PMI03-2018 Flashcards
What are the possible outcomes of acute inflammation?
Complete resolution (regeneration of native cells and restoration to normalcy)
Healing by connective tissue replacement/fibrosis
Progression to chronic inflammation
What occurs during typical acute inflammation?
Vasodilatation and increased vascular permeability
Fluid exudation and emigration of leukocytes (esp PMNs)
What are the types of aetiological cause of pulpitis?
Microbial
Thermal
Chemical
How can microbes gain access to the pulp?
Carious cavitation
Attrition/abrasion/erosion
Fractures/cracks
Perio-endo lesions
Iatrogenic
What are the different ways of classifying pulpitis?
Acute/chronic (clinical and histological features)
Reversible/irreversible (clinical features)
Open/closed
Subtotal/generalised
Sterile/infected
Describe the general course of pulpal inflammation with no treatment.
Increase in pulpal pressure due to oedema from acute inflammation (vasodilatation and increased vascular permeability)
Leads to venous stasis –> ischaemia –> necrosis
Destruction of odontoblasts and adjacent pulpal tissue
May lead to periapical periodontitis and abscesses
What local factors affect healing in pulpitis?
Blood supply
Degree of infection
Mobility of tooth
What systemic factors affect healing in pulpitis?
Age
Nutrition
Pre-existing medical conditions
What host factors affect healing in pulpitis?
Pulpal anatomy
Apical blood flow
Pre-existing state of pulp
What irritant factors affect healing in pulpitis?
Nature
Severity
Duration
What cells are characteristic of chronic inflammation?
Lymphocytes
Plasma cells
Macrophages
Can patients often tell exactly which tooth has pulpitis? Why?
No - pulps of individual teeth are NOT precisely represented in the sensory cortex so pain is poorly localised
Does pulpitis react to pressure on tooth surface (biting, percussion)? Why?
No
Infection/inflammation has not reached periodontal/periapical tissues
Describe what you would see in reversible pulpitis.
Hypersensitive to hot and cold
Hyperaemia and oedema
Chronic inflammatory cells with scattered acute inflammatory cells
Pain subsides on removal of stimulus
Positive response to sensibility testing
May have some tertiary dentine
Describe what you would see in irreversible pulpitis.
Pain becomes persistent and spontaneous
Reduced/no/abnormal response to sensibility testing
Often congestion of venules that results in focal necrosis
Fibrosis
Mix of neutrophils and chronic inflammatory cells
How would you treat reversible pulpitis?
Remove local irritant
How would you treat irreversible pulpitis?
Tooth extraction or RCT (or even vital pulp therapy)
Are most cases of pulpitis open or closed?
Closed
Describe open pulpitis.
Large exposure/infection/carious cavity but pulp survives
Often associated with open apices (seen in children) as it allows a better blood supply
Describe chronic hyperplastic pulpitis.
In deciduous molars of 6s in children with large pulp chambers
Large carious cavity in which entire pulpal roof is often missing
Chronic inflammation results in hyperplastic granulation tissue that extrudes from the pulp chamber
Apex may be open which decreases the likelihood of necrosis
Tooth is asymptomatic excepts for a possible feeling of pressure during mastication
Surface of polyp/tissue may be covered with stratified squamous epithelium that can migrate from adjacent gingiva
What is the alternative name for pulpal polyp?
Chronic hyperplastic pulpitis
