Pulp diseases
Pulp diseases result mainly from irritating stimuli, and starts usually as an inflammatory reaction.
Etiology:
1- Dental caries
i.e. bacterial, which is the most common cause of pulp inflammation, produced by either the micro-organisms, or their toxins.
2- Cracked teeth or excessive trauma
-leading to fracture of the crown or root, and pulp exposure, so bacteria in saliva will infect the pulp.
-deep periodontal pockets extending to the apical foramen or an accessory lateral root canal.
3- Exposure during cavity preparation
-will lead to pulp infection, and/or traumatic damage to pulp tissue.
4- Bruxism and abrasion or friction
-lead to non bacterial inflammatory state.
5-Electric or galvanic effect,as when two dissimilar filling metals are found in opposite teeth.
(Gold and amalgam + saliva-----àcurrent-----àirritation).
6- Anachoretic pulpitis:
-Means deposition of particles as bacteria or metals from the blood stream into an area of inflammation, Why?
-Here the tooth may not be carious but was traumatized by other causes as heat, malocclusion, or galvanism.
7- Aerodontalgia:
-Occurs in pilots or submarines due to formation of gases as nitrogen bubbles in blood ,secondary to rapid changes in pressure. Long flights at high altitudes, for persons with mildly inflamed tooth, would result in similar effect.
-Entrapment of these bubbles in minute vessels of the pulp leads to transient ischemia.
8- Thermal:
-Rapid cavity cutting without cooling, specially in deep caries, or large unlined metal restorations allow low grade thermal stimuli to irritate the pulp, i.e. Iatrogenic pulpitis.
** Dehydration and rehydration of dentinal tubules------àpain.
**Overheating-----àrupture of vessels------àfocal hemorrhage.
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9- Chemical :
Due to erosion or chemicals used in cavity preparation, specially in deep cavities, as zinc phosphate or composite without cavity liners.
Inflamation
-Is by nature is an expansile process, consisting of dilatation of blood vessels, leakage of fluids into surrounding connective tissue, migration of inflammatory cells( PMNLs, lymphocytes, and plasma cells) into the area of stimulation.
**Pulpitis:
-Is inflammation of dental pulp tissue, regardless of the presence of an infectious agent as microorganisms.
-If untreated leads to pulp necrosis.
**Pulp is:
1- Enclosed by hard tissue (enamel&dentin), i.e. do not allow fluid getting-out from vessels, to escape to soft loose tissue.
2- Void of collateral circulation to maintain vitality when blood supply is compromised ( severed or ruptured).
3- Void of proprioceptive nerve endings, so pain is the only sign resulting from any change in the pulp (as dehydration, osmotic pressure, changes in temperature, etc....).
**It is supposed that pulp response to irritation includes stimulation of odontoblasts to deposit tertiary or reparative dentin at the site of irritation, in order to protect the pulp tissue. However, if the irritation /injury is severe, it leads to necrosis of odontoblasts.
**Bacteria isolated from infected pulp, near carious lesion, includes gram positive anaerobes, bacteroides, and lactobacilli.
Classification of pulp diseases:
1- Pulp hyperaemia: or focal reversible pulpitis.
2- Acute pulpitis (focal or generalized), and acute pulp abscess.
3- Chronic pulpitis (focal or generalized), and chronic pulp abscess.
4- Chronic open pulpitis or pulp polyp (ulcerative or epithelialised).
5- Pulp necrosis, where inflammatory exudates or infection may spread to the periapical area.
Dental caries------àReversible pulpitis------àAcute pulpitis (Abscess) ------àChronic pulpitis(Abscess)-----à Necrosis.
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1- Pulp hyperaemia: (reversible pulpitis):
-The earliest change is non specific, revealing dilatation of the local vessels and increased permeability of plasma proteins, leading to tissue edema that presses on nerve endings.
-The tooth will be hypersensitive to cold or hot, and electric stimuli.
-Pain is mild/moderate, intermittent and lasts for 5-10". Pain may be localized to a particular tooth (rarely, WHY?).
**Removal of the stimulus would result in recovery of the condition.
2-Acute pulpitis:
-It may start as an acute state or due to an acute exacerbation of a chronic one .Pain is referred to another nearby location (or the whole side, WHY?). Pain threshold is low.
-The condition starts with engorgement of the dilated vessels with RBCs, and extravasation of PMNLs to the surrounding area (localized or generalized pulpitis).
-Pain becomes more persistant, with prolonged attacks (lasting more than 20", may start spontaneously, and often when the patient is sleeping (i.e. on recumbent position).
-Pain is severe, sharp and stabbing in character.
-Pain is produced due to either pressure of inflammatory exudate on nerve endings (within the rigid, confined chamber), or due to release of toxins/enzymes from the damaged tissues , PMNL,or micro-organisms.
-Pain is intensified with heat or cold.
-In case of liquefaction of pulp tissue, application of cold may eliminate pain (WHY?).
-If the pulp is exposed, symptoms may be less intense due to escape of exudate that presses on nerves.
** Acute pulp abscess:
-Due to localization of the inflammatory exudate and cells .
-Formed of centrally located necrotic tissue( purulent exudate), of micro-organisms, necrotic pulp tissue(debris), fibrin, RBCs ,surrounded by PMNLs, dilated& engorgd vessels, few lymphocytes, plasma cells and macrophages. The outermost margin is formed of granulation tissue.
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3-Chronic closed pulpitis:
-Long standing, low grade stimulus may lead to the condition, or due to high tissue resistance, or quiescence of an acute state.
-Pain is dull aching, deep, mild, lasts longer and intermittent.
-Pain threshold is increased.
Histologically:
-The pulp is infiltrated with mononuclear leukocytes, i.e. lymphocytes, plasma cells and macrophages.
-The surrounding tissue is formed of collagen fibers and newly formed capillaries (granulation tissue).
**Chronic abscess
-Occurs when localization of chronic inflammatory cells with central necrotic mass, and surrounded by granulation tissue
4- Chronic open pulpitis ( pulp polyp,
chronic hyperplastic pulpitis):
-It results in large carious lesions, exposed chamber, and often large apical foramins, i.e. deciduous & permanent molars of young patients
-Mild stimulus so inflammation is not confined to solid, rigid area, with abundant vascularity).
-Mildly painful or painless (reduction of nerve endings).
Histologically:
-Granulation tissue
-The surface is covered by either acute or chronic inflammatory cells
(Ulcerative pulp polyp) or covered by squamous epithelium (auto-transplantation of epithelial cells, from where?).
-This tissue usually protrudes from the tooth, of normal or faint color, either due to less vascularity or epithelial covering.
D.D.gum polyp, wlich is proliferating gingival tissue, from the interdental papilla, that may protrude and seated on the occlusal surface.
-It is reddish in color, more sensitive,and bleeds readily on slight probing.
5- pulp necrosis:
-Is death of pulp tissue ,i.e. no pain.
-There is no tissue or only remains of dead tissues.
**It is hard to relate the clinical features to specific histopathologic criteria.
**The patient, in most cases, can not localize the affected tooth, WHY? **No pain on percussion, or biting on hard substance, WHY?
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