Pulpal and Periapical Diseases (2) PDF

Pulpal and periapical Diseases (2) BDS10003 Date : Aim: The aim of this lecture is to review the histopathological features of common pulpal and periapical diseases as well as direct spread of oral infection Objectives: On completion of this lecture, the student should be able to: Understand the...

Pulpal and periapical Diseases (2) BDS10003 Date : Aim: The aim of this lecture is to review the histopathological features of common pulpal and periapical diseases as well as direct spread of oral infection Objectives: On completion of this lecture, the student should be able to: Understand the histopathological features of acute and chronic pulpal and periapical diseasesas well as direct spread of oral infection Understand the key cellular infiltrates of acute and chronic inflammation Periapical Diseases Pulpoperiapical pathosis is an inflammatory response of the periapical tissue due to a pulpal irritant Classification of Periapical Diseases Symptomatic Asymptomatic Acute apical periodontitis (incipient stage) Chronic apical periodontitis (incipient stage) Acute apical periodontitis (advanced stage) Chronic apical periodontitis (advanced stage) 1. Acute periapical abscess 2. Recrudescent (phoenix) abscess 3. Subacute periapical abscess 1. Chronic periapical abscess 2. Periapical granuloma 3. Periapical cyst Condensing osteitis Acute periapical abscess (acute apical periodontitis) Definition Severe symptomatic inflammatory response of periapical tissue to a non vital tooth Characterized by an increase in:  Inflammatory exudate  Leucocytic (polymorphonuclear leukocytes or acute inflammatory cells) infiltration  Suppuration Pathogenesis Irritant passes from the pulp to periapical tissue release of proteolytic enzymes pus formation vasodilatation Hypoxia → necrosis of cells & leucocytes stimulates osteoclastic activity & bone resorption Extravasation of inflammatory fluid exudate Leucocytic infiltration Acute periapical abscess (acute apical periodontitis) Clinical Features  Redness, hotness & swelling of the mucosa in the affected area  Severe throbbing pain which increases with biting or at night in the area of the non-vital tooth (due to pressure of exudate and leucocytic infiltrate & the effects of inflammatory chemical mediators on nerve tissues). Pain is localized (due to presence of proprioceptors in the periodontal ligament)  Most intense pain occurs as pus penetrates the bone & begins to raise the periosteum, then pain subsides as long as there is drainage of the suppurative material through a fistulous tract)  Percussion severe pain upon percussion Acute periapical abscess Chronic periapical abscess Severe throbbing pain It is Painless condition, characterized by formation of pus which is draining through a sinus tract In the early stages, no changes can be seen because bone changes need time to develop & the lesion is rapid. Then , widening of the periodontal membranes space. Ill defined hazy radiolucent area around the apex Acute periapical abscess severe pain upon percussion Histologically Chronic periapical abscess Slight discomfort Same as acute with chronic inflammatory cell infiltrate (plasma It is formed of: Central area containing pus (exudate + cells & lymphocytes) necrotic tissue + viable & dead neutrophils) The surrounding tissues show dilatation of blood vessels, infiltration with inflammatory cells (neutrophilic infiltrate) Recrudescent abscess (Phoenix) Acute exacerbation of a chronic lesion [Same as acute periapical abscess]  Similar to acute periapical abscess except for large radiolucent periapical area Periapical granuloma Definition Localized mass of chronic inflammatory granulation tissue related to the apex of a non-vital tooth. According to location in relation to the tooth apex, it may be classified into periapical, lateral and interradicular Pathogenesis Irritant passes from the pulp to periapical tissue vasodilatation Extravasation of inflammmatory fluid exudate the resorbed bone is replaced by granulation tissue Inflammation stimulates osteoclastic activity & bone resorption Chronic inflammatory cell infiltration Radiographic findings 1. 2. 3. Well defined radiolucent area related to the root apex. May be surrounded by radiopaque margin Root resorption may be noticed Histopathology 1. The alveolar bone & periodontal ligament are replaced by granulation tissue & surrounded by fibrous connective tissue capsule, attached to cementum [significance?] 2. Granulation tissue (newly formed collagen fibers, blood vessels & blood capillaries) 3. Strands or islands of epithelial rests of Malassez [significance?] Histopathology 4. Cholesterol clefts are spaces occupied by cholesterol and formed by collagen fibers 5. Foam cells are macrophages accumulate to phagocytose cholesterol Histopathology 6. Chronic inflammatory cells 7. Multinucleated giant cells Plasma cells lymphocytes Multinucleated giant cells Spread of oral infection With progression, the abscess spreads along the path of least resistance, resulting in osteomyelitis, or may perforate the cortex and spread diffusely through the overlying soft tissue such as cellulitis. Cellulitis If an abscess is not able to establish drainage through the surface of the skin or into the oral cavity, Definition Diffuse edematous spread of an acute inflammatory process through fascial spaces of the soft tissue [fascial spaces exist between the fascia and underlying organs and other tissues. In healthy conditions, these spaces do not exist; they are only created by pathology] Cellulitis Clinical features Fever, malaise, loss of appetite Firm, painful diffuse swelling The overlying skin is inflamed and red Regional lymphadenitis 2 dangerous forms of cellulitis Ludwig’s angina Cavernous sinus thrombosis Ludwig’s Angina  It is severe cellulitis usually arising from direct spread of infection from lower 7, 8 Infection spreads to involve submandibular, sublingual and submental spaces bilaterally (true Ludwig’s angina) WHY? Infection seeks the path of least resistance (thinner lingual cortical plate) The apices of these teeth are situated below the mylohyoid ridge Infection reaches submandibular space from where it spreads to involve other spaces Ludwig’s Angina  Elevation, enlargement, and protrusion of the tongue (woody tongue)  Firm, painful swelling in the upper part of the neck enlargement and tenderness of the neck above the level of the hyoid bone (bull neck).  Dysphagia and difficulty in breathing  High fever, dyspnea, tachycardia and leucocytosis  The condition may show possible suffocation and death Cavernous sinus thrombosis Definition  Cavernous sinus thrombosis is an edematous periorbital enlargement with involvement of the eyelids and conjunctiva.  It is a serious complication of orofacial infections or any infections involving “danger triangle of the face” [it consists of the area from the corners of the mouth to the bridge of the nose, including the nose and maxilla] due to thrombus formation in the cavernous sinus or it’s communicating branches  The infection usually involves one side but can easily spread to the other side Cavernous sinus thrombosis Clinical features  Protrusion and fixation of the eyeball  Induration and swelling of the adjacent forehead and nose.  The condition may be fatal as a result of brain abscess or meningitis Key points  Pulpoperiapical pathosis is an inflammatory response of the periapical tissue due to a pulpal irritant  This inflammatory response could be acute or chronic, symptomatic or asymptomatic  Affected tooth usually responds to percussion  Oral infections usually spread along the path of least resistance  The most dangerous forms of cellulitis are: Ludwig’s angina a severe cellulitis usually arising from direct spread of infection from lower 7, 8, if not properly treated may lead to death and suffocation Cavernous sinus thrombosis a serious complication of infections involving “danger triangle of the face” if not properly treated may lead to brain abscess or meningitis and death Aim: The aim of this lecture is to review the histopathological features of common pulpal and periapical diseases as well as direct spread of oral infection Objectives: On completion of this lecture, the student should be able to: Understand the histopathological features of acute and chronic pulpal and periapical diseasesas well as direct spread of oral infection Understand the key cellular infiltrates of acute and chronic inflammation Pulpal and periapical Diseases Reading material: Students are advised to review any relevant teaching provided in the first year. In addition, they are advised to read relevant sections of the following texts: Odell E.W. Cawson’s Essentials of Oral Pathology and Oral Medicine. 9th Edition. Elsevier, 2017 pp 77-83 and 129-133 Neville et al. Oral and Maxillofacial Pathology. 4th Edition. Elsevier, 2016 pp 117-128 Thank you