Conventional root canal therapy for non-vital teeth (Proceedings)

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Conventional root canal therapy for non-vital teeth (Proceedings)


Pulpal function

Pulpal functions are 1) formative, 2) nutritive, 3) sensory, and 4) defensive.

1. Formative: pulpal function is formative in that it produces dentin. The development of the pulp is a gradual process that varies with the individual tooth. Development of the pulp takes place after the development of the dental organ, from mesenchymal cells, known as the dental papilla, directly under the dental organ. A distinct basement membrane divides the cellular elements of the dental organ and the dental papilla from each other, and the concentration of cells in the dental papilla stands out clearly from the surrounding oral tissues.

Dentin and pulp share an integral relationship with the odontoblastic processes. When a lesion invades the dentin, the odontoblastic processes and the pulp are involved.

As maturation occurs additional layers of dentin are added. Each dental tubule containing a vital odontoblastic. The dentinal tubule tapers to a cone like shape to the dentinoenamel/dentinocementum junction. The dentinal tubules and odontoblastic process are less voluminous at the periphery of the tooth tapering to an almost closed structure at the cemental wall. The cellular, cytoplasm content of the dentinal tubules is significant in all endodontic treatment. Open dentinal tubules can lead to pulpal pathology.

2. Normal healthy pulpal tissues continue dentinal deposition at a slow rate throughout life. This is referred to as "calcifying down" of the pulp chamber. Pulpal pathology decreases dentinal deposition. Dentin deposition ceases with tooth mortality

3.Nutritive: the pulp provides nutrient to the surrounding tissues during development. After development dentin metabolism continues via the odontoblastic processes. The narrow pulp canals of older animals continue to remain vital with pulpal circulation intact and functional.

4. Sensory: the sensory function of the pulp is response to pain. This is accomplished through the nervous intervention via the apical foremen. Nerve bundles enter the pulp splitting into finer bundles then into unmylinated fibers that enter the odontoblastic layer. Pulpal nerves seem to remain unchanged in older animals. After pulpal necrosis of the coronal pulp with apical inflammation, nerves may still persist in the apical area.

5. Defensive: pulpal response to injury is inflammation. Inflammation produces a chemo tactic response that slows the destructive action to the pulp. Continual irritation will result in pulpal death in spite of a strong response to the irritation from a well-vascularized pulp.

Vessels

The dental pulp is a blood rich organ. The numerous vessels that pass through the apical foremen are distributed throughout the pulp. Most vessels are thinned walled with large lumen. When circulation is cut off, as seen with traumatic severance of vascular supply to the pulp, or periodontal involvement to the apical area, pulpal necrosis result form lack of nutrients to the pulp. It has been demonstrated that the pulp contains lymph vessels through experiments with calcium hydroxide and its rapid uptake into the pulp during pulp capping and Pulpotomy procedures.

Pupal pathology

A basic understanding of pulpal disease is needed to establish a need or lack of for endodontic therapy, and to predict the results of treatment.

Age considerations

Aging pulp tissue undergoes reduction of tissue volume, cellular components, nervous tissue, odontoblasts, and vascular supply. With the closing down of pulpal dimensions through continual calcification by odontoblasts, and reduction of pulpal components the pulpal response to injury is impaired.

Pulpal insult can set up the inflammatory process through the dentinal tubules, by direct dentinal insult of topical irritants, through Anachoresis, localization of blood-born bacteria in hyperemic pulp, or as a result of periodontal disease in combination perio. /endo. Lesions.

Pulpal inflammation is the result of trauma, pulpal exposure as the result of coronal fracture, bacteria, pulpal necrosis with abcessation, iatrogenic factors, or idiopathic in origin, such as internal resorption from unknown factors.