Chapter 3 - Periapical Lesions Flashcards
3 types of pulpitis
Reversible
Irreversible
Chronic Hyperplastic
Chronic Hyperplastic Pulpitis
Inflammation causes the pulpal tissue to bulge up and out into the crown
4 most likely Periapical Pathologies
Periapical Granuloma
Apical periodontal cyst
Periapical Abscess
Bone scar
What is the most common and most likely periapical pathology?
Periapical granuloma
What is the LEAST common periapical pathology?
Bone Scar
Sequelae of Periapical Pathology (4)
Sinus Tract
Osteomyelitis
Condensing Osteitis
Cellulitis
Parulis“Gum Boil”
Intraoral sinus tract exit - on oral mucosa
Osteomyelitis
Chronic or acute infection of the bone - bone marrow
Bacterial infection
Results in:
* Expanding lytic destruction
* Suppuration
* Sequestra Formation - bone pieces floating in the infection
Condensing Osteitis
What is the earliest change in the periodontium resulting from periapical pathology.
Periapical Granuloma
Most common periapical pathosis
Chronically inflamed granulation tissue - nonvital tooth
Usually asymptomatic
Histology - plasma cells and lymphocytes
Phoenix Abscess
Secondary acute inflammatory changes within a periapicla granuloma
Clinical Presentation of Periapical Granuloma
Asymptomatic
Tooth not typically mobile
Usually not sensitive to percussion
Does not respond to thermal or electrical pulp testing
Periapical Granuloma Treatment
Conventional endodontic treatment
Surgical endodontic treatment
Extraction
Periapical Periodontal Cyst
* Periapical cyst or Radicular Cyst*
Inflammatory stimulation of epithelium in the area – Rests of Malassez
Radiograhically –> Slow growth, punched out border
Histology –> Spiderweb pattern, epithelium lined
Patterns:
* Classical
* Lateral Apical Periodontal
* Residual apicl periodontal cyst
Classical Pattern of Periodontal Cyst
Lesion surrounds the root tip
Lateral Apical Periodontal Cyst
Lesion lateral to root tip
Lateral canal
Residual Apical Periodontal Cyst
Toot was extracted but the cyst remains
Periapical abscess
Acute inflammatory cells at the apex of a nonvital tooth
Symptomatic or asymptomatic
Histology –> large accumulation of inflammation
Earlies manifestation with widening of the PDL - when pulpal involvement
Periapical abscess treatment
Endo Treatment
Extraction
Pain Killers
Periapical Scar
Defect created by periapical inflammatory lesions may fill with DENSE collagenous tissue
Common – Following surgical endodontic therapy
When facial and lingual cortical plates have been lost
Histology –> Collagen (all pink, no blue), Fibroblasts
RADIO-Translucent
Sequelae or Periapical Pathology (4)
Sinus Tract
Osteomyelitis
Cellulitis
Condensing Osteitis
Sinus Tract
Pus dissects through the bone – destroying the bone
Perforates the cortical plate of bone extending into soft tissue
Follows the path of least resistance
Drains purulent material – may be intermittent drainage
Location of tract depends on involved tooth and path of least resistance
Parulis (Gum boil)
Intraoral sinus tract exiting through oral mucosa
Hole with red halo
Pustule (large pimple)
*Fistula*
Cutaneous Sinus Tract
Cutaneous Sinus Tract
Enlarged Nodular Mass
Red lesion with shades of Yellow, White, Purple
Mandibular teeth - most common
Osteomyelitis
Acute or Chronic inflammation in bone
Bacterial Infection
Results in:
* Expanding lytic destruction
* Suppuration (pus)
* Sequestra formation – bone pieces floating around in the infection
arise after odontogenic infections or traumatic fracture - not common in developed countries
Symptoms of acute infection of osteomyelitis
Fever
Lymphadenopathy
Sensitivity
Soft tissue swelling
DOESN’T produce x-ray changes
Involucrum
** During acute infection fragments of necrotic bone may become surrounded by new vital bone **
Cellulitis
Purulence perforates the cortex and spreads diffusely through the overlying soft tissue
Unable to establish a drainage point
Weaves through muscle bundles
Ludwig’s Angina
Cellulitis of the submandibular region
No previous treatment has been performed, infection has persisted (Infection from mandibular molar tooth)
Rapid swelling of sublingual, submandibular, and submental spaces
Death can occur – strangling
Woody Tongue
Bull Neck
Woody Tongue
Ludwig’s Angina
Sublingual involvment causes swelling and elevation of the tongue
Bull Neck
Ludwigs Angina
Submandibular space spread causes enlargment and tenderness of the neck
Ludwig Angina Symptoms and Signs
Obvious collections of pus are NOT present - no fistulas tract
Pain
Restricted Neck movement
Dysphagia, Dysphonia, Dysarthria
Drooling
Sore Throat
Respiratory Obstruction
SIGNS: Tachypnea,dyspnea, tachycardia, stridor, restlessness
Ludwig Angina Treatment
Call 911
Maintain airway
incise and drain
Antibiotic therapy
Eliminate orginal focus of infection
Cavernous Sinus Thrombosis
Abscess of a maxillary anterir or premolar tooth (canine - most common)
*Edematous periorbital enlargement – swelling along the lateral border of the nose*
Possibe sequelae of Cavernous Sinus Thrombosis
Protrusion and fixation of the eyeball
Pupil dilation with photophobia
Excessive lacrimation (tearing)
Loss of sight in the involved eye
Meningitis
Brain abscess
Death*
Cavernous Sinus Thrombosis Treatment
Surgical drainage
High dose antibiotics
Condensing Osteitis - Focal Sclerosing ostemyelitis
Bone sclerosis associated with the apex of teeth with pulpitis
Associated with inflammation - radiographically identical to idiopathic osteosclerosis
No clinical expansion of bone
X ray changes of Condensing Osteitis
* Increased radio-opacity near toot apex
* Thickened PDL or apical inflammatory lesion
* No radio-lucent border (distinguishes from focal cemento-osseous dysplasia)
* Not separated from apex (distinguishes from idopathic osteosclerosis)
Condensing osteitis vs cemento-osseous dysplasia
Xray of condensing osteitis has NO radio-lucent border
Condensing osteitis vs idopathic osteosclerosis
Condensing osteitis lesion is NOT separated from apex
Idiopathic osteosclerosis
*NOT associated with a carious tooth*
Normal tooth with radiolucent mass
