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Pulpal and Periradicular Pathosis

Dr Nawaf Al-Hazaimeh

Causes of inflamation
Microorganisms and viruses. Mechanical, thermal, and chemical 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, and Actinomyces

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

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. 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

Mechanical Irritants Pulp or periradicular tissues can also be irritated mechanically. Deep cavity preparations,
removal of tooth structure without proper cooling, impact trauma, occlusal trauma, deep periodontal curettage, and orthodontic movement of teeth are the main thermal and physical irritants of the pulp tissue.

Periradicular tissues can be mechanically irritated and inflamed by


impact trauma, hyperocclusion, endodontic procedures and accidents, causing physical and chemical damage

Chemical Irritants 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. their cytotoxicity can cause inflammatory changes in the underlying dental pulp. Most irrigants and medicaments are toxic and are not biocompatible

PULPAL PATHOSIS 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

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 immunocompetent cells to the injured pulp.

Lesion Progression Mild injuries may not result in significant pulpal changes. .

Moderate to severe injuries to the pulp


result in localized inflammation release of a high concentration of inflammatory mediators.

increased vascular permeability

fluids from blood vessels into the surrounding tissues.


If removal of fluids by venules and lymphatics ;

Pulp is encased in rigid surrounding tissues, forming a low-compliance system


increase in tissue pressure Local necrosis

Complete collapse o the venules at the site of pulpal injury

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 directly on sensory nerve receptors

CLASSIFICATION OF PULPAL DISEASES


diagnosis and classification of pulpal diseases are based on clinical signs and symptoms rather than histopathologic findings. Pulpal conditions can be classified as normal pulp, reversible and irreversible pulpitis, hyperplastic pulpitis, necrosis, and previously treated pulp. Hard tissue responses include calcification and resorption.

Normal Pulp A tooth with a normal pulp is clinically symptom free and responds normally to vitality tests. Such a tooth does not reveal any radiographic signs of pathosis. Reversible Pulpitis 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, which do not normally produce pain or discomfort, results in immediate relief

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.

Irreversible pulpitis
It is often a sequel to and a progression from reversible pulpitis. 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. It can be symptomatic or asymptomatic with no clinical signs and symptoms.

Symptoms 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. 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.

Tests and Treatment 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 Hyperplastic pulpitis is usually asymptomatic RCT or Extraction

PERIAPICAL PATHOSIS
As a consequence of pulpal necrosis, pathologic changes can occur in the periradicular tissues CLASSIFICATION OF PERIAPICAL LESIONS Periapical lesions have been classified on the basis of their clinical and histologic findings.

Teeth are non-vital