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Transcript
B. Retamozo DDS, MSD Pulpitis = Inflammation of the Pulp Irritant – Direct irritation – Chemical irritation Fillings Erosion Bleaching – Thermal changes Uninsulated large fillings Drilling – Mechanical damage Trauma Bruxism Attrition Abrasion Bacterial irritation from caries Cracked tooth Root fractures Immune response – Chemical mediators that initiate inflammation Microbial Irritant Microbes produce toxins Initially pulp is infiltrated by chronic inflammatory cells – Macrophages, lymphocytes & plasma cells Secondarily PMNs infiltrate – Area of liquefaction necrosis The Infectious Process • Sites of established infection – Main pulp canal space and walls – Accessory canals and apical delta – Dentinal tubules – Cementum surface – Extraradicular colonizations Relative importance? – few data, but the root canal infection is of course paramount – Brynolf 1966, Langeland et al. 1977 Apical periodontitis The Infectious Process Pulpitis Necrosis Canal infection Spread to apex Increasing infectious load; increasingly difficult to treat Time The Inflammartory Process Mast cells – Histamine release Kinins – responsible symptoms of acute inflammation Cellular damage releases Phospholipase A2 – Prostaglandins, thrombaxanes & leukotrienes Neuropeptides: SP & CGRP – Recruit inflammatory cells Inflammation => Necrosis Pulp can impede spread of infection Factors – Virulence of bacteria – Ability of pulp to release inflammatory factors to prevent increase in intrapulpal pressure – Host resistance – Lymph drainage Necrosis: coronal => apical More about inflammation.. Inflammation => vascular response Increased vascular permeabiltiy Infiltrate of leukocytes Decreased lymphatic drainage Edema => Increased local pressure So whats really going on? Pulp is enclosed within calcified walls – Low compliance system Circulation slows due to compression of venous return – Odontoblasts are altered or destroyed Increase in tissue pressure – Compression of venules in area of injury – Progresses coronal => Apex The sum total of the inflammatory response may cause more damage that the initial irritants alone! Time-Course of Apical Peridontitis • Dynamics of pulpal infection • Bacterial succession and variations in virulence and pathogenicity • Host factors modulating inflammation and spread of the infection • Ultimate consequences of root canal infection Baumgartner Microbes Type: – Dependent on the environment, nutrients, and competition Primary infection: – Obligate anaerobes and Gram Negative bacteria. Secondary infection: – Facultative and Gram Positive bacteria. Including E. Faecalis and candida. Natural Course of the Disease Vs. Pain • Varies in intensity and severity – Pain sometimes accompanies pulpitis and apical periodontitis • Unpredictable if untreated – Pulpitis and acute apical periodontitis dominate as sources for acute dental pain in children and adults (Zeng et al 1994, Lygidakis et at 1998) – which may be debilitating to the patient and lead to absence from work and involvement of costly health services. (Ørstavik, 2009) Inflammation of the periapical region Relationship between pulpal and periapical pathosis – Periapical pathology follows pulp pathology Periapical disease meets a more effective resistance that pulpal disease – Repair is more often achieved From Pulpal to Periapical Pathosis Resorption of bone – Separate irritants from bone – Prevents osteomyelitis Periapical Pathosis Bacterial endotoxins & inflammatory mediators trigger surrounding immune cells Defense cells – Prevent spread of infection into bone Cytokines: interleukins and TNF – activate surrounding osteoclasts to destroy bone Periapical Pathosis Bone is replaced by highly vascularized inflammatory tissue which can much better eliminate invading microbes than the original bone tissue could have. Periradicular lesions of pulpal origin Symptomatic apical periodontitis Asymptomatic apical periodontitis Apical abscess Symptomatic Apical Periodontitis Apical Abcess Periapical Inflammation Periapical Abscess Apical Periodontitis Cellulitis Osteitis Osteomyelitis Cavernous sinus thrombosis Periapical cyst Symptomatic Apical Periodontitis Clinical features – – – – – Localized Frequently spontaneous Intense throbbing pain Painful to touch None to minimal swelling Symptomatic Apical Periodontitis Histology – Inflammation of the PDL with acute and chronic inflammatory cells X-ray exam – no change to slight thickening of periodontal membrane Treatment – RCT or extraction Asymptomatic Apical Periodontitis Clinical features – Represents a “stand-off” between local resistance and noxious stimuli – Indicative of pulpal necrosis – Common – Painless – Slow growing – May transform into a cyst or granuloma Asymptomatic Apical Periodontitis Histology – Proliferation of fibroblasts and endothelial cells – Lymphocytes, plasma cells and phagocytes Foam cells and cholesterol clefts – Epithelial rest of Malassez X-ray – Large radiolucency up to 1cm Treatment => RCTx or extraction Asymptomatic Apical Periodontitis Periapical Abscess A localized collection of pus in a cavity formed by the disintegration of tissues. Indicative of pupal death Type is based on the degree of exudate formation, severity of pain and the presence of symptoms – Symptomatic apical abscess – Asymptomatic apical abscess Periapical Abscess Clinical features – – – – – – Rapid onset of extreme pain Painful to percussion Not localized – adjacent teeth can be painful SWELLING present Sinus tract can form Potentially life threatening Periapical Abscess Histology – Resembles and acute apical periodontitis – Involvement of the adjacent bone and soft tissue – Pus and tissue necrosis X-ray – Widened PDL to large alveolar radiolucency Treatment – Rx for antibiotics – Establish drainage Untreated Apical Abscess Cellulitis – Infection travels through the facial planes of least resistance – Fever Osteomyelitis – Infection within bone through the medullary spaces Parulis = “gum boil” Ludwig’s angina – Swelling in floor of mouth elevates tongue and blocks airway Cavernous sinus thrombosis – Infection from MX premolars and molars extends into the cranial vault End-Points of Root Canal Infections • Immediate abscess and sinus tract formation: incidence? • Chronic, stable encapsulation • Chronic cyst formation • Exacerbation of chronic lesion: incidence (5% per year?) • Sinus tract formation: incidence? 20 – 70% – Any available surface, sinus, nose, mucosa, skin • Spreading oral infection: incidence? – Submandibular, sublingual, local fascies – Eyes, brain, mediastinum Spread of infection… The path of least resistance Buccal plate is the most common route due to the thin buccal bone Outside on face Palate Neck below mylohyoid PDL Pulp canal Maxillary sinus Mandibular canal Apical Periodontal Cyst / Granuloma Clinical features – The most common cyst of the jaws – May be asymptomatic of become symptomatic – Slow continuous enlargement X-ray – Well-circumscribed radiolucency – Associated with apices of teeth – May cause resorption of teeth and bone Apical Periodontal Cyst Histology – Inflammatory cells – Prominent epithelial lining without keratin – Body of cyst filled with semifluid material Treatment => Usually require apical surgery if persistant Periapical Granuloma Initial Post RCT Post Apicoectomy 2 Year Post Op Apical Cyst vs. Granuloma A cyst is lined by squamous epithelium and containing necrotic material in the lumen. The cyst wall or capsule contains dense fibrous connective tissue with slight chronic inflammation and cholesterin slits surrounded by foreign body-type giant cells. There are "foam" cells in the epithelial lining. A lesion with highly vascular tissue containing macrophages, fibroblasts, collagen, and immune cells (neutrophils, plasma cells, T and B cells, lymphocytes, eosinophils Natural Course of the Disease: Conclusions • Unpredictable if untreated • It does not heal • Potentially very painful • Serious complications/sequelae are rare Filling therapy Endodontics Extraction Pulpitis ->Necrosis->Apical Perio->Acute phases->Local spread->Systemic spread condensing osteitis aka periapical osteosclerosis Bone sclerosis around apices of tooth with pulpitis Occurs when there is high tissue resistance to low grade infection Clinical features – – – – Adolescents and young adults Most common in mandibular first molars Tooth usually has large carious lesion No symptoms Condensing Osteitis Histology – Dense bony trabeculation X-ray – Area of radiopaque sclerotic bone with no radiolucent border – Entire root outline is visible – 85% disappear after extraction Condensing Osteitis Treatment – None – RCTx Bone Scar – The residual area of condensing osteitis that remains after resolution of inflammation Differential diagnosis – Idiopathic osteosclerosis – Periapical cemental dysplasia Condensing osteitis Osteomyelitis If the periapical infection and inflammation extend through the marrow spaces of the jaw, the result is osteomyelitis. In this case, you can identify the offending tooth causing the diffuse and irregular bone destruction. Tooth for Competency II Plastic Maxillary Premolar Before the exam – Mount tooth – Place your box number in the acrylic of the tooth – Take 2 initial x-rays Get nail polish and start check Access Clean, shape and obturate one canal Tooth for Competency II X-rays that must be turned in with tooth – 1 film for total length of root canal – 1 film with largest working file to working length – 1 film with master cone – 2 final films Place tooth in ziplock bag with paperwork and x-rays marked with your box # to your instructor Final words All projects must be graded before the end of the competency exam Remediation of the competency – Must be done prior to start of break to receive satisfactory grade Clinic privileges – Any molar Mounted in Endo typodont on the manikin Access, clean, shape and obturate all canals Dental Humor