Published on November 1, 2010
DISORDERS OF THE PULP & PERIPAICAL TISSUESPrepared by: Dr Sundeep Bhagwath : DISORDERS OF THE PULP & PERIPAICAL TISSUESPrepared by: Dr Sundeep Bhagwath OVERVIEW : OVERVIEW Slide 3: INTRODUCTION ETIOLOGY OF PULPITIS FACTORS AFFECTING RESPONSE OF PULP CLASSIFICATION OF PULPITIS TYPES OF PULPITIS PERIAPICAL ABSCESS PERIAPICAL GRANULOMA PERIAPICAL CYST / RADICULAR CYST CELLULITIS LUDWIG’S ANGINA CAVERNOUS SINUS THROMBOSIS OSTEOMYELITIS INTRODUCTION : INTRODUCTION Slide 5: Pulpitis is an inflammation of pulp tissue, a response to surrounding environment The vitality of the tooth depends on defence response of pulp dentine complex by: - Sclerotic dentin - Tertiary dentin - Calcified bridge of dentinal tubules ETIOLOGY : ETIOLOGY : MECHANICAL: Trauma, iatrogenic damage and barometric changes. THERMAL: uninsulated metallic restorations and dental procedures like cavity preparation, exothermic chemical reactions of dental materials etc. CHEMICAL: Irritation from certain dental materials or from erosion. BACTERIAL: Through toxins or from direct extension of caries FACTORS AFFECTING RESPONSE OF PULP : FACTORS AFFECTING RESPONSE OF PULP Slide 9: Severity and duration of irritant. Nature of irritant. Health condition of the pulp or pre-existing state of the pulp Apical blood flow Local anatomy of the pulp chamber Host defence CLASSIFICATION : CLASSIFICATION Slide 11: I. According to pathological condition: - - Focal or acute reversible pulpitis (Pulp hyperaemia) - Irreversible pulpitis II. According to its duration: - - Acute pulpitis - Chronic pulpitis III. According to presence of dentin covering the pulp chamber: - - Open pulpitis - Closed pulpitis Slide 12: IV. According to extension of inflammation in pulp tissue: - - Partial pulpitis - Complete / total pulpitis V. According to amount of pus formation: - - Exudative pulpitis - Suppurative pulpitis ACUTE REVERSIBLE PULPITIS(Focal reversible pulpitis, Pulp hyperaemia) : ACUTE REVERSIBLE PULPITIS(Focal reversible pulpitis, Pulp hyperaemia) Slide 14: Acute reversible inflammation of pulp tissue characterized by vascular dilatation AETIOLOGY: - Any mild irritants Slide 15: CLINICAL FEATURES: - Signs and symptoms: painful Duration: 10-15 minutes, severe and short Precipitating factors of pain: hot and cold agents Nature of pain: Throbbing, continuous and radiating. Pain stops when precipitating factors are removed Slide 16: The pain depends on - The size of exposed pulp (size of dental caries) Severity of pulp inflammation Age of patient Nature of covering dentine Slide 17: HISTOLOGICAL FEATURES: - Inflamed pulp tissue contains dilated blood vessels of various sizes and are lined by endothelial cells Presence of normal odontoblasts indicate vitality of the pulp tissue. Slide 18: PROGNOSIS-: It is a reversible condition. If it is treated , pulp will return back to its normal status. If it is left untreated , it will not return back to its normal status but it will enter the next phase.... ACUTE PROGRESSIVE PULPITIS : ACUTE PROGRESSIVE PULPITIS Slide 20: CLINICAL FEATURES: - Duration : - more than 10-15 minutes, severe and continuous, especially at night Precipitating factors of pain : - spontaneously as well as hot and cold agents Nature of pain : - Throbbing continuous and radiating pain The pain does not stop even when precipitating factors are removed. Slide 21: PROGNOSIS: - If it is left untreated, it will change to chronic pulpitis or pulp necrosis CHRONIC PULPITIS : CHRONIC PULPITIS Slide 26: It is a chronic inflammation of pulp tissue characterized by specific clinical features. CLINICAL FEATURES: - Signs and symptoms: - painful Duration: - long duration (few days to months). Slide 27: Precipitating factors of pain: - hot, cold agents and during biting. Nature of pain: - Mild and intermittent pain The pain stops when precipitating factors are relieved and when the tooth is treated Slide 28: The pain depends on: - The size of exposed pulp (size of dental caries) Severity of pulp inflammation Age of patient Nature of covering dentin HISTOPATHOLOGICAL FEATURES: - : HISTOPATHOLOGICAL FEATURES: - The pulp tissue contains dilated blood vessels with varying sizes. Degenerated odontoblasts seen. Areas of chronic inflammatory cells and fibrosis can be seen around inflamed areas Slide 30: PROGNOSIS: - It is dependant on the success of pulp capping. CHRONIC OPEN HYPERPLASTIC PULPITIS( Pulp Polyp ) : CHRONIC OPEN HYPERPLASTIC PULPITIS( Pulp Polyp ) Slide 32: It is a chronic inflammation of pulp tissue characterized by hyperplasia of connective tissue of pulp in the form of polypoid mass which originates from exposed pulp chamber Slide 33: CLINICAL FEATURES : - Site: A grossly carious molar (permanent/deciduous) where pulp chambers are wide, having multiple roots with highly vascular pulp tissue Shape : nodular fungated mass fills pulp chamber Slide 34: Size : variable Colour : reddish, bleeds readily Covering surface : intact or ulcerated HISTOLOGICAL FEATURES: - : HISTOLOGICAL FEATURES: - Mass consists of proliferation of granulation tissue with newly formed, dilated blood vessels of varying sizes, chronic inflammatory cells and fibrosis Generalized degenerated odontoblasts also called “Wheat Shafing” of Odontoblasts The mass is covered by hyperplastic stratified squamous epithelial surface Source of epithelial cells are from saliva or desquamated mucosa of cheeks or gingiva PULP CALCIFICATION (Pulp Stone or Denticles) : PULP CALCIFICATION (Pulp Stone or Denticles) Slide 42: It is a localized / generalized condition of pulp tissue characterized by formation of pulp stone in the form of calcified bodies CLINICAL FEATURES : - Site: coronal or radicular pulp Size: variable Signs and symptoms : painless Slide 43: RADIOGRAPHIC FEATURES: - Radiopaque mass / masses with variable sizes inside the pulp chamber or pulp canals. Slide 44: HISTOLOGICAL TYPES: - True pulp stone - consists of dentinal tubules. False pulp stone - consists of concentric calcified rings Free pulp stone - is freely located within the pulp tissue Attached pulp stone - is adherent to dentin wall Embedded pulp stone - is surrounded by secondary dentin Slide 48: COMPLICATIONS: - It interferes with root canal treatment. Can cause pain if it impinges on major pulp nerves. PULP NECROSIS : PULP NECROSIS Slide 51: It is an irreversible condition of pulp tissue characterized by dead pulp tissue and degeneration ( necrosis ) AETIOLOGY : -Severely irritant agents. CLINICAL FEATURES : - Signs and symptoms : painful Duration : 10-15 minutes, severe and short Slide 52: Precipitating factors of pain: hot and cold agents Nature of pain: Throbbing, continuous and radiating. The pain stops when precipitating factors are relieved. PERIAPICAL GRANULOMA : PERIAPICAL GRANULOMA Slide 56: It refers to a mass of chronically inflamed granulation tissue at the apex of a non vital tooth. May arise either after an acute condition like periapical abscess becomes quiet or it may arise de novo. Important – these lesions are not static and may transform into periapical cysts or undergo acute exacerbation. Slide 57: CLINICAL FEATURES: - Mostly asymptomatic. Pain & sensitivity can develop if acute exacerbation occurs. No mobility or sensitivity to percussion of involved tooth. Pulp vitality tests are negative. Slide 58: RADIOGRAPHIC FEATURES: - Lesion can be either well / ill defined. Variable sized from small to large. Loss of apical lamina dura. Root resorption is common. Cannot distinguish periapical granulomas from periapical cysts on a radiograph. Slide 59: HISTOLOGICAL FEATURES:- Lesion shows inflamed granulation tissue containing a dense lymphocytic infiltrate mixed with PMNL’s, plasma cells and macrophages. Epithelial rests of Malassez may be seen within the granulation tissue. Slide 60: Cholesterol clefts may also be seen along with associated multinucleated giant cells. Areas of extravasation of RBC’s and hemosiderin pigmentation is also common. RADICULAR CYST(Peripaical cyst / Apical periodontal cyst) : RADICULAR CYST(Peripaical cyst / Apical periodontal cyst) Slide 62: By definition, a radicular cyst arises from epithelial rests of Malassez located in the PDL as a result of inflammation. Often, radicular cyst remains behind in jaws after removal of infected tooth – then called RESIDUAL CYST. Slide 63: CLINICAL FEATURES: - Age incidence: peak in 3rd, 4th and 5th decades. Sex incidence: Slightly more in males. Site predilection: Maxillary anterior region. Frequency: Commonest cystic lesion of jaws. Slide 64: Signs & symptoms: Primarily symptom less. Discovered accidentally during routine dental X ray exam. Slide 65: Slowly enlarging hard bony swelling initially. Later, if cysts breaks through cortical plates, lesion becomes fluctuant. Diagnostic criteria – associated teeth are non vital Rare in deciduous teeth. Slide 66: RADIOLOGICAL FEATURES: Classically presents as round / ovoid radiolucency with sclerotic borders and associated with pulpally affected tooth / teeth. If infection supervenes, the margins become indistinct, making it impossible to distinguish it from a periapical granuloma. Slide 67: DIFFERENTIAL DIAGNOSIS: - Following lesions must be distinguished from other periapical radiolucencies– 1. Periapical granuloma 2. Peripaical cemento – osseous dysplasia (early lesions) Slide 68: PATHOGENESIS: - 1. PHASE OF INITIATION: Accepted generally that rests of Malassez included within a developing periapical granuloma proliferates to form the lining of radicular cyst. How these cells are stimulated is not clear. Some product of non vital pulp can be responsible which simultaneously evokes an inflammatory response in CT. Immune factors also held responsible as plenty of plasma cells are seen in a periapical granuloma. Slide 69: 2.PHASE OF CYST FORMATION: Can occur in two possible ways. One theory states that epithelium proliferates and covers the bare CT surface of the abscess cavity. Another theory – cyst cavity forms within proliferating epithelium as the cells in center move away from their nutrient source. Prepared by Dr Sundeep S Bhagwath Slide 70: 3. PHASE OF ENLARGEMENT: - Enlargement occurs by collection of fluid within the lumen of the cyst. Osmosis plays an important role here as the cyst wall appears to have the properties of a semi permeable membrane. Slide 71: HISTOLOGICAL FEATURES:- Lined partly / completely by non keratinized epithelium of varying thickness. Epithelium usually shows arcading around the CT. The CT wall shows inflammatory infiltrate mainly in the form of lymphocytes and plasma cells. Slide 72: Hyaline / Rushton bodies are found in epithelium and rarely in CT wall. These are curved or linear structures with eosinophilic staining properties. Slide 73: Cholesterol crystals in from of clefts are often seen in the CT wall, inciting a foreign body giant cell reaction. Originate from disintegrating RBC’s in presence of inflammation. Different types of dystrophic calcification are also seen in CT wall. Slide 74: Mucus cell metaplasia as well as respiratory cells may be seen in the epithelial lining. Keratinization if found is due to metaplasia and must not be confused with an OKC. PERIAPICAL ABSCESS(Acute dentoalveolar abscess) : PERIAPICAL ABSCESS(Acute dentoalveolar abscess) Slide 76: Collection of acute inflammatory cells at the apex of a non vital tooth is called periapical abscess. Acute lesions may arise either as in initial pathosis or as an acute exacerbation of a chronic periapical pathology (Phoenix abscess). Slide 77: CLINICAL FEATURES:- Initial stages – tenderness of affected tooth. Later – pain becomes intense, with extreme sensitivity to percussion. Extrusion of tooth in its socket. Systemic findings – fever, malaise, chills. Slide 78: Abscess may spread along path of least resistance through medullary spaces resulting in Osteomyelitis. Can also perforate cortical bone and spread to soft tissues – Cellulitis. It can also drain through an intraoral sinus tract. Opening of such a tract is usually covered by a granulation tissue – Parulis. Slide 79: Periapical abscesses may also channelize through the overlying skin and drain via a Cutaneous sinus. If an abscess begins to drain, it becomes asymptomatic due to lack of collection of pus within the cavity. Slide 80: RADIOGRAPHIC FEATURES: - In initial stages – thickening of periodontal ligaments. Later – ill defined radiolucency. Slide 81: HISTOLOGICAL FEATURES: - Microscopic sections are not usually made as specimen is fluid. Abscess contains abundant PMNL’s mixed with inflammatory exudate, cellular debris and histiocytes. Phoenix abscesses may also contain soft tissue component comprising of granulation tissue mixed with areas of abscess CELLULITIS : CELLULITIS Slide 83: It is a rapidly spreading inflammation of the soft tissues characterized by diffuse pus formation. This happens if an abscess is not able to establish drainage through the skin surface or into oral cavity. Slide 84: TYPES: - Cellulitis arising from dental infection and spreading through soft tissues of head and neck can take various forms. Mostly, infection spreads through tissue spaces like canine space, infratemporal space, pharyngeal space, buccal space, submental and submandibular space etc. Slide 85: Two especially dangerous forms of cellulitis are – - Ludwig’s angina - Cavernous sinus thrombosis Slide 86: Canine space infection Infection involving multiple spaces LUDWIG’S ANGINA : LUDWIG’S ANGINA Cellulitis of submandibular region involving sublingual, submandibular and submental spaces. In 70% cases develops from spread of infection from mandibular teeth. Increased prevalence in immunocompromised patients like AIDS, aplastic anemia, organ transplantation etc. Slide 88: CLINICAL FEATURES: - After reaching submandibular region, infection extends to lateral pharyngeal and retropharyngeal spaces. LA causes massive swelling of neck extending close to clavicles. There is posterior enlargement and protrusion of tongue. Pain in neck and floor of mouth. Slide 89: Other symptoms – dysphagia, dysphonia, drooling and sore throat. Lateral pharyngeal space involvement may cause respiratory obstruction due to laryngeal edema. In sever cases – tachypnea, dyspnea, tachycardia, stridor may also be noted. General signs – fever, malaise, leukocytosis, and raised ESR. CAVERNOUS SINUS THROMBOSIS : CAVERNOUS SINUS THROMBOSIS Occurs when infection from maxillary premolars / molars perforates buccal cortical plate and enters maxillary sinus, pterygopalatine space or infratemporal space and reaches the orbit. From here, infection enters cavernous sinus through cranial vault. Slide 91: CLINICAL FEATURES: - Periorbital edema including lateral border of nose, protrusion and fixation of eyeball. Pupil dilatation, lacrimation, photophobia and loss of vision may also occur. Pain along distribution of ophthalmic and maxillary branches of Vth cranial nerve. Proptosis, chemosis and ptosis seen in 90% cases. Fever, chills, headache, sweating, tachycardia, nausea and vomiting also occur. OSTEOMYELITIS : OSTEOMYELITIS Slide 93: Refers to acute / chronic inflammatory process in medullary spaces or cortical surfaces of bones. Various patterns recognized like focal and diffuse sclerosing, proliferative periostitis etc. Slide 94: TYPES OF OSTEOMYELITIS: - Acute osteomyelitis Chronic osteomyelitis Diffuse sclerosing osteomyelitis Condensing osteitis (Focal sclerosing osteomyelitis) Osteomyelitis with proliferative periostitis. Alveolar osteitis Slide 95: PREDISPOSING FACTORS: - After odontogenic infections Trauma to jaws Presence of ANUG Chronic systemic diseases Immunocompromised states Tobacco and alcohol abuse Diabetes mellitus Exanthematous fevers Malignancy Malnutrition ACUTE OSTEOMYELITIS : ACUTE OSTEOMYELITIS Acute osteomyelitis occurs when acute inflammation spreads through medullary spaces of bone. CLINICAL FEATURES: - Age incidence: Any age Sex incidence: Strong male predilection Site predilection: Mostly in mandible. Maxilla is involved primarily in children. Slide 97: Signs & symptoms: Fever, leukocytosis, lymphadenopathy and soft tissue swelling of affected area. X-rays can show an ill defined radiolucency. Occasionally, fragments of necrotic bone can be seen separating from surrounding normal bone – Sequestrum. If sequestrum is surrounded by vital bone – Involucrum. Slide 98: HISTOLOGICAL FEATURES: - Biopsy specimen usually contains necrotic bone, showing loss of osteocytes from lacunae and bacterial colonization. Bone periphery shows necrotic debris and infiltration with PMNL’s. Specimen diagnosed as sequestrum unless there is good clinico-pathologic correlation. CHRONIC OSTEOMYELITIS : CHRONIC OSTEOMYELITIS It can arise either de novo from the onset or as a continuation of acute osteomyelitis, if it is not resolved quickly. CLINICAL FEATURES: - Age incidence: Any age Sex incidence: Strong male predilection Site predilection: Mostly in mandible. Slide 100: Signs & symptoms: Pain, swelling, purulent discharge, sinus formation, sequestrum formation, tooth loss. Frequent acute exacerbations may occur if infection continues for a long time. X-rays reveal ill defined, moth eaten radiolucency often showing a central radiopacity (sequestrum). Slide 101: HISTOLOGICAL FEATURES: Biopsy material contains significant soft tissue component consisting of chronically inflamed fibrous CT filling intertrabecular areas of bone. Scattered areas of sequestrum may also be noted. DIFFUSE SCLEROSING OSTEOMYELITIS : DIFFUSE SCLEROSING OSTEOMYELITIS Characterized by pain, inflammation, varying degrees of periosteal hyperplasia, sclerosis and radiolucency of affected bone. Can be confused clinically and radiologically with certain other intrabony pathoses like florid cemento-osseous dysplasia or Paget's disease of bone etc. Slide 103: CLINICAL FEATURES: - Age incidence: Almost exclusively in adults. Sex incidence: Nil Site predilection: Primarily in mandible Signs & symptoms: Pain and swelling are uncommon. To make a definitive diagnosis of diffuse sclerosing osteomyelitis, microbiological cultures must be positive. Slide 104: RADIOGRAPHIC FEATURES: - Increased radiopacity around sites of chronic inflammation like periodontitis, pericoronitis, periapical pathology etc. Sclerosis occurs more in alveolar crest regions of tooth bearing areas. Slide 105: HISTOLOGICAL FEATURES:- Sclerosis and remodeling of bone. Significant inflammation of bone is not seen even though sclerosis occurs adjacent to inflammation. Necrosis of sclerotic bone secondary to inflammation may occur. In this case, necrotic bone separates and is surrounded by granulation tissue FOCAL SCLEROSING OSTEOMYELITIS(Condensing osteitis) : FOCAL SCLEROSING OSTEOMYELITIS(Condensing osteitis) This refers to a focal area of bone sclerosis associated with apices of pulpally involved (caries, deep restorations or pulp necrosis) teeth. To be diagnosed as condensing osteitis, association with inflammation is essential, as it resembles several other intrabony pathoses. Slide 107: CLINICAL FEATURES: - Occurs mostly in children and young adults. Mostly occurs in mandibular premolar/molar area, associated with pulpitis / pulp necrosis. Localized, uniform zone of increased radiopacity seen adjacent to tooth apex. No swelling / cortical expansion noted clinically. Slide 108: DIFFERENTIAL DIAGNOSIS: - This lesion must be distinguished from Focal cemento osseous dysplasia – it shows a radiolucent border. Idiopathic osteosclerosis – here, the lesion is separated from the tooth apex. OSTEOMYELITIS WITH PROLIFERATIVE PERIOSTITIS : OSTEOMYELITIS WITH PROLIFERATIVE PERIOSTITIS Also called Periostitis ossificans or Garrѐ’s Osteomyelitis. It is a type of osteomyelitis associated with periosteal bone formation. Slide 110: CLINICAL FEATURES: - Age incidence: Children & young adults Sex incidence: Nil Site predilection: Mostly in premolar/ molar regions of mandible. Slide 111: Signs & symptoms: Swelling may be noted on lower border of mandible. Pain may / may not be present. Radiographs demonstrate radiopaque laminations roughly parallel to each other and the underlying cortical surface (onion skin appearance). Slide 112: HISTOLOGICAL FEATURES: Shows parallel rows of higly cellular, woven bone in which the individual trabeculae are oriented perpendicular to surface. Sometimes, trabeculae are interconnected or they may be scattered, resembling fibrous dysplasia. In between trabeculae, fibrous CT is relatively non inflamed. ALVEOLAR OSTEITIS(Dry socket / Fibrinolytic alveolitis) : ALVEOLAR OSTEITIS(Dry socket / Fibrinolytic alveolitis) Sometimes, the blood clot at the extraction site fails to organize which eventually leads to delayed healing and causes a condition called “Dry socket”. Research shows it is due to transformation of plasminogen to plasmin with resultant lysis of fibrin and formation of kinin (pain mediators). Slide 114: PREDISPOSING FACTORS: - Local trauma Estrogens Bacterial toxins Inadequate irrigation of surgery site Tobacco abuse. Slide 115: CLINICAL FEATURES: - Age incidence: Between 20 – 40 years Sex incidence: Nil Site predilection: Posterior mandibular teeth, especially impacted third molars. Slide 116: Signs & symptoms: Affected extraction site filled with a dirty gray clot, which is lost, leaving behind a bare, bony socket (Dry socket). Diagnosis is confirmed by probing of socket which shows an exposed and extremely sensitive bone. Severe pain, foul smell and lymphadenopathy develop within 3 – 4 days of extraction. BIBLIOGRAPHY : BIBLIOGRAPHY Soames JV, Southam JC. Oral pathology/. 3rd ed. Oxford 2002. Shafer WG, Hine MK, Levy BM. A text book of oral pathology. 6th ed. W.B. Saunders Company. Phil, London, Toronto, 2005. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. 2nd ed. WB Saunders Company. Phil, London, Toronto, 2007. Cawson RA, Odell EW, Porter S. Cawson’s essentials of oral pathology and oral medicine, 7th Ed, Churchill Livingstone, 2002. Regezi JA, Sciubba JJ, Jordan RCK. Oral pathology: Clinical Pathologic Correlations. 4th ed. Saunders Company, 2003. ACKNOWLEDGEMENT : ACKNOWLEDGEMENT All pictures in this presentation are courtesy of the authors mentioned in the bibliography. Slide 119: THANKS FOR YOUR PATIENCE!