIVE DENTINE This may result from gingival recession or surgery producing exposed root surfaces, or it may result from a failing restoration or caries exposing dentine to oral fluids. The patient will usually complain of sensitivity to hot, cold, and sweet food and drink, but the sensitivity (rather than pain) is often poorly localized. It may indeed be generalized in several areas of the mouth. Pulp tests applied to enamel surfaces will produce a normal response, but if the exposed dentine surface is stimulated either thermally or electrically, or is scratched with a probe, there may be an increased response. The teeth are not tender to percussion. CRACKED CUSPS Cusps may crack either superficially or deep into the tooth, whether the tooth is restored or not. The crack may involve the pulp or pass only through enamel and dentine. The symptoms are often poorly localized and may occur only periodically. Sometimes there is a sharp pain on biting hard on tough food, and occasionally with thermal stimuli. Thermal and electrical pulp tests are often inconclusive and the tooth may not be tender to percussion although pressure laterally on individual cusps may produce pain. Transillumination may help to show the crack, or applying disclosing solution or other 4 stain to the tooth may reveal it. Unfortunately, many teeth show multiple cracks and do not cause symptoms (perhaps because these cracks only involve enamel), and thus it is difficult to be sure that any crack that is seen is actually the cause of the pain. A useful diagnostic test is to ask the patient to bite on a cotton-wool roll. Pain is often felt when the pressure is released rather than when it is applied. Sometimes, when the restoration is removed from a suspect tooth, the crack is seen at the base of the cavity and these deep cracks are more likely to cause symptoms. PULP HYPEREMIA This change is characterized by a short and well localized pain in response to physical or chemical stimuli which diminishes after a causing effect stops. The treatment in this case is an indirect pulp capping. REVERSIBLE PULPITIS ● A review of the dental history reveals that the patient is experiencing an intermittent, exaggerated response to a stimulus such as cold or hot. However, the discomfort does not linger after the stimulus is removed, i.e., the discomfort or pain disappears when the stimulus is removed. Diagnostic findings from clinical and radiographic exams: ● Restoration and/or caries associated with the involved tooth; ● Periodontal ligament (PDL) space is WNL; ● EPT: Positive response; ● Thermal tests: Non-lingering, exaggerated response to cold and/or hot; ● Percussion: No unusual sensitivity. ● If the etiology of the inflammation is identified and corrected, the pulp will return to a normal state and the symptoms will disappear. However, if the inflammation continues, localized areas of tissue necrosis will occur which can progress to an irreversible pulpitis. IRREVERSIBLE PULPITIS ● It is accepted that irreversible pulpal disease occurs when trauma inflicted on the pulpal tissues exceeds their reparative capacity. Such a pathological insult
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