Sensitivity to thermal changes particularly to cold.
Application of ice/cold fluids results pain and relief on its removal.
Respond to stimulation by electric pulp test at lower level of current, indicating a lower pain threshold (greater sensitivity) than the adjacent tooth.
Deep carious lesions, large metallic restorations without adequate base or restoration with defective margins show these lesions.
Dilation of pulp vessels- characteristic
Edema fluids may collect because of damage to the capillary walls, allowing actual extra vacation of RBCs over some diapedisis of WBCs.
Thrombosis-due to slowing of blood flow and heamoconcentration due to transduction of fluid from vessels.
Self-strangulation of the pulp may increase due to increased arterial pressure occluding the veins at the apical foramen.
Boling and Robinson states that the above statement is not correct because the pulp may have several making self strangulation unlikely.
When a necrosed pulp chamber is opened, there may be vital tissue in the root canal of some teeth i.e. total necrosis not always occur.
Reparative and reactionary dentin may be noted in the adjacent dentinal wall
Treatment and prognosis.
It is a reversible condition, if irritant is removed before severe damage of the pulp.
The carious lesions excised and restored or a defective filling replaced as soon as it is discovered.
Proper observation that irreversible damage has not occurred.
If the primary cause is not removed leads to extensive pulpitis results with subsequent death of pulp.
Acute pulpitis. It is a frequent immediate sequla of focal reversible pulpitis, although it may also occur as a acute exacerbation of chronic inflammatory process.
Occurs in a tooth with large carious lesions or restoration, with recurrent caries.
In early stages, when inflamtion only involves a portion i.e. is just beneth the carious lesion, severe pain is elicted by thermal change, particularly ice and cold drinks.
The skin is persisted after the stimulus has disappered or been removed- characteristic feature.
Mitchell and tarplee states that in most cases any type of pulpitis exhibited increased sensitivity to both heat and cold so the evaluation with this thermal stimulus is not accurate
This is confirmed by seltzeretal shown that severty of pain is only partially related to severty of inflammatory response. Other factors are prescence of drainage, patients orevious experience, emotions etc..
Pulpal pain is poorly localized and can be felt in any of the teeth of upper or lower jaw of the affected side, since the pulp of individual tooth are not represented precisely on sensory cortex.
As greater portion of the pulp becomes involved with intrapulpal abscess formation, pain become more severe described as lascinating/throbbing type. The pain lasts for 10-15 min but may be more / less continous and its intensity may be increased when the patient lies down.
The application of heaty may cause as acute exacerbation of pain.
Electric pulp testing positive with lower level of current than adjacent normal teeth indicating increased sensitivity of pulp.
When necrosis occur sensitivity is lost.
Severe pain also occur if the opening is not wide.
Pain is not only due to the pressure caused by lack of escape of inflammatory exudate but also pain producing substances released from inflammatory reaction .
Then there is a rapid spread of inflammation through out the pulp with pain and necrosis.
Until this inflammation or necrosis reaches beyond the root apex the tooth is not sensitive to percussion .
On wide opened case no pressure build up inside the cavity, hence spread of inflammation not rapid and the pain is dull, throbbing ache but the tooth is sensitive to thermal changes, mobility and sensitivity to percussion usually absent.
In severe acute pulpitis patient is extremely uncomfortable an atleast midly ill and ill and apprehensive and seek immediate dental treatment.
Early acute pulpitis charecterised by continued vascular dilation seen in focal revesible pulpitis, accompanied by the accumulation of edema fluid in the connective tissue surrounding the tiny blood vessels.
Pavementing of PMNLs see along the walls of the vascular channels.
PMNLs rapidly migrate through the endothelium lined structures in increasing numbers.
Then great collection of WBCs especially beneth the area of carious penetration.
By this stage the odontoblast in this area have usually been destroyed.
In early stages, PMNLs confined to a localized area and remainder of pulp relatively normal.
The rise in pressure in the pulp associated with an inflammatory exudate causes local collapse of venous part of circulation.
This leads to local tissue hypoxia and anoxia which inturn may lead to localized destruction of pulp and formation of small abscess known as pulp abscess which contains puss (breakdown of leukocyts + bacteria + digested tissue).
This necrotic zone also contains PMNLs and histiocytes.
Abscess formation is due to the entrance of pulp is tiny and lack of drainage.
The chemical mediators from necrotic tissue leads to further inflammation and edema.
Ohnishi T et al reported prescence of HGF(hepatocyte growth factor) during acute inflammation of pulp, which is a multi functional cytokine, mediates epithelial mesenchimal interaction and is involved in the development and regeneration of various tissues including teeth.
Guo X et al states that interleukin-8 level in exudate of acute pulpitis is higher than that in chronic pulpitis.
In some cases, within few days acute inflammatory process spread to all the pulp so that neutrophilic leukocytes fills the pulp.
The entire odontoblast layer degenerates.
If the pulp is closed, the entire pulp tissue undergo rapid disintegration due to pressure.
Numerous small abscess may form and then entire pulp undergoes liquefaction necrosis,this is refered to as acute suppurative pulpitis.
In later stage of pulpitis, the pulp contains large number of bacteria of mixed population especially those found in normal oral cavity.
Treatment and prognosis.
No successful treatment that is capable of preserving the pulp.
Once pulpitis occurs the damage is irrepairable.
Rarely, Acute pulpitis with an open cavity become quiescent and enter a chronic state.
This occur in patient having high tissue resistance or in case of infection with low virulent microbes.
The lesion may or may not be bleed readily, depending upon the degree of vascularity of the tissue and epithelialization.
Teeth commonly involved are desiduous molars and first permanent molars ,these have excellent blood supply because of the large root opening and coupled with high tissue resistance and reactivity in young persons results in proliferation of pulp.
Sometimes gingival polyp,i.e. gingival tissue proliferation adjascent to breakdown or carious tooth may proliferate into the carious lesion and resemble hyperplastic pulpitis.
Hyperplastic tissue is basically granulation tissue made up of delicate connective tissue fibres interspersed with variable small capillaries .
Inflammatory cell infiltration is common.
In some cases fibroblasts and endothelial cells proliferation is prominent.
This granulation tissue commonly epithelialized as aresult of implantation of epithelial cells on the surface.
This epithelium is stratified squamous and closely resembles oral mucosa.
These are desquamated cells carried to the surface of the polyp by saliva which have lost there dividing capacity.
They are also from the basal cell layer released by trauma or from gingival sulcus which have the dividing capacity.
In some cases buccal mucosa may rub against polyp and epithelial cells transplanted directly .
Epithelialisation of polyp is morefrequently seen in deciduous than permanent teeth.
The tissue reaction in this pulpitis is inflammatory hyperplasia.
Organization of the tissues leads to decreased vascularity and increased fibrosis.
Treatement and prognosis:
The condition is not reversible
Root canal therapy or extraction is the treatement
Gangrenous Necrosis of Pulp:
Untreated pulpitis ,either acute or chronic result in complete necrosis of pulp tissues.
Gangrene is the necrosis of the tissue due to ischemia with superimposed bacterial infection .
The pulpitis associated with bacterial infection so the trem pulp gangrene.
It is associated with a foul odour when opened for endodontic treatement .
It is the end result of pulpitis in which total necrosis of tissue occur.
Necrosis of the pulp reported in sickle cell anemia where there is blockage of pulp microcirculation by sickle erythrocytes .
Some times dry gangrene of pulp occurs i.e. nonpurulent nonvital pulp due to traumatic injury or infarct.