Disorders of the pulp


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Disorders of the pulp - Endodontia

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Disorders of the pulp

  3. 3. INTRODUCTION 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 1.MECHANICAL: Trauma, iatrogenic damage and barometric changes. 2. THERMAL: uninsulated metallic restorations and dental procedures like cavity preparation, exothermic chemical reactions of dental materials etc. 3.CHEMICAL: Irritation from certain dental materials or from erosion. 4.BACTERIAL: Through toxins or from direct extension of caries
  4. 4. FACTORS AFFECTING RESPONSE OF PULP 1.Severity and duration of irritant. 2.Nature of irritant. 3.Health condition of the pulp or pre-existing state of the pulp 4.Apical blood flow 5.Local anatomy of the pulp chamber 6.Host defence CLASSIFICATION 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: -
  5. 5. - Open pulpitis - Closed pulpitis 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
  6. 6.  Acute reversible inflammation of pulp tissue characterized by vascular dilatation  Pulp returns to uninflammatory state after removal of stimulus AETIOLOGY: -  Any mild irritants  Trauma or blow to teeth  Disturbed occlusal relationship(high points)  Restorative procedures without thermal instulation Chemical irritation to pulp(acid etching) -Excessive pressure due to orthodontic appliance -Attrition and abrasion -Dehydration of tooth cavity -Rapid separation of teeth by mechanical separators CLINICAL FEATURES: - Signs and symptoms: painful Duration: 10-15 minutes, severe and short Precipitating factors of pain: hot and cold agents ,especially cold.
  7. 7. Nature of pain: • Throbbing, continuous and radiating. • Pain stops when precipitating factors are removed The pain depends on - • The size of exposed pulp (size of dental caries) • Severity of pulp inflammation • Age of patient • Nature of covering dentine 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.
  8. 8. TREATMENT: -Best treatment is prevention. -Identify the cause and treat it. -Treat incipient carious lesion. -Reduce high point. -Proper insulation of restorations 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
  9. 9. 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 PROGNOSIS: - • If it is left untreated, it will change to chronic pulpitis or pulp necrosis
  10. 10. CHRONIC PULPITIS • 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). Precipitating factors of pain: - hot, cold agents and during biting. Nature of pain: -  Mild and intermittent pain
  11. 11.  The pain stops when precipitating factors are relieved and when the tooth is treated 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: -  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 TREATMENT: Extirpation of pulp PROGNOSIS: - • It is dependant on the success of pulp capping
  12. 12. CHRONIC HYPERPLASTIC PULPITIS . • 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 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
  13. 13. Size : variable Colour : reddish, bleeds readily Covering surface : intact or ulcerated
  14. 14. 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
  15. 15. • Source of epithelial cells are from saliva or desquamated mucosa of cheeks or gingiva
  16. 16. TREATMENT: Extirpation or removal of both coronal and radicular pulp PULP CALCIFICATION: 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
  17. 17. Signs and symptoms : painless RADIOGRAPHIC FEATURES: - Radiopaque mass / masses with variable sizes inside the pulp chamber or pulp canals. 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
  18. 18. COMPLICATIONS: - • It interferes with root canal treatment. • Can cause pain if it impinges on major pulp nerves. PULP NECROSIS:
  19. 19. 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 Precipitating factors of pain: hot and cold agents Nature of pain: • Throbbing, continuous and radiating.  The pain stops when precipitating factors are relieved.
  20. 20. TREATMENT: Root canal treatment CLASSIFICATION OF PERIAPICAL PATHOLOGY 1.Diseases of endodontic origin -Apical periodontitis acute and chronic -Periapical abscess acute and chronic -Apical granuloma -Periapical cyst -Osteomyelitis -External root resorption
  21. 21. 2.Diseases of non endodontic origin APICAL PERIODONTITIS ACUTE APICAL PERIODONTITS It is an acute inflammation of periodontium due to trauma,irritation or infection through root canal. ETIOLOGY VITAL TOOTH NON VITIAL TOOTH Occlusal trauma Sequelae of pulpitis Wedging of foreign body between teeth During root canal therapy Blow on teeth Orthodontic pressure
  22. 22. SIGN AND SYMPTOMS -History of pulpitis -Inflammatory exudates in periodontal space cause slight extrusion of tooth -pain on mastication -Tender on percussion -Pain on palpation of affected tooth RADIOGRAPHIC FEATURES -Thickened periodontal ligament -Pulpless tooth may show periapical rarefaction -Vital pulp shows normal periradicular tissue TREATMENT
  23. 23. if pulp is infected endodontic treatment of the affected tooth is done Radiogram of healthy periodontium and chronic apical periodontitis CHRONIC APICAL PERIODONTITIS Clinical examintaion: little or no pain on percussion X-ray: interruption of lamina dura or apical radiolucency Treatment: root canal treatment
  24. 24. PERIAPICAL GRANULOMA • 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. CLINICAL FEATURES: - • Mostly asymptomatic.
  25. 25. • Pain & sensitivity can develop if acute exacerbation occurs. • No mobility or sensitivity to percussion of involved tooth. • Pulp vitality tests are negative. 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. HISTOLOGICAL FEATURES:-
  26. 26. • 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. • Cholesterol clefts may also be seen along with associated multinucleated giant cells. • Areas of extravasation of RBC’s and hemosiderin pigmentation is also common.
  27. 27. RADICULAR CYST • 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. CLINICAL FEATURES: - Age incidence: peak in 3rd , 4th and 5th decades. Sex incidence: Slightly more in males.
  28. 28. Site predilection: Maxillary anterior region. Frequency: Commonest cystic lesion of jaws. Signs & symptoms: • Primarily symptom less. • Discovered accidentally during routine dental X ray exam. • 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. • • RADIOLOGICAL FEATURES:
  29. 29. • 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. DIFFERENTIAL DIAGNOSIS: - • Following lesions must be distinguished from other periapical radiolucencies– 1. Periapical granuloma
  30. 30. 2. Peripaical cemento – osseous dysplasia (early lesions) 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. 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.
  31. 31. • Another theory – cyst cavity forms within proliferating epithelium as the cells in center move away from their nutrient. 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. 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.
  32. 32. • Hyaline / Rushton bodies are found in epithelium and rarely in CT wall. • These are curved or linear structures with eosinophilic staining properties. • 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.
  33. 33. • 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. TREATMENT: -Surgical enucleation -Root canal therapy -some cases where cyst is large and curettage can endanger vitality of adjacent tooth there following root canal therapy of affected teeth surgical exterioration is done to collapse the cyst wall . When the cyst is reduced in size then curretage is done PERIAPICAL ABSCESS ACUTE PERIAPICAL ABSCESS(CLOSED)
  34. 34. SUPPARATIVE APICAL PERIODONTITIS(OPEN) • Collection of acute inflammatory cells at the apex of a non vital tooth is called periapical abscess.
  35. 35. • Acute lesions may arise either as in initial pathosis or as an acute exacerbation of a chronic periapical pathology (Phoenix abscess). 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.
  36. 36. • 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.
  37. 37. • 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. RADIOGRAPHIC FEATURES: - • In initial stages – thickening of periodontal ligaments. Later – ill defined radiolucency HISTOLOGICAL FEATURES: - • Microscopic sections are not usually made as specimen is fluid.
  38. 38. • 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 TREATMENT: -ACUTE ABSCESS Drainage of abscess and controlling the systemic reaction Endodontic tereatment of affected tooth
  39. 39. -CHRONIC ABSCESS Root canal therapy OSTEOMYELITIS • 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 TYPES OF OSTEOMYELITIS: - 1.Acute osteomyelitis 2.Chronic osteomyelitis 3.Diffuse sclerosing osteomyelitis 4.Condensing osteitis (Focal sclerosing osteomyelitis) 5.Osteomyelitis with proliferative periostitis. 6.Alveolar osteitis PREDISPOSING FACTORS: - 1.After odontogenic infections 2.Trauma to jaws 3.Presence of ANUG
  40. 40. 4.Chronic systemic diseases 5.Immunocompromised states 6.Tobacco and alcohol abuse 7.Diabetes mellitus 8.Exanthematous fevers 9.Malignancy 10. Malnutrition 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. Signs & symptoms: • Fever, leukocytosis, lymphadenopathy and soft tissue swelling of affected area.
  41. 41. • 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. 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.
  42. 42. • Specimen diagnosed as sequestrum unless there is good clinico-pathologic correlation. 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. Signs & symptoms:
  43. 43. • 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). HISTOLOGICAL FEATURES:
  44. 44. • 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 • 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. CLINICAL FEATURES: -
  45. 45. 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. 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.
  46. 46. 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) • 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. CLINICAL FEATURES: - • Occurs mostly in children and young adults.
  47. 47. • 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. DIFFERENTIAL DIAGNOSIS: - • This lesion must be distinguished from 1.Focal cemento osseous dysplasia – it shows a radiolucent border. 2.Idiopathic osteosclerosis – here, the lesion is separated from the tooth apex. OSTEOMYELITIS WITH PROLIFERATIVE PERIOSTITIS
  48. 48. • Also called Periostitis ossificans or Garrѐ’s Osteomyelitis. • It is a type of osteomyelitis associated with periosteal bone formation. • CLINICAL FEATURES: - • Age incidence: Children & young adults • Sex incidence: Nil • Site predilection: Mostly in premolar/ molar regions of mandible.
  49. 49. 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). 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.
  50. 50. 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.