Pulpo-periapical pathology

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Dentine hypersensitivity 1.4.1.2

A hypersensitive tooth is one that tends to overreact to various stimuli because of exposed dentin.

1.4.1.2.1 Clinical:

Dentin hypersensitivity is characterized by severe pain, short and located immediately after performing a stimulus. Presumably the pain of dentin is due to the movement of liquids within the tubules (as the hydrodynamic theory). If dentin is exposed by abrasion, erosion, attrition, gingival recession, periodontal treatment, or anatomical defects, the pulp may respond well localized, sharp pain of short duration to osmotic stimuli, thermal, chemical or mechanical. When a specific etiologic factor that causes the sensitivity (caries, fracture, microleakage, recent restorative treatment), teeth with vital pulp may have symptoms identical to dentine hypersensitivity. Although, if they appear in these situations, appropriate diagnosis of reversible pulpitis.

1.4.1.2.2 Diagnosis

We need a detailed medical history along with clinical and radiographic examination. Definitive diagnosis is more difficult when coexisting clinical causes of reversible pulpitis and exposed dentin.

1.4.1.2.3 Treatment:

We can reduce dentine hypersensitivity:

  • Decreasing the permeability of the tubules exposed (application of resins, fluorides and a thin layer of varnish, oxalate salts, laser radiation ...);
  • Reducing the sensitivity of nerve fibers in dentin with gels, toothpastes or mouthwashes desensitizing (potassium nitrate, fluoride ...).

1.4.1.2.5 Effect of pulpal inflammation in dentine sensitivity

The response to stimulation not only increases dentine with exposure of dentinal tubules, also increases with the presence of inflammatory mediators. Therefore, the pulp inflammation (pulpitis) by decay, trauma or microleakage predispose to tooth dentin sensitivity increase, lowering the threshold for nerve activation and increasing the area innervated tubules.

1.4.1.3 Reversible pulpitis

Reversible pulpitis inflamed pulp involves retaining the vitality and keeps the repair capacity sufficient to restore health by eliminating the irritant that causes it.

1.4.1.3.1 Clinical:

Sharp pain in the application of thermal stimuli and / or osmotic. Removing the pulp stimulus remains asymptomatic.

1.4.1.3.2 Diagnosis

Evidence of dental caries, restore fractured recent restorative treatment or cracked cusps. During testing the pulp vitality reacts more teeth to cold than normal, and faster than heat. The percussion is usually negative.
Radiographically, the periodontal ligament space and lamina dura are normal.

1.4.1.3.3 Treatment:

The removal of the cause of irritation should cede the pulp inflammation and symptoms.

  • Caries: removal of caries and tooth restoration.
  • Recent restorative treatment: You should adjust the occlusion to eliminate occlusal traumatsimo cause of discomfort (not a cause of irreversible pulpitis). We must allow the tooth for several weeks to recover before considering the need for endodontic treatment.
  • Microfiltration or restoration fracture: elimination of the old restoration and implementation of a new one.

1.4.1.4 cracked tooth syndrome:

It consists of the incomplete fracture of a tooth whose pulp is vital. Subsequent to enamel and dentin, and in some cases, the dental pulp.
A thin incomplete tooth fracture can result in pulpal pain.
When parts of the crown are separated by the forces of occlusion, the dentin is exposed momentarily and as a result of hydrostatic fluid movement within the tubules, the patient experiences pain. Depending on the level of the fissure, the patient may have symptoms of hypersensitivity, irreversible pulpitis, or pulp may become necrotic.

1.4.1.4.1 Clinical:

Pain on chewing, with variable patterns of referred pain and sensitivity to temperature changes. The most common symptom is severe pain that occurs when releasing the pressure to stop biting. 1.4.1.4.2 Diagnosis: A diagnosis is difficult because you do not see an obvious cause of pathology. We help the patient make a wedge bite, pain releasing pressure is a strong indication of the presence of a cracked tooth. You can supplement with the help of an optical fiber light transilluminated the fracture line, or with the use of dyes (methylene blue) to stain the fissure. Fissures rarely detected radiographically. If the crack extends to the root level, one can observe a periodontal defect in the form of a narrow and deep pocket adjacent to the fracture. We will have an increased periodontal probing at a single point. Surely it will already be necrotic pulp.

1.4.1.4.3 Treatment:

Emergency treatment involves immediate removal of occlusal contacts of teeth. The definitive treatment attempts to preserve its vitality with a full cuspal coverage to prevent the spread of the crack into the pulp and the root. Please try the tooth, the condition may progress to irreversible pulpitis or necrosis, as well as lead to a vertical root fracture. In principle the cracked tooth syndrome presents with a pathology reversible pulp, so root canal treatment is contraindicated. In fact, when the process evolves to irreversible pulp pathology (formerly would not be a cracked tooth syndrome), treatment and requires a root canal treatment, and prognosis worsens considerably, losing the repair capacity of the dental pulp. If root canal treatment is done without being needed, which is relatively common in the difficult diagnosis of the entity, the prognosis is as bad as in cases where there is irreversible pulpal pathology. If root canal is done, the tooth will run out, very likely breaking in the span of months to a couple of years, and it therefore consider the appropriateness of proceeding with it.

1.4.1.5 Irreversible pulpitis

Irreversible pulpitis can be acute, subacute (mild exacerbation of chronic pulpitis) or chronic. The pulp is symptomatic with acute inflammation, whereas chronically inflamed pulp is asymptomatic in most cases.

1.4.1.6 Symptomatic irreversible pulpitis

Because the environment in which the pulp is an intense inflammatory response may lead to a detrimental increase in tissue pressure, which exceeds the capacity of compensatory mechanisms of the vital pulp, preventing the recovery of his health. The inflammatory process extends circumferentially and progressively through the pulp, perpetuating the destructive cycle.

1.4.1.6.1 Clinical:

The intensity of clinical symptoms varies increases the inflammatory response, depend on the degree of pressure intrapulpal and viability of nerve fibers.
Irreversible pulpitis can cause severe pain with the application of thermal stimuli, which persists after removal of the stimulus (inflammatory involvement of nerve fibers A-delta).
When pain subsides exaggerated a dull ache may persist pulsatile nature (inflammatory involvement of nerve fibers C nocioceptivas). Spontaneous pain (unprovoked) is also characteristic of irreversible pulpitis. If the pain is prolonged and intense pulp, central excitatory effects can produce referred pain. When the C fiber pain predominates over that of A-delta fibers, the pain is more diffuse and decreases the possibility of identifying the offending tooth by vitality tests.
In a tooth with irreversible pulpitis sometimes cold provides relief from pain (by vasoconstriction and decreased tissue pressure). Sometimes, changes in posture (lying down or bending forward) causes pain (increased pressure), which can lead to interrupted sleep.
When, moreover, there is hypersensitivity to the bite, the irreversible pulpitis is associated with acute apical periodontitis. In this case, the pulp inflammation has spread to the periradicular tissues to produce a combination of pulp and periradicular symptoms.

Referred pain area

Dental pulp that starts the pain

Frontal (forehead)

Upper incisors

Nasolabial

Upper canine, premolars

Region above the maxillary molars

Second premolars, first molars

Temporal region

Second premolars

Area below the mandibular molars

Second and third molars

Heard

Molars. Occasionally the second and third molars

Mental region

Incisors, canines and premolars

Middle of the ramus

Second premolars

Mandibular angle

First and second molars

Superior laryngeal Zone

Third molars

Premolars

Upper canine

Molars

Upper canine, premolars

Premolars

Upper canine, premolars

First premolar

First and second molars



1.4.1.7 asymptomatic irreversible pulpitis

Asymptomatic irreversible pulpitis is an inflammatory response of the pulp tissue to an irritant. It causes pain due to reduced intrapulpal pressure below the threshold of pain receptors. This is because the wet zone products:

  • Drain into the carious lesion.
  • They are absorbed by the venous or lymphatic circulation.
  • Spread to an area adjacent tissue.
  • Use any combination of these ways do not increase blood pressure.
  • It may represent the conversion of symptomatic irreversible pulpitis to a dormant state.

1.4.1.7.1 Treatment:

The treatment of asymptomatic irreversible pulpitis, like that of the symptomatic, is endodontics.

Reversible pulpitis

Irreversible pulpitis

Discomfort or light sensitivity
Feeling short or whiplash
No severe
Infrequent episodes of discomfort
Only rarely bother to bite, unless the tooth is further broken or loose and the restoration is affecting the occlusion
May result in irreversible if not eliminate the cause
The symptoms usually disappear immediately or soon to eliminate the cause
The most common causes are exposed dentin fractured restorations, recent restorations, initial attack of caries or decay rapidly progressive occlusion altered.





Pain may or may not
There is often a history of previous pain
The pain is usually moderate to severe
Pain often spontaneous ees
The pain becomes increasingly frercuente, to become continuous
The pain is often reduced, with episodes of exacerbation
The patient often needs painkillers
The thermal stimulation often triggers a severe dull pain
They tend to identify specific stimuli or multiple
The pain radiates, or is diffuse, or may be located
There is a history of trauma, restorations, periodontal disease or extensive recurrent caries
There may be no radiographic changes, or calcifications, resorption or radiolucency

1.4.1.8 Open asymptomatic irreversible pulpitis

Chronic pulpal inflammation characterized by the formation of an abscess at the point of carious exposure.
Painless. Although this may appear if food hamper drainage impacted or there is a sudden inoculation of pollutants in the pulp tissue. This would result in a symptomatic pulpitis.

Hyperplastic pulpitis 1.4.1.9

Sometimes the low-grade chronic irritation, with abundant vascularization, typical of young people, resulting in a reddish growth, cauliflower-shaped, the pulp tissue around and through a carious exposure. This proliferation of granulomatous tissue called pulp polyp, and often covered by oral mucosal epithelium.
The polyp contains few nerve fibers, making it relatively insensitive to touch. Although bleeds easily on probing the cavity. It's painless. The thermal and electrical tests are normal responses. And there are signs radiographic periapical. Before beginning the root canal treatment it requires the removal of the polyp with a sharp curette.

Asymptomatic pulpitis closed 1.4.1.10

Pulpitis secondary to surgical intervention, trauma or periodontal lesion. There is therefore no carious exposure. If pulp damage is minimal, the infant may refer chronic pulpitis.

1.4.1.11 Internal resorption

Location painless, caused by osteoclast cells that produce dentin destruction. Exact etiology is unknown (considering the trauma, persistent chronic pulpitis ...).
Usually a chance radiographic finding. If not identified early can perforate the root. Before drilling the crown resorption can be detected as a pink spot in the area. Only pulp necrosis or root canal treatment will prevent tooth decay, because the internal resorption ceases once the pulp tissue dies.

Necrosis 1.4.1.12

It means death of the pulp. It is the evolution of an irreversible pulpitits untreated traumatic injury or any circumstance that results in prolonged interruption of blood supply to the pulp. Pulp necrosis may be total or partial (more common in teeth multirooted).

1.4.1.12.1 Clinical:

There are no true symptoms of pulp necrosis because, at this stage, the sensory fibers of the pulp is destroyed. However, it can cause pain in the periradicular tissues, because of the inflamed pulp degeneration.

When necrosis is partial, there may be various symptoms due to the persistence of vital tissue in a portion of the canal.

1.4.1.12.2 Diagnosis:

Total necrosis is painless in the tooth. There is mobility. Palpation and percussion are negative, and normal radiographic findings (unless there is a concomitant periapical inflammation). Vitality tests give no answer. You can observe a change in tooth color.

1.4.1.12.3 Treatment:

Pulp necrosis requires endodontic treatment of teeth.

1.4.2. Periapical pathology

1.4.2.1 symptomatic periapical periodontitis

Inflammatory responses are periapical tissue to pulp irritants. Pain occurs due to the large increase in pressure intraperiapical.

1.4.2.2 Acute Apical Periodontitis

Incipient painful inflammation of periapical tissues caused by pollutants coming from the root canal (inflammation may also be a result of trauma caused by mechanical or chemical endodontic instruments or equipment, or the trauma caused by the occlusal surfaces hyperocclusion or bruxism.)

1.4.2.2.1 Clinical:

Pain sensitive to percussion. In these early stages is usually not seen swelling, but if you press hard on the root end can get a positive pain response.
Vitality tests are negative, although in the initial stages, we get positive responses due to the resistance of type C nerve fibers, in multirooted teeth could also happen because different channels are found in varying levels of damage.
Although there is acute periapical periodontitis, priodontal ligament may be within normal limits or show only a slight widening, radiographically.


Table 3. Periapical pathology types of endodontic origin.

1.4.2.2.2 Treatment:

Endodontic treatment. After the root canal can cause apical periodontitis, as a result of periradicular tissue trauma, or inflammatory reaction to the debris extruded to periapex. If you have deleted the whole fabric of the canal system is preferable to administer painkillers. Apical periodontitis caused by traumatic occlusion, often causes pain to biting, eating, or by occluding teeth. Many times it will put a recent refurbishment with high contact. Treatment includes adjustment of occlusion to eliminate the premature contact.

1.4.2.3 acute apical abscess

Advanced inflammatory response, with exudation of periapical tissues caused by pollutants from the pulp canal produced steadily increasing amounts of inflammatory exudate (edema), leukocyte infiltration and drainage. It is the result of the exacerbation of acute apical periodontitis in a necrotic pulp.

1.4.2.3.1 Clinical:

Throbbing pain, often intense and continuous, which is often accompanied by a localized sensation of fullness. The patient may have fever. Unless you establish a channel of drainage, the exudative response may spread diffusely, creating peripheral areas of cellulite.
The incisor periapical inflammation can cause soft tissue swelling lip, in the upper canines can affect the tissues of the wing and the nose and upper premolars lid swelling may occur.

1.4.2.3.2 Diagnosis

The facial soft tissues may swell and become tender to palpation. The overlying cortical bone resorption and oozing location of the mass beneath the mucosa produce swelling. The swelling may be localized or diffuse (cellulitis), fluctuant or firm.
The offending tooth is sensitive to percussion, may have a slight increase mobility and vitality tests are negative. Radiograph can be viewed from a total lack of updates, if the inflammation is very fast, up to a defined radiolucency.

1.4.2.3.3 Treatment:

Whenever possible, we should let the abscess drain through the pipe (it is sometimes necessary to implement a file No 30 to drain). Drainage is facilitated by gentle finger pressure on the mucosa adjacent to the swelling and positive aspiration of the pulp chamber If you can not finish the root canal, we must make intracanal medication and close it with a temporary filling. Incision and drainage through the tissues have little information (inaccessible to the apex through the ducts). And if the swelling is localized and has a fluctuating consistency.
If drainage is achieved is considered unnecessary antibiotic therapy in patients with localized swellings. It is considered appropriate to use a systemic antibiotic for any diffuse swelling, in immunocompromised patients and patients with systemic signs of illness (fever, malaise ...).

1.4.2.4 phoenix abscess

Painful abscess derived from a preexisting chronic apical periodontitis by being contaminated or infected by elements from the necrotic root canal or endodontic.

1.4.2.4.1 Diagnosis

Symptoms of phoenix abscess and acute apical abscess are identical. When we see a large periapical radiolucency, the lesion is called a phoenix abscess.

1.4.2.5 asymptomatic periapical periodontitis

Inflammatory defensive responses to an irritant pulp tissue pulp. Do not cause pain due to reduced pressure intraperiapical, below the threshold.

1.4.2.5.1 Clinical:

Asymptomatic periapical lesion that appears only on radiographs.

1.4.2.5.2 Diagnosis

Both the percussion and mobility tests give negative results. Often the patient will say that even if the tooth does not hurt, he feels "different" or "hole" on percussion. There is sometimes mobility due to a large periradicular bone loss. It is often observed discolouration due to loss of translucency, hemolysis of erythrocytes or the breakdown of pulp tissue. All vitality tests are negative, because the nerve fibers are unfeasible. Polirradiculares teeth can give positive answers when they preserve viable nerve tissue in one of its pipelines. Radiographically one can observe a radiolucent area large or small, diffuse or circumscribed. The inflammation and destruction are always greater than what is observed on radiographs. It is impossible to diagnose periapical lesions with varying degrees of accuracy without a biopsy, although the cysts are more frequent in larger lesions.

1.4.2.5.3 Treatment:

Endodontics. They will sometimes require surgical approach (true cysts).

1.4.2.6 emerging chronic apical periodontitis

This response chronic periapical tissue to pulp any irritant is characterized by a slight widening of the apical periodontal space.

1.4.2.6.1 Treatment

Endodontics. Its aim is to remove the irritant of the canal and keeping it out through a three-dimensional obturation.
If no contaminants are removed pulp, the answer is intensified to become one of the advanced acute or chronic forms.

1.4.2.7 periapical granuloma

More advanced form of chronic apical periodontitis. Development of a granulation tissue response to pulpal irritation maintained. If contaminants invade the pulp tissue forms an acute abscess (a. Phoenix).

1.4.2.7.1 Treatment:

Endodontics. If we eliminate necrosis and infection of root canals, granuloma can complete your healing and repair.


Figure 2. Apical granuloma at the apex of a tooth extracted

1.4.2.8 chronic periapical abscess (suppurative apical periodontitis)

Appearance of active formation of phlegmon and draining pus through a sinus. It usually develops from chronic apical periodontitis, but may also be secondary to an acute periapical abscess that has found a way out and drains through the oral mucosa.

1.4.2.8.1 Diagnosis

There will be a radiograph with a gutta-percha of No 35 through the fistula to know the origin of the injury.

1.4.2.8.2 Treatment:

Endodontics.


Fig 3. Upper molar has a palatal fistula and a periapical radiolucency. Place a gutta percha point 30 gauge in the sinus tract and a radiograph taken to confirm that the origin of that route is in the periapical apparently causal.

1.4.2.9 Cyst

Periapical chronic inflammatory response that develops from chronic lesions with preexisting granulomatous tissue. But not all chronic apical periodontitis lesions develop into cysts. It is characterized by the presence of a central cavity lined by epithelium and filled with fluid, surrounded by granulomatous tissue and a peripheral fibrous capsule.
There are two distinct categories of radicular cysts:

  • Apical cyst true: cavity completely enclosed within an epithelial lining.
  • Apical cyst bag: cavity lined by epithelium, but open to the root canals.

1.4.2.9.1 Treatment:

It is likely that a periapical cyst bag and heal after conventional endodontic therapy. However, the presence of a periapical true cyst may be a cause of endodontic failure (these lesions tend to self-perpetuation and not depend on the presence of irritants in the root canal). In these cases, periapical surgery is required.


Fig 4. Periapical lesion on the tooth 2.2. Although the appearance may lead one to think in a cyst, the existence of the latter can only be confirmed through pathologic examination. It can never be diagnosed based only on the radiograph.

1.4.2.10 condensing osteitis (sclerosing osteitis, periapical osteosclerosis)

Periapical bone response to a low-grade pulp irritation and prolonged, manifested as increased periapical bone density. This condition is most often seen in young people around the apices of mandibular teeth with extensive caries, large restorations, and chronically inflamed vital pulps or necrotic.

1.4.2.10.1 Clinical:

Condensing osteitis may present with various signs and symptoms because it relates to a variety of injuries pulpoperiapicales. Depending on the intensity of the cause that leads can be asymptomatic or associated with a history of pain and discomfort.

1.4.2.10.2 Diagnosis:

Often it is an asymptomatic lesion that is discovered on routine radiographic examinations. Depending on the degree of involvement pulp vitality tests may be normal, increased or negative (in cases of pulp necrosis).

1.4.2.10.3 Treatment:

Depending on the cause of the disease should follow a treatment protocol based on the signs and symptoms. If asymptomatic and benign duct requires no treatment.
Endodontic treatment may result in recovery of normal bone trabeculation, with disappearance of radiopaque zone.

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