Diagnosis of pulpitis and apical periodontitis

The noxious stimuli responsible for pulp inflammation, necrosis, and dystrophy are legion, ranging from bacterial invasion to hereditary dwarfism. Without question, bacterial invasion from a carious lesion is the most frequent initial cause of pulp inflammation.

Paradoxically, an alarming amount of pulp involvement is induced by the very dental treatment designed to repair the carious lesion. An increase in automobile and cycle accidents, as well as accidents from body contact sports, has also brought about an increase in pulp death owing to trauma. The causes of pulp inflammation, necrosis, and dystrophy are arranged below in logical sequence, beginning with the most frequent irritant, microorganisms:

I. Bacterial

A. Coronal ingress

1. Caries

2. Fracture

a. Complete

b. Incomplete (cracks, infraction)

3. Nonfracture trauma

4. Anomalous tract

a. Dens invaginatus (aka dens in dente)

b. Dens evaginatus

c. Radicular lingual groove (aka palate-gingival groove)

B. Radicular ingress

1. Caries

2. Retrogenic infection

a. Periodontal pocket

b. Periodontal abscess

3. Hematogenic

II. Traumatic

A. Acute

1. Coronal fracture

2. Radicular fracture

3. Vascular stasis

4. Luxation

5. Avulsion

B. Chronic

1. Adolescent female bruxism

2. Traumatism

3. Attrition or abrasion

4. Erosion

III. Iatric

A. Cavity preparation

1. Heat of preparation

2. Depth of preparation

3. Dehydration

4. Pulp horn extensions

5. Pulp hemorrhage

6. Pulp exposure

7. Pin insertion

8. Impression taking

B. Restoration

1. Insertion

2. Fracture

a. Complete

b. Incomplete

3. Force of cementing

4. Heat of polishing

C. Intentional extirpation and root canal filling

D. Orthodontic movement

E. Periodontal curettage

F. Electrosurgery

G. Laser burn

H.Periradicular curettage

I. Rhinoplasty

J. Osteotomy

K. Intubation for general anesthesia

IV. Chemical

A. Restorative materials

1. Cements

2. Plastics

3. Etching agents

4. Cavity liners

5. Dentin bonding agents

6. Tubule blockage agents

B. Disinfectants

1. Silver nitrate

2. Phenol

3. Sodium fluoride

C. Desiccants

1. Alcohol

2. Ether

3. Others

V. Idiopathic

A. Aging

B. Internal resorption

C. External resorption

D. Hereditary hypophosphatemia

E. Sickle cell anemia

F. Herpes zoster infection

G. Human immunodeficiency virus (HIV) and acquired immune deficiency syndrome (AIDS)

As a consequence of pathologic changes in the dental pulp, the root canal system can harbor numerous irritants. Egress of these irritants from infected root canals into the periradicular tissues can initiate formation and perpetuation of periradicular lesions. Depending on the nature and quantity of these irritants, as well as the duration of exposure of the periradicular tissues, a variety of tissue changes can occur. Radiographically, these lesions appear as radiolucent areas around the portal(s) of exit of the main canal or lateral and/or accessory canals. Histologically, depending on their stage of development, the lesions contain numerous inflammatory cells such as polymorphonuclear neutrophil leukocytes (PMNs), macrophages, lymphocytes, plasma cells, mast cells, basophils, and eosinophils. The interaction between the irritants and the host defensive mechanisms results in release of numerous mediators that curtail progression of infection and development of severe local infection (osteomyelitis) and systemic complication such as septicemia.

Irritation of pulpal or periradicular tissues results in inflammation. The major irritants of these tissues can be divided into living and nonliving irritants. The living irritants are various microorganisms and viruses. The nonliving irritants include mechanical, thermal, and chemical irritants. Mild to moderate injuries of short duration cause reversible tissue damage and recovery of these tissues. Persistent and/or severe injuries usually cause irreversible changes in the pulp and development of periradicular lesions.

In addition to the nonspecificmediators of inflammatory reactions, immunologic reactions also participate in the formation and perpetuation of periradicular pathosis. These reactions can be divided into antibody- and cell-mediated responses.

Periradicular lesions are divided into three main clinical groups: symptomatic (acute) apical periodontitis, asymptomatic (chronic) apical periodontitis, and apical abscess.

Since there is no correlation between histologic findings and clinical signs, symptoms, and duration of the lesion, the terms acute and chronic, which are histologic terms, will not be used in this chapter. Instead, the terms symptomatic and asymptomatic, which describe clinical conditions, will be used.

Symptomatic apical periodontitis (SAP) is a localized inflammation of the periodontal ligament in the apical region. The principal causes are irritants diffusing from an inflamed or necrotic pulp. Egress of irritants such as bacteria, bacterial toxins, disinfecting medications, debris pushed into the periradicular tissues, or physical irritation of the periapical tissues can cause SAP. Impact trauma can also cause SAP.

Sensitivity to percussion is the principal clinical feature of SAP. Pain is pathognomonic and varies from slight tenderness to excruciating pain on contact of opposing teeth. Depending on the cause (pulpitis or necrosis), the involved tooth may or may not respond to vitality tests. Regardless of the causative agents, SAP is associated with the exudation of plasma and emigration of inflammatory cells from the blood vessels into the periradicular tissues. The release of mediators of inflammation causes breakdown of the periodontal ligament and resorption of the alveolar bone. A minor physical injury, such as penetrating the periradicular tissues with an endodontic file, may cause a transient inflammatory response. However, a major injury, causing extensive tissue destruction and cell death, can result in massive inflammatory infiltration of the periradicular tissues.

Also, since there is little room for expansion of the periodontal ligament, increased interstitial tissue pressure can also cause physical pressure on the nerve endings, causing an intense, throbbing, periradicular pain. Increased pressure may be more important than the release of the inflammatory mediators in causing periradicular pain. The effect of fluid pressure on pain is dramatically demonstrated on opening into an unanesthetized tooth with this condition. The release of even a small amount of fluid provides the patient with immediate and welcome relief. Radiographs show little variation, ranging from normal to a “thickening” of the periodontal ligament space in teeth associated with SAP.

Asymptomatic apical periodontitis (AAP) may be preceded by SAP or by an apical abscess. However, the lesion frequently develops and enlarges without any subjective signs and symptoms. Inadequate root canal treatment may also cause the development of these lesions. Generally, a necrotic pulp gradually releases noxious agents with low-grade pathogenicity or in low concentration that results in the development of AAP. This pathosis is a long-standing, “smoldering” lesion and is usually accompanied by radiographically visible periradicular bone resorption. This condition is almost invariably a sequela to pulp necrosis.

The clinical features of AAP are unremarkable. The patient usually reports no significant pain, and tests reveal little or no pain on percussion. If AAP perforates the cortical plate of the bone, however, palpation of superimposed tissues may cause discomfort. The associated tooth has a necrotic pulp and therefore should not respond to electrical or thermal stimuli. Radiographic findings are the diagnostic key.

Asymptomatic apical periodontitis is usually associated with periradicular radiolucent changes. These changes range from thickening of the periodontal ligament and resorption of the lamina dura to destruction of apical bone resulting in a well-demarcated radiolucency.

Asymptomatic apical periodontitis has traditionally been classified histologically as either a periradicular granuloma or a periradicular cyst. Various clinical methods have been used to attempt to differentiate these two clinically similar lesions. The only accurate way to distinguish these two entitles is by histologic examination.

Periradicular Granuloma. Nobuhara and del Rio showed that 59.3% of the periradicular lesions were granulomas, 22% cysts, 12% apical scars, and 6.7% other pathoses.67 Histologically, the periradicular granuloma consists predominantly of granulation inflammatory tissue with many small capillaries, fibroblasts, numerous connective tissue fibers, inflammatory infiltrate, and usually a connective tissue capsule. This tissue, replacing the periodontal ligament, apical bone, and sometimes the root cementum and dentin, is infiltrated by plasma cells, lymphocytes, mononuclear phagocytes, and occasional neutrophils.

Occasionally, needle-like spaces (the remnants of cholesterol crystals), foam cells, and multinucleated foreign body giant cells are seen in these lesions. Animal studies have shown that cholesterol crystals can cause failure of some lesions to resolve following nonsurgical root canal therapy. Nerve fibers have also been demonstrated in these lesions. Epithelium in varying degrees of proliferation can be found in a high percentage of periradicular granulomas.

Periradicular Cyst. Histologic examination of a periradicular cyst shows a central cavity lined by stratified squamous epithelium. This lining is usually incomplete and ulcerated. The lumen of the periradicular cyst contains a pale eosinophilic fluid and occasionally some cellular debris. The connective tissue surrounding the epithelium contains the cellular and extracellular elements of the periradicular granuloma. Inflammatory cells are also present within the epithelial lining of this lesion. Histologic features of periradicular cysts are very similar to those of periradicular granulomas except for the presence of a central epithelium-lined cavity filled with fluid or semisolid material.

Дата добавления: 2015-10-16