Periapical Pathology & Periodontitis

Periapical Pathology

• Bacterial infection from dental caries is the most common cause of pulpal disease

Pulpitis

• An infection of the pulp

Periapical Infection (Apical Periodontitis)

• Inflammation around the apex of the tooth in the periapical tissues

Periapical Pathology Definition

• Disease occurring around the apex of a tooth
• Adjacent bone and the root apex may resorb
• Healing may occur if the cause of inflammation is removed

Pathways for Pulp and Periapical Tissue Infections

• Carious cavity
• Gingival crevice

PAP (Periapical Periodontitis) vs Pulpitis

• Healing is very limited in PAP
• PAP is well localized by the patient due to proprioceptive nerve endings in the periodontal ligament

Factors Affecting PAP

• Presence of open or closed pulpitis
• Virulence of involved microorganisms
• Extent of sclerosis of dentinal tubules
• Competency of the host immune response

Etiology of Periapical Periodontitis

• Untreated pulpitis and pulp necrosis
• Occlusal trauma
• Restorative intervention
• Direct blow to a tooth insufficient to cause pulp necrosis
• Unexpected biting on a hard body in food
• Minor damage to the periodontal ligament and localized inflammation

Acute Periapical Periodontitis Treatment Indications

• Young tooth with open tubules
• Rampant caries
• Closed acute pulpitis
• Presence of highly virulent microorganisms
• Weakened host defense system

Histopathological Findings

• Vascular dilation
• Exudates of neutrophils
• Oedema in the periodontal ligament
• Confined space between the root apex and the alveolar bone

Clinical Presentation

• Intense pain when external pressure is applied to the tooth
• Tooth feels elevated in its socket
• Hot and cold stimulation does not cause pain

Sequela and Prognosis

• Resolution can occur if the inflammation is transient and due to acute trauma
• Can become chronic with adjacent bone resorption
• Acute periapical abscess can occur in complicated severe cases

Apical Periodontitis Characteristics

• Inflammation around the apex of the tooth
• Severely inflamed pulp will eventually necrose
• Pain is severe, spontaneous, and persistent, localizing to the affected tooth
• The tooth is sensitive to percussion with a metal object
• Regional lymphadenopathy may be present
• Management is root canal treatment or extraction
• Antibiotics are not always necessary

Acute Periapical Abscess Definition

• Accumulation of acute inflammatory cells at the apex of a nonvital tooth
• Exudates contain potent exotoxins and lytic enzymes that rapidly break down tissue barriers
• Can be caused by the acute exacerbation of a chronic periapical granuloma
• Pus associated with a lesion will seek the path of least resistance
• Jaw tenderness
• Hypersensitivity to tooth percussion
• Possible systemic features

Apical Abscess Characteristics

• Localized, purulent form of apical periodontitis
• Presents clinically as a fluctuant buccal or palatal swelling, with or without draining pus
• Regional adenopathy is usually present
• If pus is draining, pain usually is not severe
• Antibiotics are not necessary unless concurrent cellulitis is present
• Acute incision and drainage of a fluctuant area is needed
• Definitive therapy is root canal treatment or extraction

Periapical Abscess Appearance

• Face is swollen and the eye may be swollen shut
• Represents a potentially life-threatening infection

Histopathology of a Periapical Abscess

• Appears as a zone of liquefaction, composed of pertinacious exudates, necrotic tissue and viable and dead neutrophils (pus)
• Adjacent tissues containing dilated vessels and a neutrophilic infiltrate surround the area of liquefactive necrosis

Sequelae of Acute Periapical Abscess

• Sinus tract following local penetration of overlying periosteum and mucosa
• May extend through the medullary spaces, resulting in osteomyelitis
• May perforate the cortex and spread diffusely through the overlying soft tissue as cellulitis
• Dental abscesses may discharge through the skin and drain via a cutaneous sinus
• Periapical infection can spread to the bloodstream, resulting in systemic symptoms such as fever, lymphadenopathy, and malaise
• Cellulitis
• Ludwig's angina (submental, submandibular, and sublingual spaces)

Periapical Abscess Late Stage Problems

• Oroantral fistula
• Extension to maxillary cavernous sinus area, thrombophlebitis & brain abscess or acute meningitis

Treatment and Prognosis of Periapical Abscess

• Drainage and elimination of the focus of infection is necessary
• Antibiotics if the patient has systemic features or is immunocompromised
• NSAIDs if not contraindicated
• The tooth should be endodontically treated or extracted
• Sinus and fistula tracts should be surgically removed if not treated spontaneously after extraction

Chronic Apical Periodontitis (Periapical Granuloma)

• A mass of chronically or sub acutely inflamed granulation tissue at the apex of a non-vital tooth
• A secondary reaction to the presence of microbial infection in the root canal, with spread of related toxic products into the apical zone
• In the early stages, neutrophils predominate (acute periapical periodontitis)

Granuloma Progression

• Neutrophils activate osteoclasts leading to bone resorption
• With time, chronic inflammatory cells begin to dominate the host response

Lymphocytes Mediators

• Decrease osteoclast activity
• Increase fibroblast & microvasculature

Histopathological Features

• Periapical granulomas consist of inflamed granulation tissue surrounded by a fibrous connective tissue wall
• The central part of the lesion contains foamy macrophages
• Cholesterol crystals may be present surrounded by multinucleated giant cells
• A diffuse infiltrate of lymphocytes and plasma cells, especially when numerous plasma cells are present

Treatment & Prognosis

• Conservative
• Non-restorable teeth may be extracted, followed by curettage of all apical tissues, with non-steroidal anti-inflammatory drugs
• Antibiotics are not recommended unless systemic signs and symptoms are present
• Follow-up at 1-3-6 months and 1-2 years is needed to rule out possible causes of failure
• All tissues should be submitted for histopathological examination to exclude more serious conditions, like neoplastic process

Sequelae of PAP

• Periapical granuloma enlargement with more bone resorption
• Acute exacerbation to acute periapical periodontitis
• Suppuration to form an acute periapical abscess
• Formation of a radicular cyst
• Low-grade irritation may cause osteosclerosis (bone apposition) or cementum apposition (hypercementosis)

Radicular Cyst Definition

• Apical radicular cysts are the most common cystic lesions in the jaws
• Always associated with the apex of non-vital teeth
• Makes up 75% of all radicular cysts
• Pain is seldom a feature unless there is an acute exacerbation that could lead to abscess formation
• Cysts can rise at any age after tooth eruption, but are rare in deciduous dentition

Radicular Cyst Appearance

• Apical radicular cysts are the most common cystic lesions in the jaws and are always associated with non vital teeth
• Makes up 75% of all radicular cysts
• Small... asymptomatic & discovered accidentally in radiography
• May form a sinus
• Can grow to a large size (uncommon) about 5mm diameter/year
• May perforate the cortex and present as a bluish fluctuant sub mucosal swelling
• Pain is seldom a feature unless there is an acute exacerbation that can lead to abscess formation
• Can be seen at any age (rare in deciduous dentition)

Radicular Cyst Pathogenesis

• Inflammation (usually associated with dental caries extending into the dental pulp or trauma) stimulates cells in the rests of Malassez
• Epithelial cells proliferate to form a cystic cavity
• Cystic cavity can enlarge secondary to:
  • Osmotic pressure
  • Secondary infection and inflammation related to foreign material or bacteria
  • Ongoing inflammation and proinflammatory cytokines (IL-1 & IL-6)
  • Osteoclastic resorption of surrounding bone
• The mechanism by which an epithelial lined cyst cavity forms within granulomas is unclear. Two main mechanisms include:
  • Degeneration and death of central cells within a proliferating mass of epithelium that outgrows its blood supply
  • Degeneration and liquefactive necrosis of granulation tissue where epithelial proliferation surrounds the area of necrosis

Radicular Cyst Microscopic Presentation

• Lined by nonkeratinizing stratified squamous epithelium of variable thickness which creates an arcading pattern
• Fibrous capsule of varying thickness with acute or chronic inflammatory cells
• May have plasma cells or foamy histiocytes
• May contain cholesterol clefts, bacterial colonies, foreign material related to prior dental treatments, portions of bone/tooth/tooth root, or regional odontogenic rests and neural tissue

Cyst Contents

• Vary from a watery straw color fluid through to semi-solid brownish material
• Cholesterol crystals impart a shimmering appearance
• Complex composition, hypertonic compared with serum
• Contains breakdown products of degenerating epithelial cells and inflammatory cells/connective tissue components
• Serum proteins are present in cyst fluid and are derived as inflammatory exudates
• The fluid contains a higher level of immunoglobulin than serum
• Water and electrolytes
• Cholesterol crystals

Residual Cysts

• Radicular cysts remaining after the tooth has been extracted
• Usually asymptomatic
• Usually small size (less than 1 cm in diameter)
• Unilocular, round or oval, well-defined, usually well-corticated
• Can cause bone expansion and displacement of adjacent teeth

Treatment of Radicular Cysts

• If the tooth is restorable, root canals are filled
• Apicoectomy with complete surgical enucleation
• Tooth can be extracted and the periapical cyst is curated

Inflammatory Bone Diseases

• Categorized based on the extent of involvement of the bone
• Osteitis
  • Localized inflammation of bone that does not involve marrow spaces
  • Associated with infected sockets following removal of teeth
• Osteomyelitis
  • Extensive bone involvement extending through the marrow spaces
• Periostitis
  • Inflammation of the periosteal spaces of the bone
  • May not be associated with osteomyelitis

Osteomyelitis Today

• Rare due to availability of antibiotics
• Various clinical subtypes depending on the nature/severity of the irritant, host defense, and predisposing factors - Acute - Chronic - Suppurative - Sclerotic
• Most cases are bacterial infections with expanding lytic destruction of involved bone, suppuration, and sequestra formation
• Can be called suppurative osteomyelitis, bacterial osteomyelitis, or secondary osteomyelitis
• Idiopathic inflammatory disorder that demonstrates sclerosis of bone(without suppuration or sequestra formation) that does not respond consistently to antibacterial medications

Osteomyelitis Locations

• Primary Chronic Osteomyelitis (Diffuse Sclerosing Osteomyelitis)
• Focal Sclerosing Osteomyelitis
• Proliferative periostits
• Alveolar osteitis
• Suppurative Osteomyelitis is uncommon in developed nations, but remains a difficulty in developing nations
• The most common cause is odontogenic infections and jaw fractures
• In Africa, an important cause is acute necrotizing gingivitis

Osteomyelitis Predisposing Factors

• Chronic systemic diseases, immunocompromised status, and disorders associated with decreased vascularity of bone
• Tobacco/Alcohol/IV Drug Abuse
• Diabetes Mellitus
• Exanthematous fever and malaria
• Sickle cell anemia
• Malnutrition
• Malignancy
• Collagen vascular disease
• AIDS
• Radiation
• Osteopetrosis, dysosteosclerosis, pagets disease, end-stage cemento-osseous dysplasia may result in hypovascularized bone that is predisposed to necrosis and inflammation

Acute Suppurative Osteomyelitis

• Inflammation spreads through the medullary spaces & insufficient time has passed for the body to react to the presence of the inflammatory infiltrate

Chronic Suppurative Osteomyelitis

• Body response (granulation tissue) forms dense scar tissue that walls off infected area
• Encircled dead space acts as a reservoir for bacteria, so antibiotics are difficult to reach the site
• Starts one month after spread of acute infection, progressive & needs aggressive treatment

Acute Osteomyelitis Signs

• Signs and symptoms of an acute inflammatory process lasting less than 1 month
• Fever, leukocytosis, lymphadenopathy, significant sensitivity and soft tissue swelling of the affected area may be present

Osteomyelitis Radiographic Features

• Early stages may be unremarkable or may demonstrate an ill-defined radiolucency
• Paresthesia of the lower lip may occur with drainage or exfoliation of fragments of necrotic bone
• A fragment of necrotic bone that has separated from the adjacent vital bone is termed a sequestrum
• Fragments of necrotic bone may become surrounded by vital bone, such that the mass of encased nonvital bone is called an involucrum

Acute Osteomyelitis

• Infection of jaw bone may result from untreated pulpal and/or periapical infection
• It is a very serious condition that can cause destruction of large sections of the jaw & be difficult to cure.

Chronic Osteomyelitis Features

• Follows acute osteomyelitis that is not resolved or occurs primarily without a previous acute episode.
• There may be swelling, pain, sinus formation, purulent discharge, sequestrum formation, tooth loss, or pathologic fracture.
• Patients may experience acute exacerbation or periods of decreased pain associated with chronic smoldering progression.
• Sequestra, and Osteogenic periosteal hyperplasia can be found on radiographs

Chronic Osteomyelitis Pathogenesis

• Because of a particular arrangement, large portions of each jawbone receive their blood supply through multiple arterial loops originating from a single vessel. Involvement of this single feeder vessel can lead to necrosis of a large portion of the affected bone.

Osteomyelitis Histopathologic Features - Acute

• Biopsy material is not common because of liquid content and lack of soft-tissue component.
• Material consists predominantly of necrotic bone.
• Bacterial colonization, and Acute inflammatory infiltrate consisting of polymorphonuclear leukocytes may be confused with sequestrum unless a good clinicopathologic correlation.

Osteomyelitis Histopathologic Features - Chronic

• Significant soft tissue component that consists of chronically/sub acutely inflamed fibrous connective tissue filling the intertrabecular areas of the bone.
• Scattered sequestra and pockets of abscess formation are common

Acute Osteomyelitis Treatment and Prognosis

• If an abscess is present, drainage and antibiotics are needed as it is a mixed microbial infection
• Antibiotics of choice are Penicillin, clindamycin, cephalexin, cefotaxime, tobramycin, and gentamicin
• Antibiotic therapy can sterilize the sequestra, non vital bone fragments should be allowed to remain to allow for future bone development

Chronic Osteomyelitis Treatment and Management

• Management is difficult due to pockets of dead bone and organisms being protected from antibiotics by surrounding wall of fibrous connective tissue
• AB: intravenously in high doses
• Surgical intervention is mandatory. Decortications/saucerization is combined with a cancellous bone chips transplant
• Resection of diseased bone (followed by immediate reconstruction with an autologous graft)
• Weakened jawbones must be immobilized
• Adjunctive procedures (hyperbaric oxygen) are rarely used

Focal Sclerosing Osteitis Characteristics

• Common
• Focal bony reaction to low-grade inflammatory stimulus
• Usually seen at apex of tooth with long-standing pulpitis
• Synonyms are focal sclerosing osteomyelitis, bony scar, condensing osteitis, and sclerotic bone
• Focal periapical osteopetrosis describes idiopathic lesions associated with normal, caries-free teeth
• Asymptomatic, mostly discovered on radiographs
• Bone lesions are:
  • Uniformly opaque
  • Peripheral lucency with opaque center
  • Opaque periphery with a lucent center
  • Confluent/lobulated opaque masses
• Masses of dense sclerotic bone that have very few inflammatory cells and scant connective tissue
• There is believed to be a physiologic bone reaction to a known stimulus, and the lesion itself is not removed
• It is important to rule out more significant lesions, the inflamed pulp that stimulated the focal sclerosing osteomyelitis should be treated

Diffuse Sclerosing Osteomyelitis

• Ill-defined clinical entity that is an inflammatory reaction in the mandible/maxilla believe to be in response to low virulent organism
• Bacteria are generally suspected but are seldom specifically identified
• Chronic periodontal disease can be a portal of entry for bacteria, and is important in the etiology/progression
• Teeth with non-vital caries are less often implicated in this disease

Histology Findings in Diffuse Sclerosing Osteomyelitis

• Bone sclerosis/remodeling
• Scanty marrow spaces
• Necrotic bone separates from vital bone to be surrounded by tissue
• Secondary bacterial colonization

Differential Diagnosis of Diffuse Sclerosing Osteomyelitis

• Florid osseous dysplasia exhibits anterior periapical lesions/traumatic/simple bone cysts
• Florid osseous dysplasia is asymptomatic and appears as a fibroosseous lesion lacking inflammatory cell infiltrate
• Treatment
  • Problematic due to large size of lesions, Remove cause, and Antibiotics/Low-dose corticosteroids, (Antibiotics are less effective)
• Surgeries are inappropriate to due extent
• Hyperbaric oxygen therapy/Pamidronate

Chronic Osteomyelitis with Proliferative Periostitis (Garré's Osteomyelitis)

• Uncommon infection - a chronic osteomyelitis with subperiosteal bone and collagen deposition/prominent periosteal inflammatory reaction
• Results from a periapical abscess of a mandibular molar tooth
• Can be caused by infection associated with tooth extraction or partially erupted molars
• Most common in children
• Radiographs and a biopsy provides a definitive diagnosis
• Described in the tibia & the head and neck area- Radiographs and a biopsy provides a definitive diagnosis
• Body of mandible
• Reactive new bone typified by parallel orientation of new trabeculae under low magnification
• Osteoblasts and osteoclasts are seen centrally along the trabeculae
• Scattered lymphocytes and plasma cells
• There is no inflammatory cells, so difficult to differentiate from fibrodysplasia

Histopathology

• Reactive new bone typified by parallel rows of highly cellular and reactive woven bone
• Between trabecular, uninflamed fibrous tissue Identification of and treatment of the tooth/extraction of the involved tooth

Osteoradionecrosis

• One of the most serious complications of radiation
• Bone irradiation results in damage to the osteocytes and microvasculature system
• The affected bone becomes hypoxic, hypovascular, and hypocellular
• Bone is nonhealing dead bone, though infection is not necessarily present
• Bisphosphonates are used for patients with multiple myeloma, metastatic cancers, Paget's disease, and osteoporosis
• Inhibitory effect on osteoclastic bone resorption, and can occur through tooth extraction

Alveolar Osteitis (Dry Socket; Fibrinolytic Alveolitis)

• Alveolar process of maxilla or mandible
• Occurs after tooth extraction, as a postoperative complication -1% - 3% of all extractions. Average is 20-40 years old
• After tooth extraction, a blood clot occurs, made of granulation tissue, coarse fibrillar bone, and organized mature bone eventually.

Alveolar Osteitis (Dry Socket; Fibrinolytic Alveolitis) Predisposing Factors

• Experience
• Traumatic extractions
• Oral contraceptive
• Presurgical infections
• Inadequate irrigation at surgery
• Smoking

Alveolar Osteitis (Dry Socket; Fibrinolytic Alveolitis) Signs and Symptoms

• Severe pain and foul odour that develops 3-4 days after extraction
• Swelling and lymphadenopathy
• Symptoms last 10-40 days