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oral pathology 4-Periapical Pathology 4.ppt
- 1. Pulp and periapical Pulp and periapical disorders disorders
- 3. Introduction Introduction Calcified structure of the tooth protects the Calcified structure of the tooth protects the vital soft tissue ( pulp) but Caries and vital soft tissue ( pulp) but Caries and trauma and other things may be breached trauma and other things may be breached the protective calcified of the tooth. the protective calcified of the tooth. Dental caries can facilitate and leads to Dental caries can facilitate and leads to opening of pathways to various microbes opening of pathways to various microbes The pulp tissue resist as inflammation The pulp tissue resist as inflammation response which leads pulpitis response which leads pulpitis
- 4. Conti------ Conti------ Once pulp is exposed the microbes invade Once pulp is exposed the microbes invade the pulp then breakdown of pulp tissue the pulp then breakdown of pulp tissue The pulp loses its vitality The pulp loses its vitality An inflammatory is mounted while the An inflammatory is mounted while the microbes multiply . microbes multiply . The inflammatory of the pulp is followed The inflammatory of the pulp is followed by death or nicrosis by death or nicrosis
- 5. contii contii The presence of microbes and their toxins The presence of microbes and their toxins in the root canal can evokes an in the root canal can evokes an inflammatory response in the periapical inflammatory response in the periapical area and thus inflammation extends to the area and thus inflammation extends to the periapical area. periapical area.
- 6. Types of disorders of pulp and Types of disorders of pulp and periapical periapical Pulpits Pulpits Necrotic of pulp Necrotic of pulp Pulp degeneration /pulp denticles /pulp stones Pulp degeneration /pulp denticles /pulp stones and pulp calcifications and pulp calcifications Acute apical periodontitis of pulpal origin Acute apical periodontitis of pulpal origin Periapical abscess Periapical abscess Chronic apical periodontitis Chronic apical periodontitis Periapical abscess with sinus Periapical abscess with sinus Radicular cyst Radicular cyst others others
- 7. Causes Causes The causes of pulpal disorder can be The causes of pulpal disorder can be physical, chemical and bacteria. physical, chemical and bacteria. The dental caries is the commonest cause The dental caries is the commonest cause of pulpal disease of pulpal disease
- 8. Pulpitis = Pulpitis = Inflammation of the Pulp Inflammation of the Pulp Irritant Irritant Chemical irritation Chemical irritation Fillings Fillings Erosion Erosion Bleaching Bleaching Thermal changes Thermal changes Uninsulated large fillings Uninsulated large fillings Drilling Drilling Mechanical damage Mechanical damage Trauma Trauma Bruxism Bruxism Attrition Attrition Abrasion Abrasion Direct irritation Direct irritation Bacterial irritation from Bacterial irritation from caries caries Cracked tooth Cracked tooth Root fractures Root fractures Immune response Immune response Chemical mediators that Chemical mediators that initiate inflammation initiate inflammation
- 9. Microbial Irritant Microbial Irritant Microbes produce toxins Microbes produce toxins Initially pulp is infiltrated by chronic Initially pulp is infiltrated by chronic inflammatory cells inflammatory cells Macrophages, lymphocytes & plasma cells Macrophages, lymphocytes & plasma cells
- 10. The Infectious Process The Infectious Process Sites of established infection Sites of established infection Main pulp canal space and walls Main pulp canal space and walls Accessory canals and apical delta Accessory canals and apical delta Dentinal tubules Dentinal tubules Cementum surface Cementum surface Extraradicular colonizations Extraradicular colonizations Relative importance? few data, but Relative importance? few data, but the root canal infection is of course paramount the root canal infection is of course paramount Brynolf 1966, Langeland et al. 1977 Brynolf 1966, Langeland et al. 1977
- 11. The Infectious Process The Infectious Process Pulpitis Necrosis Canal infection Apical periodontitis Time Spread to apex Increasing infectious load; increasingly difficult to treat
- 12. Inflammation => Inflammation => Necrosis Necrosis Pulp can impede spread of infection Pulp can impede spread of infection Factors Factors Virulence of bacteria Virulence of bacteria Ability of pulp to release inflammatory factors to Ability of pulp to release inflammatory factors to prevent increase in intrapulpal pressure prevent increase in intrapulpal pressure Host resistance Host resistance Lymph drainage Lymph drainage Necrosis: coronal => apical Necrosis: coronal => apical
- 13. Inflammation => Edema => vascular response Increased local pressure More about inflammation.. More about inflammation.. Increased vascular permeabiltiy Increased vascular permeabiltiy Infiltrate of leukocytes Infiltrate of leukocytes Decreased lymphatic drainage Decreased lymphatic drainage
- 14. So whats really going on? 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
- 15. The sum total of the The sum total of the inflammatory response may inflammatory response may cause more damage that the cause more damage that the initial irritants alone! initial irritants alone!
- 16. PULPITIS PULPITIS Inflammation of dental pulp Inflammation of dental pulp Main source for dental pain Main source for dental pain Causes Causes Dental caries- the Dental caries- the most common most common cause cause Traumatic exposure to pulp Traumatic exposure to pulp Repeated dental procedure Repeated dental procedure
- 17. Pathogenesis Pathogenesis Any causes above Any causes above Exposure to pulp Exposure to pulp Invasion by bacteria- Streptococus Invasion by bacteria- Streptococus Inflammation of pulp Inflammation of pulp
- 18. Types Types Acute (rapid, severe onset, short duration) Acute (rapid, severe onset, short duration) Open communication between pulp cavity & oral cavity) Open communication between pulp cavity & oral cavity) closed closed Chronic (slow , long duration, mild pain) Chronic (slow , long duration, mild pain) Open Open Closed Closed
- 19. Acute-Closed Acute-Closed Micro organism- virulent & large no. Micro organism- virulent & large no. Clinical features Clinical features Early stage - Hypersensitivity to hot & cold Early stage - Hypersensitivity to hot & cold Later more persistent Later more persistent Pain- sharp, severe & stabbing Pain- sharp, severe & stabbing Sometimes not localized Sometimes not localized Tender Tender Tooth discoloration Tooth discoloration Swelling of gum Swelling of gum
- 20. Acute-Open Acute-Open Common Common Acute exposure with micro organisms Acute exposure with micro organisms Occurs at late stage of caries Occurs at late stage of caries Abscess formed drain out of cavity Abscess formed drain out of cavity
- 21. Clinical features Clinical features Hypersensitivity hot & cold in early stage Hypersensitivity hot & cold in early stage Less pain Less pain Slight tender Slight tender
- 22. Chronic-closed Chronic-closed No communication B/W pulp & oral cavity No communication B/W pulp & oral cavity Pulp tissue destruction at the site of micro organism entry Pulp tissue destruction at the site of micro organism entry Infection remains localized for long time with remaing Infection remains localized for long time with remaing pulp tissue intact or destruction occurs slowly pulp tissue intact or destruction occurs slowly Clinical features Clinical features Hypersensitivity Hypersensitivity Early stage- to hot and cold Early stage- to hot and cold Late stage- only to hot but relieved by cold Late stage- only to hot but relieved by cold
- 23. Chronic-open Chronic-open Usually occurs on widely opened cavity Usually occurs on widely opened cavity Pulp is destroyed & replaced by granulation tissue & Pulp is destroyed & replaced by granulation tissue & become epithelialised to form pulp polyp become epithelialised to form pulp polyp PAINLESS PAINLESS
- 24. Diagnosis Diagnosis Test of healthy pulp Test of healthy pulp Tapping of tooth directly Tapping of tooth directly Sensitivity if present indicates the spread of inflammation Sensitivity if present indicates the spread of inflammation to surrounding tissue to surrounding tissue hot & cold sensitivity hot & cold sensitivity If pain persists even after stimulus removal or If pain persists even after stimulus removal or Pain persists spontaneously Pain persists spontaneously Pulp may not be healthy to save Pulp may not be healthy to save
- 25. Test of pulp- dead or alive Test of pulp- dead or alive Electric pulp tester Electric pulp tester It helps to recognize the pulp whether its alive or It helps to recognize the pulp whether its alive or dead but dead but If person feels the electric charge delivered to the If person feels the electric charge delivered to the tooth the pulp is alive tooth the pulp is alive
- 26. Treatment Treatment If pulp viable just remove irritant n healed itself If pulp viable just remove irritant n healed itself Removal of caries n restoration by filling Removal of caries n restoration by filling If pulp dead If pulp dead RCT RCT Tooth extraction Tooth extraction antibiotic is given- penicillin in acute cases antibiotic is given- penicillin in acute cases
- 27. Time-Course of Apical Peridontitis Time-Course of Apical Peridontitis Dynamics of pulpal infection Dynamics of pulpal infection Bacterial succession and variations in Bacterial succession and variations in virulence and pathogenicity virulence and pathogenicity Host factors modulating inflammation Host factors modulating inflammation and spread of the infection and spread of the infection Ultimate consequences of root canal Ultimate consequences of root canal infection infection
- 28. Microbes Microbes Type: Type: Dependent on the environment, nutrients, and Dependent on the environment, nutrients, and competition competition Primary infection: Primary infection: Obligate anaerobes and Gram Negative bacteria. Obligate anaerobes and Gram Negative bacteria. Secondary infection: Secondary infection: Facultative and Gram Positive bacteria. Including E. Facultative and Gram Positive bacteria. Including E. Faecalis and candida. Faecalis and candida. Baumgartner
- 29. Inflammation of the periapical region Inflammation of the periapical region Relationship between pulpal and periapical Relationship between pulpal and periapical pathosis pathosis Periapical pathology follows pulp pathology Periapical pathology follows pulp pathology Periapical disease meets a more effective Periapical disease meets a more effective resistance that pulpal disease resistance that pulpal disease Repair is more often achieved Repair is more often achieved
- 30. From Pulpal to Periapical Pathosis From Pulpal to Periapical Pathosis
- 31. Periapical Pathosis Periapical Pathosis Bacterial endotoxins & inflammatory Bacterial endotoxins & inflammatory mediators trigger surrounding immune cells mediators trigger surrounding immune cells Defense cells Defense cells Prevent spread of infection into bone Prevent spread of infection into bone
- 32. Periapical Pathosis Periapical Pathosis Bone is replaced by highly vascularized Bone is replaced by highly vascularized inflammatory tissue which can much better inflammatory tissue which can much better eliminate invading microbes than the original eliminate invading microbes than the original bone tissue could have. bone tissue could have.
- 33. Periradicular lesions of pulpal origin Periradicular lesions of pulpal origin Symptomatic apical periodontitis Symptomatic apical periodontitis Asymptomatic apical periodontitis Asymptomatic apical periodontitis Apical abscess Apical abscess Symptomatic Apical Periodontitis Apical Abcess
- 34. Periapical Inflammation Periapical Abscess Apical Periodontitis Periapical cyst Cellulitis Osteitis Osteomyelitis Cavernous sinus thrombosis
- 35. Symptomatic Apical Periodontitis Symptomatic Apical Periodontitis Clinical features Clinical features Localized Localized Frequently spontaneous Frequently spontaneous Intense throbbing pain Intense throbbing pain Painful to touch Painful to touch None to minimal swelling None to minimal swelling
- 36. Symptomatic Apical Periodontitis Symptomatic Apical Periodontitis Histology Histology Inflammation of the PDL with acute and Inflammation of the PDL with acute and chronic inflammatory cells chronic inflammatory cells X-ray exam X-ray exam no change to slight thickening of no change to slight thickening of periodontal membrane periodontal membrane Treatment Treatment RCT or extraction RCT or extraction
- 37. Asymptomatic Apical Periodontitis Asymptomatic Apical Periodontitis Clinical features Clinical features Represents a Represents a stand-off stand-off between local between local resistance and noxious stimuli resistance and noxious stimuli Indicative of pulpal necrosis Indicative of pulpal necrosis Common Common Painless Painless Slow growing Slow growing May transform into a cyst or granuloma May transform into a cyst or granuloma
- 38. Asymptomatic Apical Periodontitis Asymptomatic Apical Periodontitis Histology Histology Proliferation of fibroblasts and endothelial Proliferation of fibroblasts and endothelial cells cells Lymphocytes, plasma cells and phagocytes Lymphocytes, plasma cells and phagocytes Foam cells and cholesterol clefts Foam cells and cholesterol clefts Epithelial rest of Malassez Epithelial rest of Malassez X-ray X-ray Large radiolucency up to 1cm Large radiolucency up to 1cm Treatment => RCTx or extraction Treatment => RCTx or extraction
- 40. Periapical Abscess Periapical Abscess A localized collection of pus in a cavity A localized collection of pus in a cavity formed by the disintegration of tissues. formed by the disintegration of tissues. Indicative of pupal death Indicative of pupal death Type is based on the degree of exudate Type is based on the degree of exudate formation, severity of pain and the presence formation, severity of pain and the presence of symptoms of symptoms Symptomatic apical abscess Symptomatic apical abscess Asymptomatic apical abscess Asymptomatic apical abscess
- 41. Periapical Abscess Periapical Abscess Clinical features Clinical features Rapid onset of extreme pain Rapid onset of extreme pain Painful to percussion Painful to percussion Not localized adjacent teeth can be painful Not localized adjacent teeth can be painful SWELLING present SWELLING present Sinus tract can form Sinus tract can form Potentially life threatening Potentially life threatening
- 42. Periapical Abscess Periapical Abscess Histology Histology Resembles and acute apical periodontitis Resembles and acute apical periodontitis Involvement of the adjacent bone and soft tissue Involvement of the adjacent bone and soft tissue Pus and tissue necrosis Pus and tissue necrosis X-ray X-ray Widened PDL to large alveolar radiolucency Widened PDL to large alveolar radiolucency Treatment Treatment Rx for antibiotics Rx for antibiotics Establish drainage Establish drainage
- 43. Untreated Apical Abscess Untreated Apical Abscess Cellulitis Cellulitis Infection travels through the facial planes of least resistance Infection travels through the facial planes of least resistance Fever Fever Osteomyelitis Osteomyelitis Infection within bone through the medullary spaces Infection within bone through the medullary spaces Parulis = Parulis = gum boil gum boil Ludwig Ludwig s angina s angina Swelling in floor of mouth elevates tongue and blocks Swelling in floor of mouth elevates tongue and blocks airway airway Cavernous sinus thrombosis Cavernous sinus thrombosis Infection from MX premolars and molars extends into the Infection from MX premolars and molars extends into the cranial vault cranial vault
- 45. Spread of infection Spread of infection The path of least resistance The path of least resistance Buccal plate is the most common route due to Buccal plate is the most common route due to the thin buccal bone the thin buccal bone Outside on face Outside on face Palate Palate Neck below mylohyoid Neck below mylohyoid PDL PDL Pulp canal Pulp canal Maxillary sinus Maxillary sinus Mandibular canal Mandibular canal
- 51. Apical Periodontal Cyst / Granuloma Apical Periodontal Cyst / Granuloma Clinical features Clinical features The most common cyst of the jaws The most common cyst of the jaws May be asymptomatic of become May be asymptomatic of become symptomatic symptomatic Slow continuous enlargement Slow continuous enlargement X-ray X-ray Well-circumscribed radiolucency Well-circumscribed radiolucency Associated with apices of teeth Associated with apices of teeth May cause resorption of teeth and bone May cause resorption of teeth and bone
- 52. Apical Periodontal Cyst Apical Periodontal Cyst Histology Histology Inflammatory cells Inflammatory cells Prominent epithelial lining without keratin Prominent epithelial lining without keratin Body of cyst filled with semifluid material Body of cyst filled with semifluid material Treatment => Usually require apical Treatment => Usually require apical surgery if persistant surgery if persistant
- 53. Post RCT Periapical Granuloma Periapical Granuloma Initial Post Apicoectomy 2 Year Post Op
- 54. Apical Cyst vs. Granuloma Apical Cyst vs. Granuloma A cyst is A cyst is lined by squamous epithelium lined by squamous epithelium and containing and containing necrotic material in the lumen. The cyst wall or capsule necrotic material in the lumen. The cyst wall or capsule contains dense fibrous connective tissue with slight chronic contains dense fibrous connective tissue with slight chronic inflammation and cholesterin slits surrounded by foreign inflammation and cholesterin slits surrounded by foreign body-type giant cells. There are "foam" cells in the epithelial body-type giant cells. There are "foam" cells in the epithelial lining. lining. A lesion with A lesion with highly vascular tissue highly vascular tissue containing macrophages, containing macrophages, fibroblasts, collagen, and immune cells (neutrophils, plasma fibroblasts, collagen, and immune cells (neutrophils, plasma cells, T and B cells, lymphocytes, eosinophils cells, T and B cells, lymphocytes, eosinophils
- 56. condensing osteitis condensing osteitis Bone sclerosis around apices of tooth with pulpitis Bone sclerosis around apices of tooth with pulpitis Occurs when there is high tissue resistance to low Occurs when there is high tissue resistance to low grade infection grade infection Clinical features Clinical features Adolescents and young adults Adolescents and young adults Most common in mandibular first molars Most common in mandibular first molars Tooth usually has large carious lesion Tooth usually has large carious lesion No symptoms No symptoms
- 57. Condensing Osteitis Condensing Osteitis Histology Histology Dense bony trabeculation Dense bony trabeculation X-ray X-ray Area of radiopaque sclerotic bone with no Area of radiopaque sclerotic bone with no radiolucent border radiolucent border Entire root outline is visible Entire root outline is visible 85% disappear after extraction 85% disappear after extraction
- 58. Condensing Osteitis Condensing Osteitis Treatment Treatment None None RCTx RCTx Bone Scar Bone Scar The residual area of condensing osteitis that remains The residual area of condensing osteitis that remains after resolution of inflammation after resolution of inflammation Differential diagnosis Differential diagnosis Idiopathic osteosclerosis Idiopathic osteosclerosis Periapical cemental dysplasia Periapical cemental dysplasia
- 60. Osteomyelitis Osteomyelitis If the periapical infection and inflammation extend If the periapical infection and inflammation extend through the marrow spaces of the jaw, the result is through the marrow spaces of the jaw, the result is osteomyelitis. In this case, you can identify the offending osteomyelitis. In this case, you can identify the offending tooth causing the diffuse and irregular bone destruction. tooth causing the diffuse and irregular bone destruction.
- 61. end