Classification and histopathology of pulp disease Flashcards
What does enamel organ develop from?
Dental lamina
Cells found in pulp
Fibroblasts and stem cells and some macrophages, lymphocytes (& lymphatics)
Post-eruption dentine
Secondary and tertiary
Secondary dentine
Physiological: laid down at relatively constant rate throughout life
Regular structure
Pulp gets smaller
Tertiary dentine
Reactionary: laid down in response to insult to pulp
-structure varies
Reparative: occurs through differentiation of new odontblasts after odontoblasts have been killed
-poor structure
Pulp stones
True: composed of dentine
False: amorphous calcifications
-increase in number and size with age
Classification of pulp pathology
Inflammatory (pulpitis) Degenerative -fibrosis -calcifications -internal resorption -may be age changes or 'idiopathic'
Pulpitis
Most important disease to affect pulp
Inflammation of pulp
Most common aetiology: dental caries
Defence reactions of dentine (dentine sclerosis, reactionary dentine formation)
Classification of pulpitis
Pulpitis –> acute or chronic
Acute –> open (i.e. pulp chamber open to oral cavity) or closed
Chronic –> open or closed
Acute open due to exposure, tooth fracture
Acute closed due to trauma
Chronic open due to open caries
Chronic closed due to caries
Causes of pulpitis
Infection (bacterial)
Trauma
Secondary to attrition, abrasion, erosion
Causes of pulpitis: infection (bacterial)
Dental caries (main cause) Secondary to -crack/ fracture -lateral root canals -canals in furcation -invaginated odontome Bacteraemia
Causes of pulpitis: trauma
Physical -direct blow -heat -dessication Chemical -filling materials/ liners Mechanical -cavity preparation
Clinical features of pulpitis
Often poorly localised pain
May radiate to adjacent jaw, neck, face
Continuous or intermittent
Reversible, symptomatic irreversible or asymptomatic irreversible
Correlation clinical and histological
Little to none
Pulpitis
Occurs within closed environment i.e. limited by dentine
Little/ no collateral blood supply
Closed vs open apex (open better prognosis)
Patterns of pulpitis
Starts as localised lesion directly related to proximity of caries e..g pulp horn
Inflammation will spread throughout pulp if caries untreated
Rate of progression and character of pulpitis will vary between teeth and individuals
Protective responses
Tertiary dentine
- forms in response to caries
- > distance of pulp from irritant
- this reduces and may halt pulpitis
Response to early dentine caries
Wheat sheaving indicated oedema in odontoblast layer
Tertiary (reactionary) dentine formation
> blood flow
Lymphocytes, plasma cells and macrophages
-At this stage it is possible pulpitis may resolve if caries removed or ceases to progress
Response to late dentine caries
Acute inflammation > vascularity inflammatory exudate accumulation of neutrophils death of odontoblasts
Natural history
Closed environment
- rapid rise in tissue pressure
- collapse of venous circulation
- leads to tissue hypoxia
Natural history: pulp necrosis
Hypoxia leads to
- local tissue necrosis
- release of inflammatory mediators
- further inflammation and neutrophil accumulation
- formation of pus: pulp abscess
Natural history: pulp abscess
May be:
localised to pulp horn
surrounded by granulation tissue
Natural history: spread
Pulpitis may spread to involve whole pulp
- pus may drain into oral cavity if there is pulp exposure (‘open’ pulpitis)
- bacteria destroyed by neutrophils
Following spread
Total necrosis may follow
One root may be affected first with spread of infection to apex in multi-rooted teeth
What does untreated pulpitis lead to
Necrosis and periapical pathology
Chronic hyperplastic pulpitis
‘pulp polyp’
Usually first permanent molars
-open apices - good blood suply
-open carious cavity with pulp exposure
Granulation tissue in pulp chamber
Surface ulcerated and covered by fibrin and neutrophils
May become covered by epithellium
-source of epithelium uncertain: either saliva or gingival crevice
Clinically appears red and bleeds easily (less so if epithelialsed), often painless
Healing of pulp
Use of calcium hydroxide may stimulate dentine formation
Need contact with pulp for it to be effective
Clinically need to decide whether to ‘pulp cap’ or to extirpate pulp following exposure
Pathological resorption
Internal
-secondary to pulpitis
-idiopathic (‘pink spot’)
External - many causes
