S. R. Prabhu - Handbook of Oral Pathology and Oral Medicine

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Handbook of Oral Pathology and Oral Medicine
Discover a concise overview of the most common oral diseases in a reader-friendly book Handbook of Oral Pathology and Oral Medicine
Handbook of Oral Pathology and Oral Medicine

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3.2 Pulpitis

3.2.1 Definition/Description

Pulpitis refers to inflammation of the dental pulp. Types include:Reversible pulpitis: pulpal inflammation resolves once the aetiology is removedIrreversible pulpitis: pulpal inflammation does not resolve once the aetiology is removedChronic hyperplastic pulpitis (pulp polyp)

3.2.2 Frequency

Prevalence varies from country to country. Ranges from 27%‐54% of the population

Irreversible pulpitis is more common in females

3.2.3 Aetiology/Risk Factors

Caries

Traumatic exposure of the pulp

Fracture of the crown or cusp

Cracked tooth

Thermal or chemical irritation

3.2.4 Clinical and Radiographical Features

Reversible pulpitis:Pain from cold test does not linger for longer than 30 secondsNo percussion sensitivityNo spontaneous painNo heat sensitivity

Irreversible pulpitis:Pain from cold test lingers for longer than 30 secondsMay get pain from heat testMay have spontaneous painMay be percussion sensitiveSleep or work is affectedA patient may have difficulty locating the tooth from which the pain originatesRadiographically or clinically, deep caries may be visible

Chronic hyperplastic pulpitis:Presence of a pink fleshy mass filling a carious cavity (pulp polyp; Figure 3.1)Usually single, rarely involving multiple teethNon‐tender or mildly tenderBleeds readily on probing

3.2.5 Microscopic Features

Acute pulpitis:Pulpal hyperaemiaFocus of acute inflammatory cell infiltrate Figure 3.1 Chronic hyperplastic pulpitis (pulp polyp) presenting as a fleshy mass in the carious cavity (white arrow).Destruction of odontoblastsFormation of an abscess in some cases

Chronic pulpitis:Mononuclear cell infiltrate (chronic inflammatory cells)Focus of pulp necrosisAbscesses and pus formationWall of granulation tissue

Chronic hyperplastic pulpitis:Mass composed of granulation tissueRich vasculatureChronic inflammatory cell infiltrateStratified squamous epithelial lining covers the surface of granulation tissue

3.2.6 Differential Diagnosis

Periodontal pain

Dentin hypersensitivity

Cracked tooth syndrome

Dental trauma

Idiopathic orofacial pain

Pain from restorative procedures

Pain of non‐odontogenic origin

3.2.7 Diagnosis

Based on history, clinical examination and testing

Radiography detects carious lesions causing pulpitis

Thermal tests

Radiographical examination for clinically visible and non‐visible caries and for recurrent carries under restorations, lamina dura and periodontal ligament (PDL) space

3.2.8 Management

3.2.8.1 Reversible Pulpitis

Remove the irritant or repair tooth structure (caries, exposed dentin, defective restoration)

Continue to monitor the patient's symptoms

Advise patient to return if symptoms persist or worsen

Pain management with analgesics (ibuprofen and paracetamol)

Antibiotics are not required

3.2.8.2 Irreversible Pulpitis

Pulpectomy of the offending tooth: complete removal of the pulp

Root canal treatment

Pain management with analgesics

Antibiotics are not recommended

Extraction if tooth cannot be saved

3.2.8.3 Chronic Hyperplastic Pulpitis

Extraction of the tooth

3.3 Apical Periodontitis and Periapical Granuloma

3.3.1 Definition/Description

Apical periodontitis refers to inflammation of the PDL surrounding the apex of the tooth caused by infection, bacterial products, or other irritants through the apex of the root. Usually, this occurs due to acute inflammation (acute apical periodontitis)

Periapical granuloma, also known as chronic apical periodontitis, refers to formation of granulation tissue surrounding the apex of a non‐vital tooth arising in response to pulpal necrosis

3.3.2 Frequency

Prevalence of apical periodontitis shows variation

Prevalence increases with age; by 50 years of age, one in two individuals will experience apical periodontitis

In individuals over 60 years of age, the prevalence rises to 62%

3.3.3 Aetiology/Risk Factors

Bacterial invasion from the pulp

Occlusal trauma from the high spots of restorations

Irritants and inflammatory mediators from the necrotic pulp

Endodontic procedures (iatrogenic)

Gingival infection

3.3.4 Clinical Features

Apical periodontitis:Acute form is commonPain and tenderness of the tooth on slight touchMinutely extruded toothNo changes with hot and cold drinks or foodSequelae: may proceed to dental abscess or chronic apical periodontitis

Periapical granuloma:Most cases are asymptomaticTooth involved is non‐vitalTooth is slightly tender to percussion

3.3.5 Radiographical Features

Apical periodontitis:Usually, no significant changes seenOccasionally, lamina dura may show haziness or slightly wide periodontal space

Periapical granuloma:Presents as a radiolucent lesionA radiolucent lesion of a few millimetres in size is usually indistinguishable from a periapical cystAn affected tooth typically reveals loss of the apical lamina duraRoot resorption is not uncommonA radiolucent lesion associated with the root apex often has fuzzy borders ( Figure 3.2a) Figure 3.2 Periapical granuloma. (a) Radiolucent lesion of periapical granuloma at the root apex of the non‐vital lateral incisor. (b) Photomicrograph showing apical connective tissue (black star) with chronic inflammatory cells and proliferating epithelial cells. Microscopic features demonstrate an evolving periapical cyst arising from periapical granuloma(source: by kind permission of Associate Professor Kelly Magliocca, Department of Pathology and Laboratory Medicine, Winship Cancer Institute at Emory University, Atlanta, GA, USA).(c) This photomicrograph shows cholesterol clefts and multinucleated giant cells in a mature periapical granuloma. These features are similar to those of periapical cyst.

3.3.6 Microscopic Features

Apical periodontitis:Engorged blood vesselsIntense infiltration of neutrophils

Periapical granuloma:Chronically inflamed granulation tissue around apex of a non‐vital tooth shows:Lymphocytes, macrophages, and plasma cells intermixed with neutrophils and proliferating epithelial cells (cell rests of Malassez) within the granulation tissue ( Figure 3.2b)Cholesterol clefts with multinucleated giant cells, red blood cells, and areas of hemosiderin pigment ( Figure 3.2c)Uninflamed layers of fibrous tissue at the peripheryPresence of osteoclasts

Sequelae of periapical granuloma:Acute exacerbation can cause rapid enlargement of the lesion and may progress to abscess formationProliferation of the epithelial cell rests of Malassez associated with the inflammation may lead to the development of an inflammatory radicular cyst

3.3.7 Differential Diagnosis

Cracked‐tooth syndrome and acute periapical abscess to be differentiated from acute apical periodontitis

Periapical lesions presenting as radiolucent lesions in the apical region of the roots (e.g. periapical cyst, chronic periapical abscess) to be differentiated from periapical granuloma

Sometimes nasopalatine duct cyst (in maxillary anterior teeth) presents radiographical features mimicking those of periapical granuloma

3.3.8 Diagnosis

History

Clinical examination

Radiography

3.3.9 Management

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