Diseases of the Pulp and Periapical Tissues PDF

DISEASES OF THE PULP AND PERIAPICAL TISSUES BY DR/ Eman Allam. LECTURER OF ORAL PATHOLOGY SPHINX UNIVERSITY. SIGNIFICANCES OF PULP ANATOMY IN INFLAMMATION: 1.The pulp is enclosed within unyielding hard dentine, does not allow edema. 2.Nerves, arteries and veins e...

DISEASES OF THE PULP AND PERIAPICAL TISSUES BY DR/ Eman Allam. LECTURER OF ORAL PATHOLOGY SPHINX UNIVERSITY. SIGNIFICANCES OF PULP ANATOMY IN INFLAMMATION: 1.The pulp is enclosed within unyielding hard dentine, does not allow edema. 2.Nerves, arteries and veins enter through a small apical foramen.  3. Lack of collateral circulation 4. Response to sudden temperature changes. (20°C to 45°C). 4. The pulp lacks the power of regeneration. 6-The nerve supply of the pulp (free nerve endingd only) does not permit localization of the offending tooth. ETIOLOGY OF PULP DISEASES: 1: Living irritants (bacteria). 2: Non-living irritants: 2. NON-LIVING IRRITANTS: A. Physical: Mechanical, thermal, electrical, aeronautical, irradiation. B.Chemicals: Acids, alkalis, poisons. "Odonto-iatrogenic Pulpitis  LIVINING IRRITANT(BACTERIA) 1.Through an open cavity: a. Dental caries is the most common cause of pulpitis. b.Trauma(tooth fracture). c. Pulp exposure during cavity preparation( odonto-iatrogenic ). 2. Though periodontal ligament(periodontal disease). 3. Extension of adjacent periapical infection. 4. Hematogenous (anachoretic pulpitis).  1.LIVING IRRITANTS Through an open cavity Via the periodontal membrane Haematogenous infection: Spread from adjacent infected teeth:  HEMATOGENOUS INFECTION. Anachoretic Pulpitis: Circulating bacteria in the blood ,localize in inflamed pulp(pulp may be inflamed during cavity preparation).  2.NON LIVING IRRITANT: 1. Mechanical irritant: a. Trauma (tooth fracture). b. Odonto-iatrogenic: 1) Pulp exposure during cavity preparation. 2) Excessive grinding of tooth. 3) Rapid separation of teeth. 4) Use of modern high-speed instruments. 5) Traumatic occlusion.  Thermal irritation: Teeth respond to sudden temperature changes (20°C to 45°C).temperature below 20°C and above 45°C may cause Pulp inflammation.  ODONTOIATROGNIC: a.Excessive heat generated during cavity or crown preparation of teeth. b. Large metallic fillings without base. c. Prolonged cooling of teeth with ethyl chloride. d. Rapid polishing of teeth or restorations. e.Prolonged contact of thermal pulp testers, whether hot or cold. f.Direct contact of a very hot cauterizing loop to the crown  AERONAUTICAL ODONTALGIA : Aeronautical odontalgia (aerodontalgia): Toothache affects personnel, having vital pulp with deep caries or recent metallic restoration, when flying at high altitudes or entering the low pressure chamber. Pain is due to decompression of an inflamed pulp (pulp may be inflamed during cavity preparation).odonto-iatrogenic.  a. Avoid pulp irritation from heat during cavity preparation, or from chemicals in filling. b. Zinc- oxide and eugenol in the cavity after preparation to prevent pain during decompression. Electrical irritation (Galvanism): When different metallic restorations (gold versus amalgam)come in contact with each other, an intermittent electrical current, causes pain.  CHEMICAL IRRITATION: 1. Deep dental caries : (acids through dentinal tubules irritate the pulp). 2.Odonto-iatrogenic. a. Use of irritating material for drying the cavities, such as alcohol. a. Improper mixing and use of zinc phosphate cement or silicate cement.  IDIOPATHIC. Excessive gingival recession exposes the cementum of the tooth to the chemical agents(acids or alkalis) in some foods.  DISEASES OF THE PULP Classification of pulpitis: According to: 1. Type of inflammation. 2. Extent of pulp inflammation. 3.Direct communication between pulp and oral environment.  TYPE OF INFLAMMATION 1. Type of inflammation : a. Reversible: Focal reversible pulpitis. b. Irreversible : Acute pulpitis. Chronic pulpitis. 2.Extent of pulp involvement : a.Partial pulpitis : a portion of the pulp, usually the pulp horn and coronal portion is inflamed. b.Total pulpitis ,the entire pulp is inflamed. 3.Direct communication between pulp and oral environment: a. Open pulpitis: pulp is communicated with the oral cavity. b. Closed pulpitis: No direct communication between the pulp and the oral cavity.  1.FOCAL REVERSIBLE PULPITIS (PULP HYPEREMIA) Definition: Focal Reversible Pulp Inflammation. (the earliest form of pulpitis). Etiology and Clinical Features: Deep caries, deep metallic restoration without base or defective marginal restoration. A tooth is sensitive to thermal changes, particularly cold. Pain is sharp shooting pain that disappears within seconds after removal of the irritant. Pulp tester: the tooth responds at a lower level than normal tooth.  HISTOLOGIC FEATURES: Starts in localized area usually the pulp horn: 1.Vasodilatation. 2.Inflammatory fluid exudate. 3.Intact odontoblastic layer. Treatment: 1.Remove the cause. 2.Temporary filling zinc oxide and eugenol is used. It is reversible on removal of the irritant.  2.ACUTE PULPITIS Definition: Acute pulp inflammation. Etiology: High virulence bacteria and low body resistant. Living irritant or non living irritant( mechanical, thermal, electrical……..).  CLINICAL FEATURES: Deep caries ,deep metallic restoration without base or defective marginal restoration. Severe continuous , sharp lancinating or throbbing pain. Pain increases while the patient is laying down, and with thermal changes particularly cold. Pain persists after removal of the cause. In later stage: Hot increases pain but cold may relief pain (HOT TOOTH). Pain becomes spontaneous and awakes patient from sleep. The extreme pain is due to: 1. Pressure of fluid exudate on nerve endings, as the pulp is enclosed within hard dentine chamber, that does not allow edema. 2.The products of inflammation such as histamine and serotonin, act upon the nerve endings. With electric or thermal pulp tester the tooth reacts at a far lower threshold than normal.  Histopathological features: 1.Destruction of odontoblastic layer. 2. Vasodilatation. 3. Fluid exudate. 4. Acute inflammatory cells: (Polymorph nuclear leucocytes P.M.N.Ls.). 5.Pus formation (minute pulp abscess) mostly in the (Pulp horn). *Pus consists: of dead and alive bacteria, dead and alive PMNLs and liquified necrotic cells. 6.Numerous abscesses which finally coalesce together and total liquefaction of pulp occurs ( total suppurative pulpitis.) Treatment: Endodontic treatment or tooth extraction.  3.CHRONIC PULPITIS A. Chronic closed pulpitis. B. Chronic open pulpitis. 1.Chronic open hyperplastic pulpitis (pulp polyp). 2.Chronic open ulcerative pulpitis.  A. Chronic closed pulpitis. Definition: chronic closed pulp inflammation. Etiology :It may follow acute pulpitis. It Can Start Chronic: 1.low virulence bacteria and good body resistance. 2.Chronic caries, recurrent caries or incomplete removal of caries. 3.When the pulp is capped following traumatic exposure. 4.Hematogenous (Anachoretic pulpitis). Clinically: Intermittent dull achy pain,less sensitive to hot and cold. Pulp tester: responds at a higher level than normal. (chronic irritations degenerate nerve endings). Histopathology: 1.Reparative dentin( as the irritant is mild). 2.Granulation tissue: a. Proliferating fibroblasts. b. Proliferating blood vessels. c. Newly formed collagen fibrils. 3.Chronic inflammatory cells(lymphocytes &plasma cells)  B.CHRONIC OPEN PULPITIS. 1.Chronic hyperplastic pulpitis (pulp polyp). 2.Chronic ulcerative pulpitis. (Large carious cavity.Wide pulp exposure.)  1) Chronic Hyperplastic Pulpitis. (pulp polyp is a misnomer) DEFINITION : Chronic hyperplastic pulp inflammation. ETIOLOGY AND CLINICAL FEATURES: 1.Child or young adult. 2. Good resistance. 3. Deciduous molars or first permanent molar. 4.Large carious cavity 5. Wide pulp exposure. 5.Wide apical foramen (good blood supply & adequate drainage). so the pulp is vital. Painless red mass filling the carious cavity. The lesion is less sensitive to manipulation because it contains degenerated nerve endings. Differential diagnosis: Gingival polyp: attached to gingiva and sensitive to manipulation. But pulp polyp attached to pulp and less sensitive. Histopathological features: 1.GRANULATION TISSUE: a. proliferating fibroblasts. b. proliferating blood vessel c. newly formed collagen fibrils. 2.CHRONIC INFLAMMATORY CELLS :(lymphocytes & plasma cells). 3. Stratified squamous epithelium ,will cover the granulation tissue. Source of the epithelium:1. Oral mucosa(tongue or gingiva ).by rubbing of the granulation tissue against oral mucosa. 2. Desquamated epithelial cells of the oral mucosa in saliva.  2)CHRONIC OPEN ULCERATIVE PULPITIS. Large carious cavity and wide pulp exposure: pulp tissue is replaced by granulation tissue& chronic inflammatory cells (lymphocytes& plasma cells) Non or slight dull pain increase by thermal changes.as fluid exudate escapes from the pulp through the exposure. PULP NECROSIS AND PULP GANGRENE Untreated pulpitis may lead to death of the pulp. The inflammatory exudates compressed within a hard shell of dentine leads to compression of blood vessels particularly the apical, which then leads to infection and necrosis. The term pulp gangrene has been applied to this condition.. CLINICAL FEATURES: The tooth is symptomless ,but it may be dark in color. Microscopically: Either an empty pulp chamber and canals or isolated areas of necrotic structureless masses.  PATHOLOGY OF THE PERIAPICAL AREA The principal pathologically different types of change are: production of new bone very mild irritation and long Sclerosis. standing Mild irritation Dental granulomas. Moderate irritation Cyst. Sever irritation Periapical abscess. Radiograph of periapical sclerosis : radiopacity at the apex of the root.  DENTAL GRANULOMA Definition :It is a localized mass of chronic inflammatory granulation tissue to localize the inflammation. Types according to Location: 1.Periapical granuloma.(around the apical foramen) 2.Lateral granuloma, (Related to lateral accessory root canal). 3.Inter-radicular granuloma.(in the bifurcation or trifurcation related to accessory root canal) 4. Odonto-iatrogenic granuloma(related to perforation of root canal during endodontic treatment).At any site.  AETIOLOGY OF GRANULOMA : 1. Low grade pulpitis. 2. Infection through the gingival cravice. 3. Trauma. 4. Hematogenous infection. 5. Odonto-iatrogenic. a. Deep seated restoration. b. Use of unsterilized R.C. instruments. c. Application of strong antiseptics in R.C. therapy.  CLINICAL FEATURES: 1.Related to non vital tooth. 2.The involved tooth is slightly sensitive to percussion due to hyperemia, edema, and inflammation of the apical periodontal ligament. 3.Mild pain when biting or chewing on solid food. 4.The tooth feels slightly elongated in its socket or extruded from its socket.  MECHANISM OF FORMATION Chronic pulpitis, pulp necrosis ,chronic periodontitis. Granulation tissue (to wall off the inflammation). Pressure on bone, bone resorption by osteoclasts. Resorbed bone is replaced by granulation tissue.  RADIOGRAPHIC FEATURES Well defined radiolucent lesion.  Histopathology: 1. Fibrous capsule attached to cementum. (during extraction ,granuloma is attached to the tooth) 2.Granulation tissue: (a. Proliferating fibroblasts b. proliferating capillaries. c. Newly formed collagen fibrils). 3.Chronic inflammatory cells:(lymphocytes& plasma cells). 4.Cholesterol clefts(empty spaces were occupied by cholesterol crystals that dissolve in xylol during preparation) ,surrounded by:.Macrophages& foam cells(macrophages ingest lipid that dissolve in xylol during preparation). Multinucleated foreign body giant cells.  5. EPITHELIAL RESTS(MASSES OR STANDS): Source of epithelium: 1.Epithelial rests of Malassez. 2.Oral epithelium through sinus tract or deep periodontal pocket) 3. Respiratory epithelium of maxillary sinus. Fate of epithelium: May give rise to inflammatory periodontal cyst.  PERIAPICAL ABSCESS: (DENTOALVEOLAR ABSCESS) Definition: Localized suppurative process of the dental periapical region. It usually arises as a result of: 1. Pulp necrosis and Infection following acute pulpitis. 2. Trauma. 3. Acute exacerbation of periapical granuloma 4.Haematogenous infection in an inflamed area. 5.Odonto-iatrogenic. a) Deep seated restoration. b) Use of unsterilized R.C. instruments. c) Application of strong antiseptics in R.C. therapy. d) Mechanical irritation in R.C.T.  CLINICAL FEATURES: Systemic manifestations: Acute Onset, fever, swelling, pain redness and Lymphadenitis. 1. Local manifestations: The associated tooth usually shows a deep carious lesion or a restoration, but it may be intact. a) Severe pain on percussion. b) Feeling that the tooth extruded from the socket. c) The abscess may "point" intraorally or extra-orally. Histologic features: Abscess cavity (was filled with pus ), surrounded by neutrophils.  SEQUELA OF PULPITIS PULPITIS Acute Chronic Apical Periodontitis Acute Chronic Periapical Abscess Periapical Granuloma Periodontal Cyst Acute Chronic Spread of Dental Infection  SPREAD OF DENTAL INFECTION 1.Direct 2.Lymphatic 3.Vascular Lymphadenitis Cavernous Sinus Thrombosis Through pulp champer Maxilla Through gingival crevice Thrombosis Embolism Maxillary sinustits Periodontal abscess Osteomylitis Lung Acute Chronic Subperiosteal abscess Acute Chronic brain muscosal abscess Focal defuse abscess cellulitis Ludwig’s Angina THANK YOU