Pink Tooth Of Murmmery- Internal Resorption

Internal Resorption Or Pink Tooth of Mummery

Internal resorption was first reported by Bell in 1830. It is known as the Pink Tooth of Mummery because of the pink discoloration of the crown and is named after the anatomist Mummery.

Internal resorption is an idiopathic slow or fast progressive resorption occurring in the dentin of the pulp chamber or root canals of the teeth.

Read And Learn More: Endodontics Notes

Etiology:

The exact etiology is unknown. A patient may present a history of trauma or persistent chronic pulpitis, or a history of pulpotomy.

Internal Resorption Symptoms:

• Usually asymptomatic, recognized clinically through routine radiograph.
• Pain occurs if resorption perforates the root.
• “Pink tooth” is the pathognomonic feature of internal root resorption.
• Pulp shows either partial or complete necrosis. In actively progressive lesions, pulp is partially vital and may show symptoms of pulpitis.
• In anterior teeth, it is typically seen in the middle of the tooth in the mesiodistal direction but in multirooted teeth, it can be present mesial, distal, or center.
  

Internal Resorption Diagnosis:

1. Clinically: “Pink tooth” appearance

2. Radiographic changes:

• The classical description of internal resorption, that is, clearly well-defied radiolucency of uniform density which balloons out of root canal was given by Gartner el al.
• The original root canal outline distorted

Bone changes are seen only when root perforation into the periodontal ligament takes place.

3. Pulp tests:

Positive, though a coronal portion of the pulp is necrotic, the apical pulp could be vital.

Internal Resorption Diffrential Diagnosis:

It is difficult to differentiate internal resorption from external resorption when it progresses to periodontal space causing root perforation.

It can be diffrentiated by

• History: Giving the history of trauma, pulpotomy, etc.
• Pink tooth appearance
• Taking radiographs at different angles; radiolucency does not move when a radiograph is taken at different angles, whereas in external resorption, radiolucent lesion changes position on changing angle.
  • Uniform ballooning of the root canal is seen in internal resorption, whereas an irregular border with alteration of adjacent bone is seen in external resorption.

Internal Resorption Treatment:

• Pulp extirpation stops internal root resorption.
• Surgical treatment is indicated if conventional treatment fails.

Pulp Degeneration

Pulp degeneration is generally present in old age. In young age, it may result from persistent mild irritation. Common causes of pulp degeneration are attrition, abrasion, erosion, operative procedures, caries, pulp capping, and reversible
pulpitis. Forms of pulp degeneration:

Pulp Degeneration Calcifi Degeneration:

In calcific degeneration, part of pulp tissue is replaced by calcified material. Mainly three types of calcifications are seen in pulp:

• Dystrophic calcifications
• Diffuse calcifications
• Denticles/pulp stones

Pulp Degeneration Dystrophic Calcification :

• They occur by the deposition of calcium salts in dead or degenerated tissue. The local alkalinity of destroyed tissues attracts the salts.
• They occur in minute areas of young pulp affected by minor circulatory disturbances, in blood clots, or around a single degenerated cell.
• They can also begin in the connective tissue walls of blood vessels and nerves and follow their course.

Pulp Degeneration Diffuse Calcifiations:

• They are generally observed in root canals.
• The deposits become long, thin, and fibrillar on fusing

Pulp Degeneration Denticles/Pulp Stones:

These are usually seen in pulp chambers.

Classification of pulp stones:

• According to Location:
  • Free
  • Embedded
  • Attached

According to Structure:

• • True
  • False

True denticle:

It is composed of dentin formed from detached odontoblasts or fragments of Hertwig’s enamel root sheath which stimulates the undifferentiated cells to assume dentinoblastic activity.

False denticle:

Here degenerated tissue structures act as a nidus for the deposition of concentric layers of calcified tissues.

Atrophic Degeneration:

• It is wasting away or decreasing in size which occurs slowly as the tooth grows old.
• Here fewer stellate cells are found and pulp is less sensitive than normal.

Fibrosis Degeneration:

• There is a gradual shift in the ratio and quality of tissue elements. Here, the number of collagen fiers/unit area increases leading to fibrosis. Pulp has a characteristic leathery appearance.
• The number and size of cells decrease so cells appear as “shrunken solid particles in a sea of dense fiers”.
• Fibroblastic processes are lost, and cells have round and pyknotic nuclei.
• Dentinoblasts decrease in length and appear cuboidal or flattened.

 

Pulp Necrosis

Pulp necrosis or death is a condition following untreated pulpitis. Pulpal tissue becomes nonvital and if the condition is not treated, noxious materials will leak from pulp space forming the lesion of endodontic origin. Necrosis may be partial or total, depending on the extent of pulp tissue involvement.

Types of pulp necrosis:

1. Coagulation necrosis:

In coagulation necrosis, the protoplasm of all cells becomes fied and opaque. Cell mass is recognizable histologically, and intracellular details are lost.

2. Liquefaction necrosis:

In liquefaction necrosis, the entire cell outline is lost. The liquefied area is surrounded by a dense zone of PMNL (polymorphonuclear leukocytes) and chronic inflammatory cells.

Etiology:

Necrosis is caused by noxious insult and injuries to the pulp by bacteria, trauma, and chemical irritation.

Pulp Necrosis Symptoms:

• Discoloration of a tooth due to extravasation of pulpal blood into dentin as a result of trauma.
• Lack of translucency/dull or opaque appearance
• History from patient
• A tooth might be asymptomatic
  

Pulp Necrosisv Diagnosis:

1. Pain:

It is absent in complete necrosis

2. Pulp Necrosis History of the patient:

History reveals past trauma or past history of severe pain which may have lasted for some time followed by complete and sudden cessation of pain.

3. Pulp Necrosis Radiographic changes:

The radiograph shows a large cavity or restoration or normal appearance unless there is concomitant apical periodontitis or condensing osteitis.

4. Pulp Necrosis Vitality test:

Usually, vitality tests show a negative response. But multirooted teeth may show mixed responses because only one canal may have necrotic tissue. Sometimes teeth with liquefaction necrosis may show a positive response to an electric test when an electric current is conducted through moisture present in a root canal.

5. Pulp Necrosis Visual examination:

The tooth shows color changes like dull or opaque appearance due to a lack of normal translucency.

6. Pulp Necrosis Histopathology:

Necrotic pulp tissue, cellular debris, and microorganisms are seen in the pulp cavity. If there is concomitant periodontal involvement, there may be presence of slight evidence of inflmmation.

Pulp Necrosis Treatment:

Complete removal of pulp followed by restoration or extraction of the nonrestorable tooth.

Pathologies Of Periradicular Tissues

Periradicular tissue contains apical root cementum, periodontal ligament, and alveolar bone.

Etiology:

• Bacterial
  • A root canal is a unique, stringent ecological niche for bacterial growth because of a lack of oxygen. The primary nutrient source for root canal biotics is host tissues and tissue fluids.
  • Microorganisms in chronically infected root canals are mainly anaerobic and Gram-negative type.

The most common microorganisms seen in periradicular diseases are

• Streptococcus
• Peptostreptococcus
• Prevotella

Black-pigmented microorganisms

• Porphyromonas
• Enterococcus
• Campylobacter
• Fusobacterium
• Eubacterium

Pathologies Of Periradicular Tissues Routes:

• The untreated pulpal infection leads to total pulp necrosis and further periapical infection.
• Anachoresis
• Invasion of microorganisms into pulp from the periodontal pocket and accessory canals resulting in the formation of lesions of endodontic origin
  

Pathologies Of Periradicular Tissues Trauma:

• Physical trauma to a tooth or operative procedures result in dental follicle desiccation or heat transfer causing sufficient damage to pulp and its blood supply.
• Severe trauma to the tooth and heat production during tooth preparation causes immediate interruption of blood supply resulting in pulp necrosis even though it is not infected.
• Persistent periapical tissue compression from traumatic occlusion may lead to the apical inflammatory response.

Factors Related to Root Canal Procedures:

• It is impossible to extirpate pulp without initiating an inflammatory response.
• Using strong or excessive amounts of intracanal medicaments between appointments may induce periapical inflammation.
• Improper manipulation of instruments within the root canal or over instrumentation can force dentinal debris, irrigating solution, and toxic components of necrotic tissue in the periapex.
• Overextended endodontic filling material may induce periapical inflammation by directly inducing foreign body reaction which is characterized by the presence of leukocyte infiltration, macrophages, and other chronic inflammatory cells.
  

Pathologies Of Periradicular Tissues Diagnosis:

• Chief Complaint:

The patient usually complains of pain on biting, pain with swelling, pus discharge, etc.

• Dental History:

The patient gives a history of recurring episodes of pain and sometimes swelling with discharge.

• Objective Examinations:

1. Extraoral examination:

General appearance, skin tone, facial asymmetry, swelling, extraoral sinus, sinus tract, tender or enlarged cervical lymph nodes.

2. Intraoral examination:

It includes an examination of soft tissues and teeth to look for
discoloration, abrasion, caries, restoration, etc.

• Clinical Periapical Tests:

1. Percussion:

Indicates inflammation of the periodontium.

2. Palpation:

Determines how far the inflammatory process has extended periodically.

3. Pulp vitality:

• Thermal tests which can be heat or cold
• Electrical pulp testing

4. Periodontal examination

It is important because the periapical and periodontal lesions may mimic each other and require differentiation.

1. Probing:

Determines the level of connective tissue attachment. The probe can penetrate into an inflammatory periapical lesion that extends cervically.

2. Mobility:

Determines the status of periodontal ligament

Radiographic examination:

Periradicular lesions of pulpal origin have four characteristics :

• Loss of lamina dura apically
• Radiolucency at apex regardless of cone angle
• Radiolucency resembling a hanging drop
• Cause of pulp necrosis is usually evident

Recent advances in radiography:

• Digital subtraction radiography
• Xeroradiography
• Digital radiometric analysis
• Computed tomography
• Radiovisiography
• Magnetic resonance imaging
  

Classifiation Of Periradicular Pathologies

Grossman’s Classification:

1. Symptomatic periradicular diseases:

• Symptomatic apical periodontitis previously known as acute apical periodontitis (AAP):
  • Vital
  • Nonvital
• Acute alveolar abscess
•  Phoenix abscess

2. Asymptomatic periradicular diseases:

Asymptomatic apical periodontitis (chronic apical periodontitis)

• Chronic alveolar abscess
• Radicular cyst
• Condensing osteitis

3. External root resorption

4. Persistent Apical periodontitis

5. Disease of the periradicular tissues of nonendodontic origin.

WHO Classification:

• K 04.4 — Acute apical periodontitis
• K 04.5 — Chronic apical periodontitis (apical granuloma)
• K 04.6 — Periapical abscess with sinus
• K 04.60 — Periapical abscess with sinus to the maxillary antrum
• K 04.61 — Periapical abscess with sinus to the nasal cavity
• K 04.62 — Periapical abscess with sinus to the oral cavity
• K 04.63 — Periapical abscess with sinus to skin
• K 04.7 — Periapical abscess without sinus
• K 04.8 — Radicular cyst (periapical cyst)
• K 04.80 — Apical and lateral cyst
• K 04.81 — Residual cyst
• K04.82 — Inflammatory paradental cyst

Ingle’s Classification of Pulpoperiapical Pathosis:

1. Painful pulpoperiapical pathosis:

• Symptomatic Acute apical periodontitis
• Advanced apical periodontitis:
  • Acute apical abscess
  • Phoenix abscess
  • Suppurative apical periodontitis (chronic apical abscess)

2. Nonpainful pulpoperiapical pathosis:

• Condensing osteitis
• Chronic apical periodontitis both incipient and advanced stages
• Chronic apical periodontitis:
  • Periapical granuloma
  • Apical cyst
  • Suppurative apical periodontitis