Sequelae of Endodontic Infection

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NDBE Oral Path Flashcards on Sequelae of Endodontic Infection, created by Laura Gennaro on 05/02/2018.
Laura Gennaro
Flashcards by Laura Gennaro , updated more than 1 year ago
Laura Gennaro
Created by Laura Gennaro about 6 years ago
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Question Answer
Upon exposure, contaminated pulp acts as a conduit between... the oral cavity and alveolar bone
What is an important defense mechanism alerting to need for therapeutic intervention? Pulpitis-related pain
Pulpitis: Main types of causative noxious stimuli -Bacterial= caries -Mechanical= trauma, iatrogenic damage from dental procedures -Thermal= extensive cavity preparation, large uninsulated metal restoration
What is the crossover point from reversible to irreversible pulpitis? Invasion of the pulp by bacteria
Reversible pulpitis tissue capable of returning to a normal state of health if noxious stimuli removed
Irreversible pulpitis dental pulpal tissue damaged beyond point of recovery
Reversible pulpitis details -Tooth acutely painful to stimuli >>discomfort resolves within few seconds >>responds to electric pulp testing (EPT) at lower levels of current than control tooth -Mobility and sensitivity to percussion absent -Dentin sensitivity may produce similar symptoms -Cracked tooth and defective restoration often present if pain upon biting
Irreversible pulpitis details -Tooth acutely painful to stimuli >>Discomfort continues for longer period of time >>Responds to electric pulp testing (EPT) at lower current than control tooth -Throbbing pressure in later stages -With increasing discomfort patient may be unable to identify offending tooth >>Pulpal pain may be referred between arches, but should not cross the midline
Pulpal necrosis -Tooth fails to respond to EPT or thermal sensitivity testing -Symptoms vary from none to acute pain
Chronic hyperplastic pulpitis (pulp polyp) -Unique, uncommon pattern of pulpal inflammation -Occurs with large exposures of pulp in which entire dentinal roof is missing -High level of chronic inflammation produces hyperplastic granulation tissue that extrudes from chamber
Is a biopsy necessary for the diagnosis of pulpitis? No, there is a surprising lack of correlation between histopathologic findings and clinical symptoms
Primary dentin formed before completion of crown
Secondary dentin formed after completion of crown -dentin physiologically continues to be deposited along inner walls -Leads to smaller pulp chambers/canals w/ age -Significant traumatic injury may lead to early obliteration of pulp chamber/canal (calcific metamorphisis)
In what disease is early widespread formation of secondary dentin seen in association with? Progeria
Tertiary dentin laid down in response to focal injury -triggered by injury of peripheral odontoblastic -in response to caries, trauma, dental procedures
Dental Calcifications Prevalence: approx. 20% of radiographs -Idiopathic, associated with aging -Increased prevalence in context of chronic pulpal irritation (attrition, caries, dental restorative procedures) -Noted in association w/ certain disease processes (uncommon)
Condensing Osteitis -localized areas of bone sclerosis associated w/ teeth exhibiting pulpitis -uniform area of increased radiodensity adjacent to apex of tooth -thickened PDL or apical inflammatory lesion often present -no clinical expansion
What percent of condensing osteitis cases regress with extraction/treatment of the involved tooth? ~85%
Bone scar residual area of condensing osteitis remaining after resolution of inflammatory focus
Idiopathic Osteosclerosis -asymptomatic focus of increased bone production -tends to arise in 1st-2nd decade -Prevalence: 5-10% -Seen in various tooth & non-tooth bearing areas of the jaws -Associated dentition vital -needs to be distinguished from condensing osteitis
Acute Apical Periodontitis -early stage of infection in which neutrophils predominate -widening of PDL space radiographically -pain on biting/percussion -constant dull, throbbing pain
Chronic Apical Periodontitis -neutrophils release prostaglandins which activate osteoclasts to resorb bone, leading to detectable periapical radiolucency, and chronic inflammatory cells dominate -often asymptomatic -pain and sensitivity in context of acute exacerbation
Acute Inflammation -initial, rapid response to infection or tissue damage -exudation of fluid/plasma proteins -migration of PMNs (neutrophils)
Chonic inflammation -response of prolonged duration to infection or tissue damage -characterized by varying combinations of: >>continued inflammation >>continued tissue injury >>attempted tissue repair (granulation tissue, angiogenesis, fibrosis)
G wound healing tissue comprised of: -fibroblasts (deposit collagen) -endothelial cells (form capillaries; angiogenesis) -scattered leukocytes (mainly macrophages)
Fibrosis -healing by connective tissue replacement (scarring) -represents end result of granulation tissue: >>fibroblasts in granulation tissue secrete collagen >>granulation tissue ultimately converts to fibrous tissue (called organization)
Abscess -specific pattern of ACUTE inflammation -represents a localized collection of purulent inflammatory tissue (pus) -most frequently due to infection with bacteria that are pyogenic
Pus exudate rich in neutrophils, dead cell debris, microbes
Resolution of periapical pathology cannot occur as long as... pulpal infection is active -rationale behind RCT/extraction
Periapical Pathology: Progression to chronic inflammation -periapical granuloma -radicular/periapical cyst
Periapical granuloma -a tumor-like mass of granulation tissue -inflammatory response can be associated w/ orifice of main canal or can be associated w/ a lateral canal that is infected -usually asymptomatic and associated w/ infected tooth (pain & sensitivity may occur w/ acute exacerbation) NOT a real granuloma
Radiographic appearance of Periapical Granuloma -radiolucency varies from small to >2cm in diameter -apical lamina dura usually lost -circumscribed or ill-defined -cortical expansion, root resorption may rarely occur
Pathology of Periapical Granuloma -removed tissue consists chiefly of granulation tissue w/ admixture of acute/chronic inflammation & variable amounts of organizing fibrous tissue
Granuloma -collection of activated macrophages, often w/ T-lymphocytes -represents attempt to contain an offending agent that is difficult to eradicate (foreign material that is relatively inert, persistent microbes) -limited number of diseases cause granulomatous inflammation
Radicular (periapical) cyst -represents the exact same inflammatory response seen in periapical granuloma PLUS epithelium -in the presence of surrounding inflammatory milieu, otherwise quiescent epithelium may be stimulated to proliferate -proliferation may assume the morphology of a cyst or may proliferate haphazardly amongst the granulation tissue
Where does the epithelium in Radicular cysts come from? Incomplete disintegration of HERS (Hertwig's Epithelial Root Sheath) yields clusters (rests) of quiescent epithelial cells in PDL space -Epithelial rests of Malassez
Residual Radicular Cyst consequence of tooth extraction without curettage
Periapical Fibrous Scar -on occasion fibrous tissue (organized granulation tissue) is not remodeled into alveolar bone during healing -most commonly occurs when facial & lingual cortical plates destroyed by initial periapical insult -results in periapical radiolucency indistinguishable from periapical granuloma/radicular cyst
Management of Non-abscessed periapical radiolucencies -often resolve following root canal therapy or extraction w/ curettage -persistent lesions may require apicoectomy (tissue should be submitted to pathology since expected resolution did not occur w/ RCT) -periapical fibrous scars= no treatment theoretically but difficult to diagnose preoperatively
Other things seen microscopically -Endodontic materials -Pseudostratified ciliated epithelium (sinus mucosa due to oroantral communication; occasionally metaplastic change to cyst lining) -Rushton bodies -Hyaline ring granulomas
Rushton bodies -peculiar structures seen in <10% of odontogenic cyts -represents amalgamation of keratin secretion and hemorrhage (from ruptured cysts)
Hyaline Ring Granulomas -granulomatous inflammation around poorly-digestible, hyalinized, ring-shaped material -plant-based food penetrate tissues through extraction sockets or grossly carious dentition -incidental finding
Periapical abscess -abscess at the apex of a non-vital tooth -may arise as initial periapical pathosis or from acute exacerbation of chronic periapical inflammation -may be symptomatic or asymptomatic
Symptomatic Periapical Abscess caused by accumulation of purulent material within alveolus -tenderness/pain upon percussion and palpation -tissue swelling -constitutional signs/symptoms may be present
Asymptomatic Periapical Abscess especially if abscess is able to drain -intraoral sinus tract w/ parulis -cutaneous sinus tract
Complications of abscess -cellulitis (soft tissue) -osteomyelitis (bone) -sepsis (blood) (Risk of dissemination less for abscesses that drain freely)
Where do most dental abscesses perforate? Where do maxillary lateral incisors, palatal roots of maxillary molars, and mandibular 2nd-3rd molars frequently drain? -perforate buccally because the bone is thinner -Drain palatally/lingually
Management of Periapical Abscess -Drainage & elimination of focus of infection (treatment w/ NSAIDs pre-op & for post-op pain control) -Antibiotic coverage for well-localized and easily drained abscess in healthy patient unnecessary -Signs/symptoms diminish within 48hrs -Sinus tract resolves spontaneously after treatment of offending tooth
Parulis (gumboil) -small, exophytic mass of granulation tissue at opening of sinus tract into oral cavity -compressible & fluctuant -typically asymptomatic (abscess can drain) -patient may report foul/salty taste in saliva (from pus) -resolves w/ treatment of underlying periapical/periodontal disease
Antral Pseudocyst -focus of inflammation located within maxillary sinus -typically asymptomatic and discovered incidentally on radiographs -cause unknown but adjacent odontogenic infection contributory in some cases (treatment of offending tooth when applicable) -treatment otherwise unnecessary; surgical removal if symptomatic
Radiographic features of Antral Pseudocyst -Spherical -Dome-shaped -Uniform radiodensity arising from floor of maxillary sinus -Inflammatory exudate located immediately beneath mucosal sinus lining -Cortical bone remains intact below lesion (would be displaced superiorly if disease was intraosseous)
Actinomycosis -serious, chronic infectious bacterial infection caused primarily by genus Actinomyces
Top 3 clinical presentations of Actinomycosis -Cervicofacial (55%) -Abdominal (20%) -Thoracic (15%)
Actinomyces -members of endogenous flora of mucous membranes (oral cavity, colon, vagina, bronchi) -disruption of mucosal barrier integral pathogenicity of Actinomyces (tooth extraction, grossly carious tooth, mandibular fracture)
Periapical actinomycosis -clinical presentation may or may not be more aggressive than routine periapical disease -sinus tract formation or perforation of buccal/lingual cortical plates -asymptomatic
Prognosis/Treatment -Excellent prognosis with minimal antibiotic coverage -Removal of all tissue at time of apicoectomy/surgical excision prerequisite -Antibiotic coverage for 1 week at discretion of clinician
Osteomyelitis -inflammation of bone and marrow spaces -virtually always secondary to infection: >>complication of open fractures, surgical procedures, diabetic infections of foot >>secondary to bacteremia stemming from minor skin infections or trivial mucosal injury
The vast majority of osteomyelitis cases are caused by... Most common types of osteomyelitis -bacterial infection -Suppurative osteomyelitis (Acute, Chronic) -Tuberculous osteomyelitis -Proliferative periostitis
Osteomyelitis of gnathic bones -mandible affected more frequently (poor vascular supply) -75% male predilection Etiology: -Acute dental infection -Radiation treatment -Hypovascular bone conditions
Acute dental infection -usually in context of predisposing condition (fracture, irradiation, diabetes mellitus, steroid therapy) -most dental infections do not cause osteomyelitits
Hypovascular bone conditions -cemento-osseous dysplasia -paget disease of bone -osteopetrosis
Acute suppurative osteomyelitis of the gnathic bones
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