Pulpitis

It’s the inflammation of the dental pulp. The sequence of events leading to pulpitis are:

  • Dental caries -> Cavitation of enamel -> Penetration of tooth pulp -> Pulpitis
  • At early stage when pulp infection is limited, tooth becomes sensitive to percussion and hot or cold and pain resolves immediately when irritating stimulus is removed
  • If infection spreads throughout the pulp: irreversible pulpitis occurs: pulp necrosis.
  • At this late stage, pain is severe and is sharp or throbbing worsening on lying down
  • Once pulp necrosis is complete, pain may be constant or intermittent but cold sensitivity is lost
  • Very painful condition and is the most common cause of sever dental pain
  • If untreated: death of pulp -> spread of infection to periodontal space -> periodontitis

Etiology:

  • Dental caries: extending up to pulp: most common cause
  • Traumatic:
  • Exposure of pulp
  • Mechanical damage
  • Fracture of crown
  • Cracked tooth
  • Splitting of tooth which usually occurs in Pre Molar due to masticatory stress
  • Splitting allows microorganisms to reach pulp
  • Thermal effect:
  • E.g.: heat production during drilling especially when done without using water: over rapid cavity penetration: also in silver filling
  • To prevent thermal effect, underneath filling Zn(PO4) is used as insulator
  • Nonspecific infection
  • Due to streptococcus, other organisms via deep caries or via hematogenous route (bacterial invasion)
  • Chemical injury
  • Cements (silicate), mercury alum

Aerodontalgia: mimics pulpitis pain but is due to decompression in high altitude

Pathogenesis:

  • Infection localized to pulp chamber (crown) and pulp cavity (root) which are closed, fixed and rigid space -> accumulation of exudates in pulp space -> increased pressure (limitation for apical foramen) -> increased circulation -> impaired venous return and impaired arterial supply -> pulp necrosis.
  • If treated in early stage: reversible and localized
  • Late stage: irreversible
  • Pulpitis is a nonspecific infection because multiple bacteria are involved: streptococcus and other bacteria present in carious cavity are mostly responsible

Types of Pulpitis:

  • Open: pulp cavity and oral cavity communicate
  • Closed: no such communication exists
  • Acute: rapid, onset, sever and of short duration
  • Chronic: slow development, long duration

Acute Closed Pulpitis

  • When virulent micro organisms enter the pulp in large numbers, part of pulp becomes quickly destroyed resulting in an acute inflammatory reaction.
  • This reaction leads to acute hyperemia with escape of fluids and cellular exudates into the surrounding tissues
  • A minute abscess is formed
  • Rest of pulp is undamaged i.e. infection remains localized
  • In severe cases, however inflammation doesn’t remain localized: it spreads quickly to pulp and progressively destroys it.

Chronic Closed Pulpitis

  • Pulp destruction is seen at the entry at site of injection
  • Mild hyperemia and abscess formation occurs
  • Infection can remain localized for long periods with remaining part of pulp infected and healthy
  • In other words, destruction progresses slowly and finally thru apex, reach periapical tissue
  • Clinically:
  • Acute and chronic pulpitis recognized by type and degree of pain:
  1. Acute pulpitis:
  • Early stage: tooth is hypersensitive to hot and cold
  • Later: pain becomes more persisted and aggravated while lying down or sleeping
  • Pain is due to: pressure on nerve endings by inflammatory exudates in the closed and rigid pulp chamber
  • OR release of pain producing mediators (histamine, 5-HT) from damaged site
  1. Chronic pulpits:
  • May develop without symptoms
  • However there may be bouts of full pain with hot and cold stimuli spontaneously
  • Pain of both acute and chronic pulpitis is poorly localized due to lack of proprioceptive fibers in the pulp and because individual pulp is not represented in sensory homunculus.

Acute Open Pulpitis

  • It occurs in late stage of caries
  • Pulp chamber may open up due to destruction of part of crown
  • Usually the pulp is already dead by this time but it may remain viable and proliferative
  • Following an acute exposure and introduction of infection, an acute inflammatory reaction ensues that leads to abscess formation and escape of pus thru to exposed part
  • Pus escapes: pain relived
  • Rapid spread of infection and destruction of pulp

Chronic Open Pulpitis

  • Occasionally widely exposed pulp survives in a stage of chronic open pulpitis especially in teeth with open apex
  • Crown of tooth with pulp are destroyed and replaced by granulation tissue which may proliferate to fill the carious cavity and then undergoes epithelialization and fibrosis
  • Fibrosis leads to formation of nodules called ‘pulp polyps’ and the condition is called chronic hypertrophic (plastic) pulpitis (CHP)
  • CHP : irritation, infection, chronic inflammation of pulp, proliferation of granulation tissue, epitelization and fibrosis
  • Painless , occurs usually when apex is wide open and high blood supply maintain viability
  • Pathophysiology of chronic open pulpitis:
  • Infection: chronic inflammation of pulp: formation of granulation tissue and proliferation: epithelization and fibrosis: nodule formation

Investigation and Diagnosis

  • Early stage: see by applying hot and cold (ethyl chloride)
  • Initially tooth is sensitive to both hot and cold but later the cold relives while hot aggravates
  • Electric pulp tester: first test in a healthy tooth
  • Start with low current and raise it till response comes
  • Then test in affected tooth
  • Low current produces responds in early stage and high current in late stage
  • Helps to judge the extent of pulpitis

Management of Pulpitis

  • Extraction: effective but destructive way of treating pulpits
  • Not always treatment of choice
  • In severe pulpitis, LA may not work
  • However it is safe in that there are no complications like spread of infection
  • Pulp capping:
  • In recently exposed pulp cavity with opening >1mm without any infection or pain: pulp capping is done (direct pulp capping or DPC) Ca(OH)2 applied at exposed parts
  • If pulp cavity opening >1mm: needs extirpation and RCT.
  • Pulpotomy
  • Partial removal of pulp
  • Coronal pulp is amputated leaving the remaining radicular pulp to heal
  • Pulpotomy is an intermediate treatment modality when apex is wide ( e.g. in children with incomplete development) and RCT is not possible
  • Newly exposed pulp cavity is treated with pulpotomy instead if RCT which is done later as pulp grows

Treatment of pulpitis is offered based on patient

  • Attitude: whether he wants to preserve or remove the tooth
  • Financial status: RCT is expensive
  • Latest technique for desensitization : iontophoresis (back to condition of sensation)
  • Once irreversible pulpitis occurs: RCT is necessary and contents of pulp chamber and root canals are removed followed by thorough cleaning antisepsis and filling teeth with an inert material

Complications of Pulpitis

  • If pulp infection doesn’t decrease: periapical abscess formation (pain on chewing)
  • If mild and chronic infection: periapical granuloma or eventually periapical cyst which produces radiolucency at root apex
  • When untreated a periapical abscess can erode into the alveolar bone producing osteomyelitis, penetrate and drain through the gingiva (parvis or gumboil) or track along deep fascial planes producing a virulent cellulits (Ludwig’s Angina) involving submandibular space and floor of mouth
  • Elderly patient with DM and pt taking glucocorticoids may experience little or no pain and fever as these complications develop.
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