Pulpal and Periradicular Pathosis

Irritants: Irritation of pulpal or periradicular tissues can result in inflammation The major irritants of these tissues can be divided into those that are living and nonliving The living irritants are various microorganisms and viruses The nonliving irritants include mechanical, thermal, and chemical irritants

Microbial irritants: Microorganisms present in dental caries are the main sources of irritation of the dental pulp and periradicular tissues. Carious dentin and enamel contain bacteria such as Streptococcus mutans, lactobacilli & Actinomyces The population of microorganisms decreases to few or none in the deepest layers of carious dentin. However, direct pulp exposure to microorganisms is not a prerequisite for pulpal response and inflammation. Microorganisms in caries produce toxins that penetrate into the pulp through tubules In response to the presence of microorganisms and their byproducts in dentin, the pulp is infiltrated locally (at the base of tubules involved in caries), primarily by chronic inflammatory cells such as macrophages, lymphocytes, and plasma cells As the decay progresses toward the pulp, the intensity and character of the infiltrate change When actual exposure occurs, the pulp tissue is infiltrated locally by polymorphonuclear (PMN) leukocytes to form an area of liquefaction necrosis at the site of exposure Pulpal tissue may remain inflamed for long periods of time and may undergo eventual or rapid necrosis. This depends on several factors:(1) The virulence of bacteria, (2) The ability to release inflammatory fluids to avoid a marked increase in intrapulpal pressure, (3) The host resistance, (4) The amount of circulation, and most importantly, (5) Lymph drainage

The lesions extended first horizontally and then vertically If the irritants persist, the ensuing damage will become extensive and will spread throughout the pulp Subsequently, bacteria, or their byproducts, and other irritants from the necrotic pulp will diffuse from the canal periapically, resulting in the development of inflammatory lesions Bacteria play an important role in the pathogenesis of pulpal and periradicular pathoses

Mechanical Irritants Pulp or periradicular tissues can also be irritated mechanically Main thermal and physical irritants of the pulp tissue: Deep cavity preparations, Removal of tooth structure without proper cooling, Impact trauma, Occlusal trauma, Deep periodontal curettage, and Orthodontic movement of teeth

Periradicular tissues can be mechanically irritated and inflamed by: Impact trauma, Hyperocclusion, Endodontic procedures and accidents, pulp extirpation, over-instrumentation of root canals, perforation of the root, and overextension of the root canal filling materials

Chemical Irritants: Chemical irritants of the pulp include various dentin cleansing, sterilizing, and desensitizing substances, as well as some of the substances present in temporary & permanent restorative materials & cavity liner Antibacterial agents, such as silver nitrate, phenol with and without camphor, and eugenol, have been used in an attempt to sterilize dentin after cavity preparations. However, their effectiveness as dentin sterilizers is questionable, and their cytotoxicity can cause inflammatory changes in the underlying dental pulp Antibacterial irrigants used during cleaning and shaping of root canals, intracanal medications, and some compounds present in obturating materials are examples of potential chemical irritants of periradicular tissues Most irrigants and medicaments are toxic and are not biocompatible

PULPAL PATHOSIS: Pulpal injury results in cell death and inflammation The degree of inflammation is proportional to the intensity and severity of tissue damage Slight injuries, such as incipient caries or shallow cavity preparations, cause little or no inflammation in the pulp In contrast, deep caries, extensive operative procedures, or persistent irritants usually produce more severe inflammatory changes Depending on the severity and duration of the insult and the host capacity to respond, the pulpal response ranges from transient inflammation (reversible pulpitis) to irreversible pulpitis and then to total necrosis. These changes often occur without pain and without the knowledge of the patient or dentist

Inflammatory Process: Irritation of the dental pulp results in the activation of a variety of biologic systems such as nonspecific inflammatory reactions mediated by histamine, bradykinin, and arachidonic acid metabolites Unlike the connective tissues in other parts of the body, normal and healthy dental pulps lack mast cells. However, these cells are found in inflamed pulps Physical injury to mast cells by an antigen on their cell surfaces, results in the release of histamine and/or other bioactive substances present in mast cell granules The presence of histamine in the blood vessel walls and a marked increase in histamine levels indicate the importance of histamine in pulpal inflammation The dental pulp is densely innervated with sensory fibers containing immunomodulatory neuropeptides Experiments indicate that pulpal neuropeptides undergo dynamic changes after injury. In addition stimulation of the dental pulp by caries results in the formation of various interleukins and recruitment of inflammatory cells to the site of injury Studies indicate that pulpal nerves are protective in nature and that they may be involved in the recruitment of inflammatory and immune-competent cells to the injured pulp.

Lesion Progression: Mild injuries to the pulp may not result in significant pulpal changes Moderate to severe injuries to the pulp result in: Localized inflammation and the Release of a high concentration of inflammatory mediators As a consequence of the release of a large quantity of inflammatory mediators, increased vascular permeability and migration of leukocytes to the site of injury occur Elevated capillary pressure and increased capillary permeability move fluids from blood vessels into the surrounding tissues If removal of fluids by venules and lymphatics does not coincide with the filtration of capillaries, an exudate forms Pulp is encased in rigid surrounding tissues, forming a low-compliance system; therefore a small increase in tissue pressure causes passive compression and even complete collapse of the venules at the site of pulpal injury Pressure increases occur in small compartmentalized regions and progress slowly Increased tissue pressure, the inability of the pulp to expand, and the lack of collateral circulation may result in pulpal necrosis and the development of subsequent periradicular pathosis Pain is often caused by several factors The release of mediators of inflammation causes pain directly by lowering the sensory nerve threshold These substances also cause pain indirectly by increasing both vasodilation in arterioles and vascular permeability in venules, resulting in edema and elevation of tissue pressure. This pressure acts on sensory nerve receptors

CLASSIFICATION OF PULPAL DISEASES: Because there is little or no correlation between the histological findings of pulpal pathosis and clinical symptoms, the diagnosis and classification of pulpal diseases are based on clinical signs and symptoms rather than histopathological findings Pulpal conditions can be classified as normal pulp, reversible and irreversible pulpitis, hyperplastic pulpitis, and necrosis Hard tissue responses include calcification and resorption Normal Pulp: Clinically symptom free Responds normally to vitality tests Does not reveal any radiographic signs of pathosis

Reversible pulpitis: By definition, reversible pulpitis is a clinical condition associated with subjective and objective findings indicating presence of mild inflammation in the pulp tissue If the cause is eliminated, inflammation will reverse and the pulp will return to its normal state Causes: Mild or short-acting stimuli such as incipient caries, cervical erosion, or occlusal attrition; most operative procedures; deep periodontal curettage; and enamel fractures resulting in exposure of dentinal tubules can cause reversible pulpitis. Symptoms: Reversible pulpitis is usually asymptomatic However, when present, symptoms usually follow a particular pattern Application of stimuli, such as cold or hot liquids, as well as air, may produce sharp, transient pain Removal of these stimuli, results in immediate relief Cold and hot stimuli produce different pain responses in normal pulp Pain in response to heat in normal pulp, is delayed; and the intensity of pain increases as the temperature rises Pain in response to cold in normal pulp is immediate; and the intensity tends to decrease if the cold stimulus is maintained

Treatment The removal of irritants and sealing and insulating the exposed dentin or vital pulp usually results in diminished symptoms and reversal of the inflammatory process in the pulp tissue If irritation of the pulp continues or increases in intensity for reasons stated earlier, moderate to severe inflammation develops with resultant irreversible pulpitis and eventually pulpal necrosis

Irreversible pulpitis: By definition, irreversible pulpitis is a clinical condition associated with subjective and objective findings indicating presence of severe inflammation in the pulp tissue It is often a sequel to and a progression from reversible pulpitis It can be symptomatic (with spontaneous and lingering pain) or asymptomatic (with no clinical signs and symptoms) Severe pulpal damage from extensive dentin removal during operative procedures or impairment of pulpal blood flow as a result of trauma or orthodontic movement of teeth may also cause irreversible pulpitis Irreversible pulpitis is a severe inflammatory process that will not resolve even if the cause is removed Symptoms: Irreversible pulpitis is usually asymptomatic Patients may, however, report mild symptoms Irreversible pulpitis may also be associated with intermittent or continuous episodes of spontaneous pain (with no external stimuli) Pain resulting from an irreversibly inflamed pulp may be sharp, dull, localized, or diffuse and can last anywhere from a few minutes up to a few hours Localization of pulpal pain is more difficult than localization of periradicular pain and becomes more difficult as the pain intensifies

Tests and Treatment In the presence of severe pain, pulpal responses differ from those of un-inflamed teeth or teeth with reversible pulpitis For example, application of heat to teeth with irreversible pulpitis may produce an immediate response; also, occasionally with the application of cold, the response does not disappear and is prolonged Application of cold in patients with painful irreversible pulpitis may cause vasoconstriction, a drop in pulpal pressure, and subsequent pain relief If inflammation is confined to the pulp and has not extended periapically teeth respond within normal limits to palpation and percussion The extension of inflammation to the PDL causes percussion sensitivity and allows better localization of pain Root canal treatment or extraction is indicated for teeth with signs and symptoms of irreversible pulpitis

Hyperplastic Pulpitis: Hyperplastic pulpitis (pulp polyp) is a form of irreversible pulpitis that originates from overgrowth of a chronically inflamed young pulp onto the occlusal surface. It is usually found in carious crowns of young patients Adequate vascularity of the young pulp, adequate exposure for drainage, and tissue proliferation are associated with the formation of hyperplastic pulpitis Symptoms: Hyperplastic pulpitis is usually asymptomatic

Treatment: Pulpotomy or root canal treatment or Extraction

Pulp necrosis: Necrotic pulp is a clinical condition associated with subjective and objective findings indicating death of the dental pulp Pulp is encased in rigid walls, it has no collateral blood circulation, and its venules and lymphatics collapse under increased tissue pressure. Therefore irreversible pulpitis leads to liquefaction necrosis If exudate produced during irreversible pulpitis is absorbed or drains through caries or through a pulp exposure into the oral cavity, necrosis is delayed; the radicular pulp may remain vital for long periods of time In contrast, closure or sealing of an inflamed pulp induces rapid and total pulpal necrosis and periradicular pathosis In addition to liquefaction necrosis, ischemic necrosis of the pulp occurs as a result of traumatic injury from disruption of the blood supply. Symptoms: Pulpal necrosis is usually asymptomatic

Tests and treatment: Cold, heat, or electrical stimuli applied to teeth with necrotic pulps usually produce no response Because of the spread of inflammatory reactions to periradicular tissues, teeth with necrotic pulps are often sensitive to percussion Sensitivity to palpation is an additional indication of periradicular involvement Root canal treatment or extraction is indicated for these teeth

Hard tissue changes caused by pulpal inflammation: As a result of irritation, two distinct hard tissue changes may occur: calcification or resorption Pulp calcification: Extensive calcification (usually in the form of pulp stones or diffuse calcification) occurs as a response to trauma, caries, periodontal disease, or other irritants Factors associated: thrombi in blood vessels, collagen sheaths around vessel walls and aging are possible sources for these calcifications Calcific metamorphosis: An extensive formation of hard tissue on dentin walls, often in response to irritation or death and replacement of odontoblasts As irritation increases, the amount of calcification may also increase, leading to partial or complete radiographic (but not histological) obliteration of the pulp chamber and root canal A yellowish discoloration of the crown is often a manifestation of calcific metamorphosis Often the teeth are unresponsive Palpation and percussion are usually within normal limits In contrast to soft tissue diseases of the pulp, which have no radiographic signs and symptoms, calcification of pulp tissue is associated with various degrees of pulp space obliteration This condition is not pathologic in nature and does not require treatment

Internal (Intracanal) Resorption: Inflammation in the pulp may initiate resorption of adjacent hard tissues (stimulate pulpal cells to clastic state) The pulp is transformed into a vascularized inflammatory tissue with dentino-clastic activity; this condition leads to the resorption of the dentinal walls, advancing from its center to the periphery Most cases of intracanal resorption are asymptomatic Advanced internal resorption involving the pulp chamber is often associated with pink spots in the crown Teeth with intracanal resorptive lesions usually respond within normal limits to pulpal and periapical tests Radiographs reveal presence of radiolucency with irregular enlargement of the root canal space Immediate removal of the inflamed tissue (pulpectomy) and completion of root canal treatment are recommended If left untreated, these lesions tend to be progressive and eventually perforate to the lateral periodontium. When this occurs, pulp necrosis ensues and treatment of the tooth becomes more difficult (unfavorable prognosis)

Classification of periapical lesions: As a consequence of pulpal necrosis, pathological changes can occur in the periradicular tissues Periapical lesions have been classified on the basis of their clinical and histological findings As with pulpal disease, little correlation exists between the clinical signs and symptoms and duration of lesions compared with the histopathological findings Because of these discrepancies and for convenience, these lesions are classified into the following six main groups: normal periapical tissues, symptomatic (acute) apical periodontitis, asymptomatic (chronic) apical periodontitis, condensing osteitis, acute apical abscess, and chronic apical abscess Lesions associated with significant symptoms (such as pain or swelling) are referred to as acute (symptomatic), whereas those with mild or no symptoms are identified as chronic (asymptomatic) Normal Periapical Tissues This condition represents a clinical and radiographic diagnostic category in which the tooth has normal periapical tissues and will not be abnormally sensitive to percussion or palpation testing The teeth in this category have normal lamina dura and periodontal ligament structures

Acute (Symptomatic) Apical Periodontitis: Etiology: The first extension of pulpal inflammation into the periradicular tissues Eliciting irritants include: inflammatory mediators from an irreversibly inflamed pulp or egress of bacterial toxins from necrotic pulps, chemicals (such as irrigants or disinfecting agents), Hyperocclusion, over-instrumentation of the root canal and extrusion of obturating materials (overfills)

Signs and Symptoms: Moderate to severe spontaneous discomfort as well as pain on biting or percussion Application of pressure by the fingertip or tapping with the butt end of a mirror handle (percussion) can cause marked pain May or may not be associated with an apical radiolucent area Thickening of the PDL space may be a radiographic feature However, usually there is a normal PDL space and an intact lamina dura

Histological Features: Bone and root resorption may be present histologically; however, resorption is usually not visible radiographically

Treatment Adjustment of occlusion (when there is evidence of Hyperocclusion), removal of irritants or a pathologic pulp (RCT) or removal of periapical exudate usually results in relief

Chronic (Asymptomatic) Apical Periodontitis: Etiology: Results from pulp necrosis and usually is a sequel to acute apical periodontitis

Signs and Symptoms: By definition, chronic apical periodontitis is a clinical asymptomatic condition of pulpal origin associated with inflammation and destruction of periapical tissues Mostly asymptomatic Radiographic features range from interruption of the lamina dura to extensive destruction of periapical and inter-radicular tissues

Histological Features Histologically, chronic apical periodontitis lesions are classified as either granulomas or cysts A periapical granuloma characterized by chronic inflammatory tissue around apex of pulpally involved tooth Fibroblasts, collagen fibers, plasma cells, lymphocytes, macrophages and giant cells The apical (radicular) cyst has a central pathological cavity filled with an fluid or semisolid material or cell debris and is lined by epithelium The origin of the epithelium is the remnants of Hertwigs epithelial sheath, the cell rests of Malassez Fibroblasts, collagen fibers, plasma cells, lymphocytes, macrophages and giant cells

Treatment Removal necrotic pulp and complete Obturation of the root canal system or extraction usually result in resolution

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