▪ PROGRAMA “SERVICIO RESPONSABLE”
TOTAL, PERSONAS ATENDIDAS SEGÚN TIPO DE ADICCIÓN
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❑ Radiation Injury to Pulp
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❑❑ Progression of Pulpal Pathologies
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❑ Diagnostic Aids for Pulpal Pathology
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❑ Classification of Pulpal Pathologies
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❑ Normal Pulp and Pulpitis
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❑❑ Reversible Pulpitis/Hyperemia/Hyperactive Pulpalgia
❑❑ Internal Resorption
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❑ Etiology of Periradicular Diseases
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❑ Diagnosis of Periradicular Pathologies
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❑ Clinical Periapical Tests
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❑❑ Classification of Periradicular Pathologies
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❑❑ Acute Apical Periodontitis (AAP)
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❑ Acute Apical Abscess
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❑ Phoenix Abscess/Recrudescent Abscess
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❑ Chronic Alveolar Abscess
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❑ External Root Resorption
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❑ Diseases of Periradicular Tissue of Nonendodontic Origin
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❑❑ Bibliography
INTRODUCTION
Dental pulp consists of vascular connective tissue contained within the rigid dentin walls. It is the principle source of pain within the mouth and also a major site of attention in endodontics and restorative treatment.
Some important features of pulp are as follows (Fig. 3.1)
• Pulp is located deep within the tooth, so defies visualization
• It gives radiographic appearance as radiolucent line
• Pulp is a connective tissue with several factors making it unique and altering its ability to respond to irritation
• Normal pulp is a coherent soft tissue, dependent on its normal hard dentin shell for protection. Therefore once exposed, it is extremely sensitive to contact and to temperature but this pain does not last for more than 1-2 seconds after the stimulus removed.
• Pulp is totally surrounded by a hard dental tissue, dentin which limits the area for expansion and restricts the pulp’s ability to tolerate edema.
• The pulp has almost a total lack of collateral circulation, which severely limits its ability to cope with bacteria, necrotic tissue and inflammation
• The pulp consists of unique cells the odontoblasts, as well as cells that can differentiate into hard-tissue secreting cells.
These cells form dentin and/or irritation dentin in an attempt to protect pulp from injury (Fig. 3.2).
• Pulpal responses are unpredictable, “Some pulps die if you look at them cross eyes, while others would not die even if you hit them with an axe”.
• Correlation of clinical signs and symptoms with corresponding specific histological picture is often difficult.
• Thus the knowledge to pulp is essential not only for providing dental treatment, but also to know the rationale behind the treatment provided.
After all, “This little tissue has created a big issue”.
ETIOLOGY OF PULPAL DISEASES
I. Etiology of pulpal diseases can be broadly classified into:
1. Physical
• Mechanical
• Thermal
• Electrical 2. Chemical
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Textbook of Endodontics
3. Bacterial 4. Radiation
II. WEIN classifies the causes of pulpal inflammation, necrosis or dystrophy in a logical sequence beginning with the most frequent irritant, microorganisms.
1. Bacterial
Bacterial irritants: In 1891, WD Miller said that bacteria are a possible cause of pulpal inflammation (Fig. 3.3). Most common cause for pulpal injury-bacteria or their products may enter pulp through a break in dentin either from:
• Caries (Fig. 3.4)
• Accidental exposure
• Fracture
• Percolation around a restoration
• Extension of infection from gingival sulcus
• Periodontal pocket and abscess (Fig. 3.5)
• Anachoresis (Process by which microorganisms get carried by the bloodstream from another source localize on inflamed tissue).
Bacteria most often recovered from infected vital pulps are:
• Streptococci
• Staphylococci
• Diphtheroids, etc.
2. Traumatic
Fig. 3.1: Relation of pulp with its surrounding structures
Fig. 3.2: Formation of irritation dentin
Fig. 3.3: Radiograph showing carious exposure of pulp in first molar
Fig. 3.4: Tooth decay causing pulpal inflammation
• Acute trauma like fracture, luxation or avulsion of tooth (Fig. 3.6).
• Chronic trauma including para-functional habits like bruxism.
3. Iatrogenic (Pulp inflammation for which the dentists own procedures are responsible is designated as Dentistogenic pulpitis). Various iatrogenic causes of pulpal damage can be:
a. Thermal changes generated by cutting procedures, during restorative procedures, bleaching of enamel, electrosurgical procedures, laser beam, etc. can cause severe damage to the pulp if not controlled.
b. Orthodontic movement c. Periodontal curettage d. Periapical curettage
A use of chemicals like temporary and permanent fillings, liners and bases and use of cavity desiccants such as alcohol.
4. Idiopathic a. Aging
b. Resorption internal or external (Fig. 3.7).
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Pathologies of Pulp and Periapex
Fig. 3.7: Resorption of tooth involving pulp
RADIATION INJURY TO PULP
Radiation therapy affect pulps of fully formed teeth in patients exposed to radiation therapy. The pulp cells exposed to ionizing radiation may become necrotic, there may occur vascular damage and the interference in mitosis of cells. Irradiations also affect the salivary glands causing decreased salivary flow, thereby increased disposition to dental caries and pulp involvement.
Radiation damage to teeth depends on dose, source, type of radiation, exposure factor and stage of tooth development at the time of irradiation.
PROGRESSION OF PULPAL PATHOLOGIES Pulp reacts to above mentioned irritants as do other connective tissues. Degree of inflammation is proportional to intensity and severity of tissue damage. For example, slight irritation like incipient caries or shallow tooth preparation cause little or no pulpal inflammation, whereas extensive operative procedures may lead to severe pulpal inflammation.
Depending on condition of pulp, severity and duration of irritant, host response, pulp may respond from mild inflammation to pulp necrosis (Fig. 3.8).
These changes may not be accompanied by pain and thus may proceed unnoticed.
Pulpal reaction to microbial irritation (Fig. 3.9) Carious enamel and dentin contains numerous bacteria Bacteria penetrate in deeper layers of carious dentin↓ Pulp is affected before actual invasion of bacteria via their↓
toxic byproducts
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Byproducts cause local chronic cell infiltration When actual pulp exposure occurs pulp tissue gets↓ locally infiltrated by PMNs to form an area of liquefaction
necrosis at the site of exposure
Eventually necrosis spreads all across the pulp and periapical↓ tissue resulting in severe inflammatory lesion.
Fig. 3.5: Periodontal disease causing pulpal inflammation
Fig. 3.6: Fracture of tooth can also cause pulpal inflammation
Fig. 3.8: Response of pulp to various irritants
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Textbook of Endodontics
Degree and nature of inflammatory response caused by microbial irritants depends upon
1. Host resistance
2. Virulence of microorganisms 3. Duration of the agent 4. Lymph drainage
5. Amount of circulation in the affected area 6. Opportunity of release of inflammatory fluids
DIAGNOSTIC AIDS FOR PULPAL PATHOLOGY
• Subjective symptoms—most common being pain
• Objective symptoms
1. Visual and tactile inspection — 3Cs – i. Color
ii. Contour iii. Consistency 2. Thermal tests
i. Heat tests — isolation of tooth — use of:
– Warm air – Hot water – Hot burnisher
– Hot gutta-percha stick ii. Cold tests:
– Ethyl chloride spray – Ice pencils
– CO2 snow — temperature 18ºC 3. Electrical pulp testing
4. Radiographs 5. Anesthetic tests 6. Test cavity
Recent advances in diagnostic aids for pulpal pathology include:
1. Laser Doppler flowmetry 2. Liquid crystal testing 3. Hughes probeye camera 4. Infrared thermography 5. Thermocouples 6. Pulpoximetry
7. Dual wavelength spectrophotometry 8. Plethysmography
9. Xenon-133 radioisotopes
CLASSIFICATION OF PULPAL PATHOLOGIES
• Baume’s classification: Based on clinical symptoms 1. Asymptomatic, vital pulp which has been injured or
involved by deep caries for which pulp capping may be done.
2. Pulps with history of pain which are amenable to pharmacotherapy.
3. Pulps indicated for extirpation and immediate root filling.
4. Necrosed pulps involving infection of radicular dentin accessible to antiseptic root canal therapy.
• Seltzer and Bender’s classification: Based on clinical tests and histological diagnosis.
1. Treatable
a. Intact uninflamed pulp b. Transition stage c. Atrophic pulp d. Acute pulpitis
e. Chronic partial pulpitis without necrosis 2. Untreatable
a. Chronic partial pulpitis with necrosis b. Chronic total pulpitis
c. Total pulp necrosis Engel’s classification
• Grossman’s clinical classification 1. Pulpitis
a. Abnormally responsive to cold b. Abnormally responsive to heat ii. Chronic
a. Asymptomatic with pulp exposure b. Hyperplastic pulpitis
c. Internal resorption 2. Pulp degeneration
a. Calcific (Radiographic diagnosis) b. Other (Histopathological diagnosis) 3. Necrosis
Fig. 3.9: Gradual response of pulp to microbial invasion
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Pathologies of Pulp and Periapex
Fig. 3.11: Infectious sequelae of pulpitis
Fig. 3.12: Spread of pulpal inflammation to surrounding tissues
NORMAL PULP AND PULPITIS
A normal pulp gives moderate response to pulp test and this response subsides when the stimulus is removed. The tooth is free of spontaneous pain. Radiograph shows an intact lamina dura, absence of any pulpal abnormality, calcifications, and resorption (Fig. 3.10).
Pulpitis is inflammation of the dental pulp resulting from untreated caries, trauma, or multiple restorations. Its principal symptom is pain. Diagnosis is based on clinical finding and in confirmed in X-ray. Treatment involves removing decay, restoring the damaged tooth, and, sometimes, performing root canal therapy or extracting the tooth.
Pulpitis can occur when caries progresses deeply into the dentin, when a tooth requires multiple invasive procedures, or when trauma disrupts the lymphatic and blood supply to the pulp. It starts as a reversible condition in which the tooth can be saved by a simple filling. If untreated, it progresses as swelling inside the rigid encasement of the dentin compromising the circulation, making the pulp necrotic, which predisposes to infection.
Infectious sequelae of pulpitis include apical periodontitis, periapical abscess cellulitis, and osteomyelitis of the jaw (Fig. 3.11). Spread from maxillary teeth may cause purulent sinusitis, meningitis, brain abscess, orbital cellulitis, and cavernous sinus thrombosis. Spread from mandibular teeth may cause Ludwig’s angina, parapharyngeal abscess, mediastinitis, pericarditis and empyema (Fig. 3.12).
BARODONTALGIA/AERODONTALGIA
It is pain experienced in a recently restored tooth during low atmospheric pressure. Pain is experienced either during ascent or descent. Chronic pulpitis which appears asymptomatic in normal conditions, may also manifests as pain at high altitude because of low pressure.
Rauch classified barodontalgia according to chief complaint:
Class I: In acute pulpits, sharp pain occurs for a moment on