Dental Pulp Diseases and Anatomy

Pulp Diseases

• Pulp is a type of connective tissue found at the center of a tooth.
• It contains collagen fibers, cells like fibroblasts and odontoblasts, nerves, blood vessels, and lymphatics.
• Pulpitis is the inflammation of the dental pulp.
• Pulp is a special connective tissue, enclosed by hard dental tissue.
• During pulp inflammation, intrapulpal pressure increases because the pulp cannot swell.
• Untreated pulp inflammation leads to pulp necrosis.
• Infection can spread through the apical foramina into the periapical tissues.
• Pulp tissue lacks collateral circulation and receives blood only from the apical foramen.
• Cutting off the blood supply results in necrosis.

Anatomic Features of Dental Pulp

• Pulp tissue is enclosed by rigid calcified walls of dentin, which prevents excessive swelling during inflammation.
• There is no collateral circulation to maintain vitality if the primary blood supply is obstructed.
• Nerves, arteries, and veins enter through the small apical foramen.
• During inflammation, artery dilation puts pressure on veins, causing constriction.
• Degeneration and necrosis occur when venous blood outflow is blocked.
• Pulp responds to temperatures between 20°C and 45°C.
• Temperatures outside this range can cause pulp inflammation.
• Pulp lacks the ability to regenerate.

Etiologic Factors of Pulp Diseases

• Noxious stimuli are common causes of pulp inflammation.
• Bacterial effects are a main cause of pulp disease
• Dental caries is the most common cause of pulp disease via bacterial effects
• Direct communication between the pulp and oral environment
• Advanced periodontal disease
• Anachoresis refers to bacteremia from blood
• Retrograde infections originate from the apical foramen.
• Mechanical damage is a main cause of pulp disease
• Accidental damage due to trauma and fracture
• Odonto-iatrogenic damage refers to pulp exposure during cavity preparation; complications are caused by dentists
• Tooth attrition, tooth abrasion
• Thermal injury is a main cause of pulp disease
• Odontoiatrogenic thermal injury involves excessive heat from burs or stones during teeth preparation
• Large metallic fillings without lining
• Heat generation from dental cement setting
• Prolonged tooth cooling
• Chemical irritation is a main cause of pulp disease
• Dental erosion involves the loss of tooth surface from acids in food, drink, or stomach acid (excessive vomiting)
• Odontoiatrogenic chemical irritation occurs due to excessive acid etching,
• Strong drugs like alcohol or chloroform used to dry cavities
• and/or improper mixing of dental cements

Galvanic Shock and Aerodontalgia

• Galvanic shock arises from metal fillings with differing electromotive potential, such as gold versus amalgam.
• Aerodontalgia, or tooth squeeze, is pain caused by changes in ambient pressure.
• This can occur at high altitudes where recent or leaky restorations trap gases that expand, causing severe pain.

Dental Pulp Neurophysiology

• Nerve bundles enter the pulp through the apical foramen/foramina, branching extensively, especially in the coronal pulp.
• The pulp-dentin border zone (pulp tips) is densely innervated, with nerve endings extending 100-150 μm into dentinal tubules.
• Dental pulp consists of A-delta and C-fibers.
• A-fibers are myelinated, conduct fast, cause sharp, sudden pain, are located in the PDJ (peripheral), and allow good localization.
• With A-fibers there is no referred pain, responds to cold/heat, and experiences hyperosmotic solutions
• C-fibers are unmyelinated, conduct slowly, cause dull, continuous pain, are located in the core of the pulp, and allow poor localization.
• With C-fibers there is referred pain, responds to heat, increase in pulp pressure, and inflammatory exudate
• The hydrodynamic theory explains pulp pain as a result of dentinal fluid movement due to stimuli.

Mechanism of Pulp Pain Production

• Stimuli (thermal, evaporative, mechanical, chemical, osmotic pressure) expose dentin and open tubules, changing the rate of dentin fluid flow.
• Action potentials are generated in intradental nerves, travel to the brain, and cause pain.
• Initial pain affects A-delta fibers, then degeneration of A-delta fibers leads to pain transmission via C-fibers.
• C-fiber stimulation occurs due to heat (vasodilation and edema inside the pulp) and pressure.

Classification of Pulp Diseases

• According to the severity of inflammation: acute and chronic pulpitis
• According to the extent of pulp involvement: partial and complete pulpitis
• According to communication between the dental pulp and the oral environment: open and closed pulpitis
• According to the fate: reversible and irreversible pulpitis
• According to presence or absence of infection: infected and sterile pulp

Focal Reversible Pulpitis

• Focal reversible pulpitis, also known as pulp hyperemia, is an early form of pulpitis
• It is localized mainly to the pulpal ends of irritated dentinal tubules.
• Causative factors include irritants like deep carious destruction, large metallic fillings without insulation, and sensitivity to hot and cold.
• Teeth with focal pulpitis are sensitive to thermal changes and mild-moderate pain especially from cold that subsides when removed.
• Histological features include dilation and engorgement of blood vessels (hyperemia), acute inflammatory cellular infiltrate, intact odontoblastic layer, and reparative dentin
• Edema fluid may collect due to damaged capillary walls, causing extravasation of red blood cells or diapedesis of white blood cells (PMNL).
• Slowing of blood flow and hemoconcentration from fluid transudation could cause thrombosis.
• Focal pulpitis is generally reversible if the irritant is removed before severe damage, such as excavating and restoring a carious lesion or replacing a defective filling.
• If the primary cause is not addressed, extensive pulpitis and subsequent pulp "death" may occur.

Acute Pulpitis

• Acute pulpitis is an acute inflammatory reaction of the pulp resulting from progression of focal reversible pulpitis or acute exacerbation of chronic pulpitis
• Acute pulpitis follows pulp hyperemia or acute exacerbation of chronic pulpitis.
• Early stages present with severe pain from thermal changes, especially cold, in the area beneath a carious lesion.
• The pain continues after stimulus removal, may be spontaneous, and can be exacerbated when lying down.
• Later stages involve intense throbbing pain that can keep patients awake, making it hard to identify the offending tooth.
• Heat increases pain, cold may provide relief and the electric pulp vitality tester indicates increased sensitivity.
• If there is an opening symptoms decrease due to exudate escape, reducing pressure and chemical irritation.
• Early histological features include polymorphonuclear leukocytes confined to a localized area with the rest of the pulp relatively normal.
• Increased pressure from inflammatory exudate causes venous collapse.
• Local tissue hypoxia and anoxia lead to localized destruction and pulp abscess formation containing pus.
• The odontoblastic layer is destroyed.
• Later histological features show the acute inflammatory process spreading to involve most of the pulp, with neutrophilic leukocytes filling the pulp and odontoblastic layer degenerating.
• Numerous abscesses cause pulp liquefaction necrosis (acute suppurative pulpitis).
• Treatment involves root canal treatment or extraction

Chronic Pulpitis

• Chronic pulpitis may arise through a quiet phase from a previous acute pulpitis but more typically is chronic initially
• It results from long-term, low-grade injury (slowly progressing caries or low virulence organisms) or from quiescence of an acute process.
• Pain is not prominent, but a mild, dull, intermittent ache may occur.
• Reaction to thermal change is dramatically reduced due to partial nerve tissue degeneration.
• The threshold for stimulation by electric pulp vitality tester is often increased.
• Histological features include infiltration of pulp tissue by mononuclear chronic inflammatory cells.
• Namely lymphocytes, plasma cells, macrophage, more connective tissue reaction, dilated capillaries and evident fibroblastic activity with collagen fibers (attempt to wall off infection).
• A small area of pulp necrosis and pus formation may be localized by a well-defined wall of granulation tissue, forming a minute abscess.

Chronic Hyperplastic Pulpitis (Pulp Polyp)

• Chronic hyperplastic pulpitis is a unique form where the inflamed pulp reacts by excessive proliferation instead of perishing.
• May occur as a chronic lesion from the onset or as a chronic stage of a previously acute pulpitis.
• This reaction is related to the open root foramen, which allows a rich blood supply.
• It occurs in young people (children with deciduous teeth or first permanent molars) and requires treatment as it is not reversible.
• A soft tissue mass grows out of the affected pulp with little to no pain.
• Most common teeth involved are deciduous or first permanent molars with a large pulp chamber, large apical foramen a good blood supply.
• Root development isn't completed, apical foramen is not constricted, and blood vessels enter through a wide apical foramen.
• Histological features include the pulp being replaced by a well-vascularized granulation tissue mass and deeper tissue showing chronic inflammatory cell infiltrate.
• Namely lymphocytes, plasma cells, macrophage sometimes admixed with polymorphonuclear leukocytes
• Gradually the surface becomes epithelized covered by stratified squamous epithelium due to implanting desquamated epithelial cells carried to the surface of the saliva.
• The differential diagnosis is gingival hyperplasia, which is sensitive, highly vascular, and attached to the gingiva.
• Treatment includes extraction of the tooth or pulp extirpation (pulpotomy)

Gangrenous Necrosis of Pulp

• Untreated pulpitis results in complete necrosis of the pulp.
• It is associated with bacterial infection, resulting in pulp gangrene and a foul odor when the pulp is opened.
• With sickle cell anemia blockage of pulp vessels by defective RBC results in pulp necrosis
• Non-vital pulp maintains general histology but is non-purulent.
• It is due to trauma or infarct.