Diseases Of Pulp & Periapical Tissues PDF

Presentation Title Diseases Of Pulp & Periapical Tissues  Etiology: FACTORS PHYSICAL INJURY CHEMICAL INJURY MICROBIAL FACTORS Acute Injury Bacterial invasion by: Injury on toot...

Presentation Title Diseases Of Pulp & Periapical Tissues  Etiology: FACTORS PHYSICAL INJURY CHEMICAL INJURY MICROBIAL FACTORS Acute Injury Bacterial invasion by: Injury on tooth Medicaments or materials applied to Dental caries Cavity preparation without water Fractured tooth where pulp is spray dentin diffuses exposed Vigorous polishing through dentinal Anchoretic infection due to Root planning in PDL therapy tubules. presence of bacteria in circulating Restoration – improper insulation blood stream. Chronic Injury Attrition -abrasive food & bruxism Abrasion -abnormal tooth brushing  Focal Reversible Pulpitis (Pulp Hyperemia) Mild, transient, localized inflammatory response. Histopathology: Dilation of pulp blood vessels. Dentin Collection of edematous fluid due to damage of vessel wall with extravasations of RBC or diapedesis of WBC. Dilation of blood vessels Decreased blood flow & hemoconcentration due Inflammatory cell infiltrate to transudation can cause thrombosis. Reparative or reactionary dentin in adjacent dentinal wall.  Acute Pulpitis Irreversible condition characterized by acute, intense inflammatory response in pulp. Intrapulpal abscess formation cause severe pain lancinating or throbbing type (10 – 15mins) Intrapulpal abscess Intensity of pain can increase when patient lies down. Histopathology: Edema in pulp with vasodilation. Infiltration and migration of PMN’s along vascular channels. Destruction of odontoblasts at pulp dentin border. Rise in pressure due to inflammatory exudate local collapse of venous part of circulation Tissue hypoxia & anoxia Destruction of pulp & abscess formation. Abscess consists pus, leukocytes & bacteria. Numerous abscess formation  pulp liquefaction & necrosis. (acute suppurative pulpitis)  Chronic Pulpitis Persistent inflammatory reaction in pulp with little or non constitutional symptoms. Pain is mild, dull & intermittent. Reaction to thermal changes is reduced because of degeneration of nerves. Manipulation with small instruments elicits bleeding but with little pain. Histopathology: Infiltration of mononuclear cells, lymphocytes & plasma cells, with vigorous connective tissue reaction. Prominent capillaries with fibroblastic activity & bundles of collagen fibers. If granulation tissue formation occurs in wide open exposed pulp surface –> ulcerative pulpitis. If pulpal reaction oscillates between an acute & chronic phase  pulp abscess formation surrounded by fibrous CT wall, called as Pyogenic Membrane  Chronic Hyperplastic Pulpitis (Pulp Polyp) Overgrowth of pulp tissue outside the boundary of pulp chamber as protruding mass. Pulp - pinkish red globule of tissue protruding from chamber & extend beyond caries. Commonly affected are 1° molar & 1st permanent molars. Pulp is relatively insensitive because few nerves in hyperplastic tissue. Lesion bleeds profusely upon provocation. Sometimes, gingival tissue may proliferate into carious lesion & superficially resemble hyperplastic pulpitis.  Histopathology: Hyperplastic tissue with granulation tissue, consisting delicate collagen fibers & young blood capillaries. Inflammatory cells as lymphocytes, plasma cells & polymorphs. Stratified squamous epithelium with well formed rete pegs. Grafted epithelial cells may be seen & origin of these cells is unknown, but they are degenerated superficial squames, which have lost dividing capacity. When pulp polyp is present for a long time, persistent rubbing of buccal mucosa may help in grafting of epithelial cells.  Stratified sq. epithelium covering polyp Granulation tissue Carious tooth Pulpal tissue  Diseases Of Periapical Tissues  Pulpitis Acute chronic Apical periodontitis Acute chronic Periapical abscess Periapical granuloma Acute chronic Periapical cyst Osteomyelitis Acute chronic Focal Diffuse Periosteitis Cellulitis Abscess  Apical Periodontitis Inflammation of PDL around apical portion of root. Cause: Spread of infection following pulp necrosis, occlusal trauma, inadvertent endodontic procedures etc. Types: 1.Acute Apical Periodontitis 2.Chronic Apical Periodontitis Histopathology: PDL shows signs of inflammation -vascular dilation -infiltration of PMNs Inflammation is transient, if caused by acute trauma. If irritant is constant, Inflammation invades surrounding bone resorption. Abscess formation may occur if associated with bacterial infection Acute periapical abscess / Alveolar abscess.  Chronic Apical Periodontitis (Periapical Granuloma) Common sequelae of pulpitis /apical periodontitis. Acute (exudative) left untreated chronic (proliferative). Periapical granuloma is localized mass of chronic granulation tissue formed in response to infection. HISTOPATHOLOGIC FEATURES: Granulation tissue comprising of fibroblasts, endothelial cells & numerous immature blood capillaries bone resorption. Capillaries lined with swollen endothelial cells. Macrophages, lymphocytes & plasma cells are seen. Lymphocytes produces IgG, IgA, IgM & IgE modulators of disease activity.  Plasma cells with Russel’s body are seen. T lymphocytes produce cytotoxic lymphokines, collagenase & other enzymes & destructive lymphokines. Cholesterol clefts, with multinuclear giant cells. Epithelial rests of Malassez may proliferate in response to chronic inflammation resulting in cyst formation. Bacteriologic Features: Strep. viridans, strep. Hemolyticus, non hemolytic strep, staph. aureus, staph. Albus, E coli & pneumococci are isolated from lesion.  Periapical Abscess (Dento-Alveolar abscess, Alveolar Abscess) Developed from acute periodontitis or periapical granuloma. Acute exacerbation of chronic lesion  Phoenix Abscess Etiology : Pulp infection, traumatic injury  pulp necrosis, irritation of periapical tissues Histopathology: Area of suppuration composed of PMN leukocytes, lymphocytes, cellular debris, necrotic materials & bacterial colonies. Dilation of blood vessels in PDL & bone marrow space. Inflammatory infiltrate, cellular debris, necrotic materials etc..  Osteomyelitis Inflammation of bone & its marrow contents. Secondary changes due to inflammation of soft tissue content of bone. Predisposing Factors: - Trauma, accident, gunshot wounds, radiation damage, Paget’s disease & osteoporosis. - Systemic conditions malnutrition, acute leukemia, uncontrolled DM, sickle cell anemia & chronic alcoholism. Types: 1. Acute suppurative osteomyelitis 2. Chronic suppurative osteomyelitis i. Chronic Focal Sclerosing Osteomyelitis ii. Chronic Diffuse Sclerosing Osteomyelitis  Histopathology : Acute osteomyelitis Chronic Osteomyelitis  Inflammatory Exudate in  Chronic inflammatory reaction in medullary spaces. bone - exudate & pus accumulation  PMN’s, occasional in medullary spaces. Bacterial Chronic inflammation colonization & lymphocytes & plasma  Lymphocytes, plasma cells & & reactive fibrous inflammatory response cells. macrophages. connective tissue filling intertrabecular spaces. Peripheral  Destroyed bony trabeculae  Osteoblastic & osteoclastic activity resorption without osteoblasts. occur parallelly with irregular  With time trabeculae loss bony trabeculae formation with viability & undergo slow reversal lines. resorption.  Later stages - Sequestrum may develop  Histopatholog Chronic Focal Sclerosing y Chronic : Diffuse Sclerosing Osteomyelitis Osteomyelitis  Dense mass of bony  Dense irregular trabeculae, some trabeculae with little bordered by active layer of interstitial marrow tissue. osteoblasts.  Osteocytic lacunae is empty.  Mosaic pattern, indicates  Trabeculae show reversal & periodic resorption & repair. resting lines giving Pagetoid  Soft tissue in between trabeculae – appearance. fibrous & show proliferating  Fibrotic connective tissue & fibroblast, capillaries with infiltrate of few lymphocytes. lymphocytes & plasma cells.  Osteoblastic activity  Sometimes, inflammatory completely absent. component is completely burned out, leaving sclerotic bone & fibrosis. Chronic Osteomyelitis with Proliferative Periosteitis (Garre’s Osteomyelitis, Chronic nonsuppurative sclerosing osteitis, periostitis ossificans) A distinctive type of osteomyelitis with focal gross thickening of periosteum, & peripheral reactive bone formation resulting from mild infection or irritation. Essentially a periosteal osteosclerosis analogous to chronic focal endosteal sclerosis & diffuse sclerosing osteomyelitis.  Histopathology: Supracortical but subperiosteal mass is composed of much reactive new bone & osteoid, with osteoblast Cellular & reactive bordering many trabeculae. vital bone with individual trabeculae Trabeculae orient perpendicular to cortex, with oriented perpendicular to the trabeculae arranged in parallel to each other or reticular surface form. Connective tissue is rather fibrous & show diffuse or patchy sprinkling of lymphocytes & plasma cells. Periosteal reaction – infection from caries perforating cortical plate & become attenuated, stimulating periosteum rather than producing usual suppurative periosteitis.  Diseases of Periodontium  GINGIVAL DISEASES Broadly classified into plaque induced and non-plaque induced Plaque induced – Local factors – Systemic Factors: affected by local factors modified by the specific systemic factors of the host  Histopathology Chronic gingivitis: – Presence of lymphocytes, monocytes, & plasma cells – PMN’s are seen, particularly beneath the crevicular epithelium. Crevicular epithelium is irregular and may be ulcerated Increased blood supply in connective tissue Hyperemia, edema, and hemorrhage may be present.  Junctional Epithelium – Weak point to the oral environment(non-keratinized) – Collection of PMN and lymphocytes are always found Glycogen content of the granular and spinous layers of the epithelium increases as the inflammation increases Mast cells: Show increased granules of sulfonated mucopolysaccharide Alkaline phosphatase activity increases  Necrotizing Ulcerative Gingivitis (NUG) Also known as:  Vincent’s infection  Trench mouth  Acute ulceromembranous gingivitis  Phagedenic gingivitis  Fusospirochetal gingivitis  Acute ulcerative gingivitis Necrotizing Ulcerative Gingivitis (NUG) Specific type of gingivitis with characteristic signs & symptoms. Disease manifests as both acute & recurrent (subacute) phases. Inflammatory involves free gingival margin, crest of the gingiva, and interdental papillae Spread of inflammation to the soft palate and tonsillar areas  Vincent’s angina Triad: Pain, interdental ulceration & gingival bleeding  Etiology Endogenous, polymicrobial infection + Predisposing factors destructive inflammation Fusiform bacillus and Borrelia vincentii (a spirochete) Disturbed host-parasite relationship  facilitates overgrowth of the organisms of the fuso-spirochaetal complex Increase in IgG and IgM antibody titers to spirochetes and increase in IgG titers to Bacteroides melaninogenicus  Histopathologic Features Acute gingivitis with extensive necrosis Surface epithelium is ulcerated and replaced – Thick fibrinous exudate – Pseudomembrane, containing many PMN Lack of keratinization of the gingival tissues Connective tissue shows infiltration by numerous PMN with intense hyperemia Numerous spirochetes & fusiform bacilli are found on the surface and beneath the necrotic pseudomembrane  Pericoronitis Inflammatory lesion around the impacted / partially erupted tooth Incomplete eruption of the tooth provides a large stagnant area for food debris under the gingival flap that becomes infected easily inflammation of the pericoronal flap It exhibits chronic inflammation for a long period Debris & bacteria if are deeply entrapped can result in pericoronal abscess. Mixed infection and various bacteria of the dental plaque (particularly anaerobes) are present in the pericoronal abscess  Histopathologic Features Epithelium of the pericoronal flap show – Hyperplasia – Intercellular edema – Leukocytic infiltration Underlying connective tissue exhibits Increased vascularity, Dense diffused infiltration with lymphocytes, and plasma cells Varying number of PMN  Gingival Enlargement Oversized ballooning gingiva with soft tissue filling the interproximal spaces May be localized to one papilla or may involve several or all of the gingival papillae throughout the mouth Enlargement is more prominent on the labial & buccal surfaces. It does not involve the vestibular mucosa  Etiology Classified based on etiologic factors & pathologic changes as follows: – Inflammatory gingival enlargement – Drug induced gingival enlargement – Enlargement associated with systemic factors – Conditioned enlargement – Enlargements due to systemic diseases – Idiopathic gingival enlargement – Neoplastic enlargement – False enlargement  Histopathology : Surface epithelium is hyperplastic, shows intracellular edema & micro abscesses Connective tissue – Densely infiltrated with chronic inflammatory cells – Predominantly a polyclonal mixture of plasma cells Marked vascular dilatation with severe thinning of epithelium over the connective tissue pegs  PERIODONTITIS An inflammatory disease of the supporting tissues of the tooth caused by specific microbes or group of specific microbes, resulting in progressive destruction of the PDL and alveolar bone with pocket formation, recession, or both. It is classified as – Chronic – Aggressive – Manifestation of systemic diseases – Occlusal trauma: Acute periodontitis that results from acute trauma  Chronic Periodontitis Also known as Periodontoclasia, pyorrhea, pyorrhea alveolaris, Schmutz pyorrhea Common PDL disease associated with local irritation Begins as marginal gingivitis, which usually progresses, if untreated or improperly treated  Histopathology: Early signs: Osteoclasts on the surface of the bone crest Sooner forms little bays of bone resorption: Howship’s lacunae Alveolar bone changes occurs prior to PDL changes Later if irritation persist, epithelial attachment proliferates apically down onto the cementum  Alveolar crest of bone is resorbed further apically. Principal PDL fibers become disorganized & detached from the tooth PDL pocket exists between the free gingiva and the tooth being more than 2 mm apically. Leukocytic cellular exudate from the inflamed soft tissue of the pocket wall progresses the disease Vicious cycle of irritant collection, inflammation and detachment continues, along with periodontal bone resorption in an apical direction  Lateral Periodontal Abscess Also known as Lateral abscess Related directly to a preexisting periodontal pocket Precipitating factors – Subgingival flora, – Host resistance, – Or both. When such a pocket reaches sufficient depth, around 5–8 mm, the soft tissues around the neck of the tooth approximate the tooth so tightly that the orifice of the pocket is occluded.  Bacteria multiply in the depth of the pocket  acute abscess with exudation of pus. Foreign body, particularly food debris, may also lead to abscess formation This may result in enough swelling to destroy the cortical plate of bone. If it still exists, allow the abscess to balloon the overlying tissues, forming a ‘gum boil’, or parulis  Histopathology: Resembles an abscess elsewhere in the body Consists of a central cavity filled with pus walled off on one side by the root of the tooth and on the other by connective tissue Most of cases the epithelial lining of the crevice would have been destroyed by the inflammatory process.