5 Pulpal and Periapical Diseases Flashcards
3 signs of pulpal injury:
- external stimuli reaches a noxious level
- degranulation of mast cells
- inflammatory mediators are released
Inflammatory mediators released with pulpal injury:
They cause (3):
- histamine, bradykinin, prostaglandins
- cause vasodilation, increased blood flow, vascular leakage with edema
describe normal pulp tissue and how pulpal injury occurs
- increased blood flow promotes healing through removal of inflammatory mediators and swelling of the injured tissue usually occurs
- dental pulp is a confined area
- activate dilation of the arterioles leads to increased pulpal pressure
- secondary compression of the venous return can lead to strangulation
What causes pulpal injury?
increased pulpal pressure + accumulation of mediators = vessel damage, pulpal inflammation, and tissue necrosis
4 causes of pulpal inflammation (pulpitis):
1) Mechanical damage- traumatic accidents, iatrogenic damage from dental procedures, attrition, abrasion
2) Thermal injury- severe thermal stimuli can be transmitted through large uninsulated metal restorations , dental procedures (cavity preps, polishing, chemical rxns of dental materials)
3) Chemical irritation- from erosion, acidic dental materials (unsafe use of them)
4) Bacterial effects- toxins, extension from caries
reversible vs irreversible pulpitis
Reversible
- tissue is capable of returning to a normal state
- pain does not occur without stimulation
- stops within seconds if stimulus is removed (more dramatic response to cold)
- electric pulp testing (EPT) response at lower levels of current than control tooth
- no mobility
- no sensitivity to percussion
- tx: removal of local irritant
- if untreated, duration of the pain upon stimulation can become longer –> can become irreversible
Irreversible
- higher level of inflammation has developed
- pulp is damaged beyond the point of recovery
- invasion by bacteria is often the transition between the two
- pain may be spontaneous, continuous, or worse when the pt lies down
- initially the tooth responds to EPT at lower levels
- thermal stimulus = sharp, severe pain that continues after the stimulus is removed (cold is worse, sweet and acidic foods also cause pain) nd
- mobility and sensitivity to percussion are usually absent
- if pulpal drainage occurs, the symptoms may resolve (crown fracture, fistula, pain can return if drainage is blocked)
- tx: endo or extraction
early vs later signs of irreversible pulpitis
Early
- pain can usually be localized to the specific tooth
- as it worsens, harder to identify exact tooth
Later
- pain increases in intensity
- throbbing pressure, keeps awake at night
- heat increases pain, cold may produce relief
- tooth responds to EPT at higher levels of current or demonstrates no response
- affects children and young adults
- large pulpal exposures (entire dentinal roof is gone),
- tooth is asymptomatic
- irritation and bacteria lead to chronic inflammation
- hyperplastic granulation tissue comes out of the pulpal chamber
pulp polyp (chronic hyperplastic pulpitis)
most common teeth affected by pulp polyp
primary molars
primary vs secondary vs tertiary dentin
Primary- formed before completion of the crown
Secondary- odontoblasts continue to deposit dentin slow and gradual, leads to smaller pulp chambers and canal systems, deposition increases after age 35-40, deposition begins in the coronal portions of the tooth and proceeds apically, believed to be result of aging
Tertiary- new dentin laid down in areas of injury, laid down in areas of injury to peripheral odontoblastic processes, reactionary or reparative
significant traumatic injury can lead to early obliteration of the pulp chamber and canal, may be noticed clinically by a yellow discoloration of the crown
calcific metamorphosis
radiographic appearance: premature closing of the pulp chamber and canal (compared to adjacent or contralateral teeth), pulpal space is obliterated or reduced dramatically
calcific metamorphosis
tx for calcific metamorphosis: primary vs permanent teeth (vital and non-vital)
Primary teeth
- asymptomatic: monitor, wait for them to exfoliate
- symptomatic: extract and space maintain
Permanent teeth
- non-vital: endo therapy
- vital: periodic reevaluation
- esthetics: bleaching or full coverage
occurs in about 20% of all people, characterized by an increased # of calcifications in older teeth or teeth with a history of trauma or caries
pulp calcifications
Where are pulp calcifications usually formed?
within the coronal portions of the pulp
90-95% of periapical lesions are ?
5-10% of periapical lesions are?
90-95% of periapical lesions are inflammatory, tooth-related lesions (cyst, granuloma, abscess),
5-10% are something else (other odontogenic cysts, non-odontogenic cysts, dysplastic bone disease, benign neoplasms, malignant neoplasms)
Radiographic features: periapical cyst vs granuloma
Periapical cysts and granulomas are more likely to be: slow growing, well-defined, corticated
Larger lesions = more likely to be cyst than granuloma
3 periapical inflammatory lesions:
periapical granuloma
periapical cyst
periapical abscess
Name the periapical inflammatory lesion: aka apical periodontitis
periapical granuloma
Name the periapical inflammatory lesion: collection of chronically inflamed granulation tissue at the apex of a nonvital tooth
periapical granuloma
Most apical inflammatory lesions are ______.
periapical granulomas
Name the periapical inflammatory lesion: defensive reaction secondary to the presence of bacteria in the root canal, spread of related toxic products into the apical zone
periapical granuloma
Name the periapical inflammatory lesion:
- asymptomatic or painful
- soft tissue overlying the apex may be tender
- usually no mobility or significant sensitivity to percussion
- thermal or EPT: no response or may see some response if pulpal necrosis is limited to a single canal in a multi-rooted tooth
periapical granuloma clinical findings
radiographic findings: radiolucent lesion of variable size, loss of apical lamina dura, circumscribed or ill-defined, root resorption can be seen (not uncommon)
periapical granuloma
histopathology: inflamed granulation tissue and fibrous CT, cells seen: lymphocytes, neutrophils, plasma cells, macrophages
periapical granuloma
tx of periapical granuloma in restorable vs non-restorable teeth
Restorable
- endo therapy (should be evaluated at 1 and 2 year intervals to rule out possible lesional enlargement and ensure proper healing, strong emphasis should be placed on the importance of recall visits)
Non-restorable
- extraction
- curettage of all apical soft tissue
Name the periapical inflammatory lesion: use of systemic antibiotics NOT recommended unless associated swelling or systemic changes are present
periapical granulomas
Tx of periapical granuloma may fail to heal for several reasons (6)
1) Cyst formation
2) Persistent pulpal infection- poor access design, missed or perforated canals, vertical root fractures, inadequate technique or instrumentation, leaking restorations
3) Periapical foreign material
4) Associated periodontal disease
5) Penetration into maxillary sinus
6) Fibrous scar formation (“periapical scar”)
defect created by peripheral inflammatory lesions may fill with dense collagenous tissue rather than normal bone
“periapical scar” (associated with failure of periapical granulomas)
Name the periapical inflammatory lesion: arises from epithelial rests of Malassez most commonly, may be traced to crevicular epithelium or sinus lining
periapical cyst / lateral radicular cyst
Name the periapical inflammatory lesion: stimulus is inflammation (epithelium at the apex of a nonvital tooth is stimulated by inflammation to form a true epithelium-lined cyst)
periapical cyst / lateral radicular cyst
Name the periapical inflammatory lesion:
- non-vital tooth
- radiolucent lesion of varying size
- may be corticated
- loss of apical lamina dura
- can see root resorption
- recurrence is rare
periapical cyst / lateral radicular cyst
Name the periapical inflammatory lesion: site is root apex or lateral root surface
periapical cyst / lateral radicular cyst
Name the periapical inflammatory lesion: dx by pulp testing or biopsy
periapical cyst / lateral radicular cyst
tx for periapical cyst / lateral radicular cyst
extraction, endo therapy
histopathology: fibrovascular CT and granulation tissue supporting a mixed infiltrate of chronic and acute inflammatory cells, nonkeratinized stratified squamous epithelial lining, may see foreign material
periapical/lateral cyst
tx of periapical/lateral radicular cyst
- extraction or endo therapy (some believe large cystic lesions cannot be resolved with conventional endo)
- follow up at 1 and 2 years is advised (at minimum)
- biopsy required for nonresolving cases
tool for the resolution of periapical inflammatory disease, lesions that fail to respond to proper therapy
Periapical surgery (apicoectomy)- curetage of all periradicular tissue and submission for histopathologic examination, amputation of the apical portion of the root, seal the foramen of the canal
Why submit tissue removed from a periapical disease for microscopic exam?
Things to consider carefully in patient history:
possibility of more serious process unrelated to periapical inflammatory disease
Consider:
- does the patient have previous tx for a jaw lesion
- previous malignancy
- metastatic tumor history (breast, lung, colon, prostate)
can develop in any edentulous space that at one point was dentulous, periapical cyst that did not resolve following extraction of the affected tooth
residual cyst
radiographic appearance: unilocular RL of varying size, corticated or non-corticated
residual cyst
dx: biopsy + extraction history
residual cyst
tx for residual cyst
surgical removal (recurrence unlikely)
Name the periapical inflammatory lesion: accumulation of acute inflammatory cells at the apex of a non-vital tooth
periapical abscess
Name the periapical inflammatory lesion: may be the initial periapical pathology OR a secondary flare up of a chronic periapical inflammatory lesion
periapical abscess
Name the periapical inflammatory lesion: source of the infection is usually obvious, pulpal death may be trauma-related (tooth doesn’t have a cavity or restoration)
periapical abscess
Name the periapical inflammatory lesion: becomes symptomatic as purulent material accumulates within the alveolus (tenderness of affected tooth)
periapical abscess
Progression of a periapical abscess:
pain becomes more intense –> extreme sensitivity to percussion –> extrusion of tooth may occur –> swelling of tissues
Name the periapical inflammatory lesion:
- tooth does not respond to cold or EPT
- headache, malaise, fever, and chills may be present
periapical abscess
How does a periapical abscess spread?
along the path of least resistance
Radiographic findings—widening of apical PDL space, ill-defined radiolucency, sometimes no changes can be detected if not enough time has passed for detectable bone destruction
periapical abscess
when purulence of a periapical abscess spreads through medullary spaces in bone
osteomyelitis
How does a periapical abscess perforate the cortex?
- spread diffusely through the overlying soft tissues as cellulitis
- channel through overlying soft tissue and perforate the oral epithelium creating an intraoral sinus tract (drainage)
accumulation of inflamed granulation tissue located at the opening of the sinus tract
parulis
*associated with periapical abscess
If an abscess is not able to establish drainage through the skin or into the oral cavity, what happens?
may spread through fascial planes of soft tissue (cellulitis)
2 dangerous forms of cellulitis
Ludwig’s angina
cavernous sinus thrombosis
cellulitis of the submandibular region, aggressive and rapidly spreading
Ludwig’s angina
angina comes from the Latin word _____ meaning to strangle
angere
70% of cases develop from spread of an acute infection from mandibular molars
Ludwig’s angina
causes: acute infection from mandibular molars, peritonsillar or parapharyngeal abscesses, oral lacerations, fractures of the mandible, submandibular sialadenitis
Ludwig’s angina
Ludwig’s angina has an increased prevalence in people who are ?
immunocompromised
spaces involved in Ludwig’s angina
- sublingual, submandibular, and submental spaces
- once it enters the submandibular space, may extend to lateral pharyngeal (parapharyngeal) space and then to retropharyngeal space
- may result in spread to the mediastinum
tx of Ludwig’s angina
- maintenance of the airway
- elimination of original focus of infection
- IV antibiotic therapy
- incision and drainage
mortality rate of Ludwig’s angina
10% (pericarditis, pneumonia, mediastinitis, sepsis, empyema, respiratory obstruction)
a major dural sinus encased between the meningeal and periosteal layers of the dura, receives venous drainge from the orbit via the superior and inferior ophthalmic veins
cavernous sinus
___% of cases of cavernous sinus thrombosis are the result of dental infections.
Other causes:
10%
Other: sinusitis, conditions prone to blood clotting, lupus, an infection in the ears or eyes
Cavernous sinus thrombosis: developing from anterior vs posterior pathway
Anterior pathway: infection in maxillary anterior teeth perforate the facial maxillary bone and spread to the canine space
Posterior pathway: infections in maxillary premolar or molar teeth spreads to buccal or infratemporal space
- swollen eyelids and conjunctiva with cavernous sinus thrombosis
- protrusion around eye, forehead, and nose
- pupil dilation and loss of vision
periorbital edema
- induration and swelling of forehead and nose
- fever, chills, tachycardia
- nausea and vomiting
- mental state changes
cavernous sinus thrombosis
tx for cavernous sinus thrombosis
- aggressive IV antibiotics (3-4 weeks)
- removal of source of infection if identifiable (draining an infected sinus, extract a tooth and drainage)
- anticoagulation therapy
mortality rate of cavernous sinus thrombosis
~30%
- purulence from a periapical abscess can spread through medullary spaces in the bone
- majority of cases caused by bacterial infections
- expanding lytic destruction of involved bone that extends away from the initial site involvement
- suppuration and sequestra formation
osteomyelitis
3 classifications of osteomyelitis:
- acute suppurative osteomyelitis
- chronic suppurative osteomyelitis
- diffuse sclerosing osteomyelitis
Name the osteomyelitis: acute inflammatory process spreads through the medullary spaces of the bone, < 1 month duration
acute suppurative osteomyelitis
Name the osteomyelitis: signs and symptoms include fever, leukocytosis, lymphadenopathy, significant sensitivity, soft tissue swelling, paresthesia of the lower lip may occur, drainage or necrotic bone spicule exfoliation
acute suppurative osteomyelitis
tx for acute suppurative osteomyelitis
Surgical intervention
- resolve infection
- establish drainage
- remove infected bone
- culture the bacteria
Antibiotics are key!!
- penicillin, clindamycin, metronidazole
Name the osteomyelitis: if left untreated, acute suppurative osteomyelitis progress to this
chronic suppurative osteomyelitis
Name the osteomyelitis: signs and symptoms include swelling, pain, sinus formation, purulent discharge, sequestrum formation, tooth loss, or pathologic fracture
chronic suppurative osteomyelitis
radiographic appearance: patchy, ragged, and ill-defined radiolucent, often contains central radiopaque sequestra
chronic suppurative osteomyelitis
Name the osteomyelitis: surgical intervention is mandatory, removal of all infected material down to bleeding bone is mandatory in all cases
chronic suppurative osteomyelitis
localized areas of bone sclerosis, associated with the apices of traumatized teeth (caries, excessive occlusal forces)
condensing osteitis
radiographic appearance: uniform zone of radiopaque change directly associated with root surfaces, widened PDL space may be seen
condensing osteitis
most common locations of condensing osteitis
most commonly mandible, premolar and molar
tx for condensing osteitis
- resolution of the odontogenic infection
- extraction or endo tx of the involved tooth
about 85% of cases regress, partially or totally
condensing osteitis
residual area of condensing osteitis remaining after resolution of the inflammatory focus
bone scar
