Periapical inflammatory lesions of endodontic origin

The dental organ, in all its beauty and complexity, is an intertwined composition of the odontium and the periodontium. The health of one conditions the other.

It is in this same concept that endocanal infections cause complications of the deep periodontium. This is due to the constant relationship between the canal and the periapical region, through the presence of the apical foramen but also through its lateral, secondary and accessory canals.

1. Anatomophysiology of the deep periodontium:

Four structures determine the periradicular periodontium:

The apical 1/3 of the root

Apical cementum

The apical desmodont

Alveolar bone

1. The apical third of the root:

In its apical portion, the root canal narrows to the cemento-dentin junction which marks the border between the endodontium and the periodontium.

This is where the periapical region begins, the site of apical periodontitis.

This region includes the deep periodontal tissues, the root cementum, the alveolar bone and, interposed between the two, the desmodont or dentoalveolar ligament.

 Hence the change in the name of periodontitis.

KUTTLER diagram

2. The importance of pulp anatomy in endodontics:

Ignorance of pulp-radicular morphology can be the cause of endodontic treatment failures. In teeth with a straight trajectory,

operative maneuvers are easier than those with a single or double curvature at the apical third.

Unfortunately, clinical conditions mean that the anatomical reality of dental roots and canals can only be understood through the

X-ray that provides a two-dimensional image of a three-dimensional reality.

Faced with all these difficulties, good practice of endodontics requires perfect knowledge of pulp-radicular anatomy.

3.  Terminology:

Specialists replaced the notion of tooth with that of dental organ when they became aware of the close links uniting the tooth to its supporting tissues and the link between these tissues and the cementum; an integral part of the tooth; and this in 1953 (HESS JC) .

 According to Jean -Jacques LASFARGUES: (PA) are inflammatory lesions of the deep periradicular periodontium, mainly of the periapical region,

following bacterial infection of the endodontium.

They result from various attacks that can alter the dental pulp, including caries, trauma, surgical procedures, periodontal diseases, as well as

the lack of sealing of endodontic fillings and associated coronal restorations.

We will also speak of lesion of endodontic origin or (LOE) or periradicular inflammatory lesion of endodontic origin (LIPOE).

This inflammatory reaction is favored by the anatomical and connective continuity which exists at the level of the communication pathways between the pulp canal space and the desmodontal space.

Often discovered by chance during a dental visit, simply by examining a panoramic x-ray, without warning clinical signs, they represent one of the most frequent pathologies in dentistry. (BRAU JJ et al.).

The existence of apical periodontitis means the systematic presence of a pulp contamination pathway associated with a defense reaction of the periapical tissues.

The majority of pulpal and periapical lesions are induced by oral bacteria.

IV-Immunopathology:

Apical lesions are reactive in nature; they reflect a dynamic battle between the agents attacking the pulp in an intra-canal situation and the host defense reactions in the periapex.

 The factors of aggression : bacteria and their by-products “toxins” released in the canal and migrating into the periapex. They play a key role in the development of the infectious process and the apical lesion. Thus they cause

inflammation that can lead to the development of granulomatous tissue in the apical periodontium with cementum, dentin and bone resorptions.

 Host defense factors : immune cells, mediators and antibodies; Malassez epithelial cells.

The presence of a periapical lesion signifies a dynamic struggle between root canal infection and host response.

PA is a manifestation of the body’s defense against intraductal aggressors. Without this defense reaction, canal infection would cause

septicemia.and it would be impossible to control root canal infections with our endodontic treatments.

4. Etiologies:

1-) Pulpopathies:

The bacterial pulp infection causing PA is of exogenous origin and comes mainly from caries, non-watertight restorations, chronic attacks by erosion-abrasion-attrition, and trauma, which lead to pulpitis, then necrosis, either initially or secondarily septic.

2-) Traumas:

• Trauma can lead to septic necrosis through direct exposure of the pulp (fracture) or indirect exposure (crack).
• Dislocations or simple dental shocks, which damage the vascular-nervous bundle, will result in necrosis by ischemia which is asymptomatic and aseptic at the start. Bacterial contamination occurs secondarily.

3-) Iatrogenic causes:

• All poorly performed restorative dentistry procedures can lead to overheating, drying out and irreversible damage to the pulp, which in extreme cases can lead to necrosis.

Bacterial microinfiltrations at the interface of leaking fillings are a major cause of chronic pulpitis and necrosis, which may be associated with condensing osteitis or apical granulomas.

• Extrusion of endodontic materials into the periapex can induce chronic foreign body inflammation, related to the irritant properties of certain root canal cements, including eugenol-based products.
• The lack of sealing of the surgical field, promoting salivary contamination, is often the cause of canal infection.
• insufficient canal debridement leaves a bacterial potential in place.
• The leaky root canal allows surviving bacteria to have the nutrients they need to reproduce.
• Iatrogenic inoculation of bacteria into the periapex by apical over-instrumentation is also a major cause of the appearance or non-healing of PA during endodontic treatments.
• It is also worth mentioning, as an indirect cause of PA in teeth with filled canals, the lack of sealing of coronal restorations.
• The apical crossing of endodontic files induces the backflow of septic debris into the periapex, or even dentin chips that carry bacteria. These septic backflows, particularly on teeth with pre-existing lesions and during endodontic retreatments, cause purulent periapical inflammations (abscesses and exacerbation phenomena also called “infectious outbreaks” “Flar up”); they can also promote the implantation and survival of specific germs in extra-radicular situations.

5.  Microbiology:
6. Endodontic bacterial infection:

This is a necessary condition for the development of PAs.

Necrotic pulp tissue provides an excellent substrate for bacterial multiplication.

2. Ecology of endodontic bacterial flora

The endodontic flora responsible for PA is polymicrobial, but limited, never exceeding twenty bacterial species.

It is composed mainly of strict and facultative anaerobic bacteria, such as Gram- fusobacterium rods and Gram+ cocci.

 This flora evolves over time depending on the structural integrity of the tooth,

the age and duration of the infection.

 The multiplication of bacteria in the necrotic pulp is due to the selection of proteolytic bacteria.

6.  Pathogenesis:

 1-acute initial response and primary exacerbation:

It is an intense and short-lived host response. It is characterized by:

• Hyperemia.
• Vascular congestion.
• Edema of the periodontal ligament.
• Extravasation of neutrophils and monocytes.
• Limited bone resorption.
• Histologically, tissue changes are limited to the periapical desmodontal space and the adjacent newly formed bone.

2. chronic transformation and secondary exacerbation:

• The continued presence of intraductal irritants promotes the transition from initial inflammation to a chronic lesion corresponding to the granuloma.
• Granuloma is an infiltrated and vascularized granulation tissue limited by a fibro-connective membrane
• It contains macrophages and lymphocytes producing antibodies and cytokines.
• The granuloma reflects a stage of equilibrium between confined aggressors and a self-controlled defense.

3.  Transformation into a cyst:

A granuloma can develop into a periapical cyst. Two types of cysts are commonly described:

The bay or pocket cyst (the cavity lumen communicates with the endodontic canal and the true cyst (cavity completely delimited by the epithelium

And without contact with the canal).

• The pathogenesis of a true cyst involves three stages: Phase 1 : Proliferation of Malassez epithelial debris. Phase 2 : Development of a cavity lined by epithelium. Phase 3 : The cyst increases in size.

7.  CLASSIFICATION:

A simplified classification classifying apical periodontitis according to the acute or chronic nature of the pathogenic line is the most suitable for clinical practice, while being consistent with the inflammatory dynamics of these lesions.

1.  Symptomatic pulp-apical pathologies:
   • Early acute apical periodontitis or pulpododontitis.
   • Acute apical periodontitis established.
   • Acute apical abscessed periodontitis or primary acute periapical abscess.
2.  Asymptomatic pulpo-periapical pathologies:
   • Chronic apical periodontitis with granuloma or cyst
   • Chronic apical periodontitis with fistula of endodontic origin:
   • Chronic apical periodontitis with abscess or secondary acute periapical abscess: Phoenix abscess.
   • “ Condensing osteitis ”.
3.  Diagnostic approach:

The three key criteria for making a diagnosis of PA are:

1. the existence of an endoperiodontal bacterial contamination pathway,
2. a negative response to pupal vitality tests,
3. a radiolucent bone image of endodontic origin.

Other signs and symptoms – pain, positive responses to percussion and palpation tests, fistula and swelling, are inconstant and depend on the status of the different forms of periapical lesions.

 J. LASFARGUES; CLINICAL REALITIES Vol. 12 No. 2, 2001 pp. 149-162

XI- MEANS OF DIAGNOSTIC:

1. Assessment of symptomatology:

CRITERIA	Questions to ask patients	Probable meaning
Location	Can the patient identify the painful tooth?	If yes, periapical involvement is very likely.
Intensity	Is the patient disturbed in his daily life by the pain?	If yes, irreversible pulpitis or acute apical periodontitis.
Duration	Does it extend after the stimulus and tend to be permanent?	If yes, irreversible pulpitis or acute apical periodontitis.
Stimuli	What are the causes and triggers?	If pressure is involved, periapical involvement is very likely.
Relief	Is the pain relieved by ice or painkillers?	If yes, periapical involvement, to be excluded.
Spontaneity	Appearance of pain for no apparent reason?	If yes, irreversible pulpitis or acute apical periodontitis.
Background	Presence of painful crises in the past?	If the history is painful, periapical involvement is very likely.
General signs	Fever, lymphadenopathy, fistula, swelling ?	If yes, certain periapical involvement.

2. Assessment of objective signs:

•  The exoral examination:

Will look for signs of a dental infection by visualization and palpation: facial asymmetry, swelling, cutaneous fistula, large and painful lymph nodes,

limitation of mouth opening, difficulty swallowing.

• The intraoral examination: will allow the objective clinical signs of the pathology to be recognized:

• dental signs : deep caries, cracks and fractures, abrasions and erosions, extensive and defective restorations, dental dyschromia and other anomalies;
• mucosal signs: inflammatory appearance (redness, edema) of soft tissues, ulcerations, fistular ostium;
• functional signs: occlusal interferences, abnormal mobility.

3. Clinical diagnostic tests:

The tests are therapeutic trials, which aim to reproduce the symptoms described by the patient, while avoiding triggering predictable pain, for example by hitting a tooth already identified by the patient as painful on simple contact.

1-3- Pulp sensitivity tests:

They will include thermal (cold and hot) and electrical tests.

A negative response to these three tests indicates that the pulp is necrotic and constitutes the second key criterion essential for the diagnosis of PA. False positives (purulent pulpitis) or negatives (pulp mineralization) will have to be distinguished.

2-3- Percussion test : “technique see 3rd Year diagnostic driving course”

• False positives, i.e. vital teeth reacting to percussion (total pulpitis, periodontal diseases of non-pulpal origin, colds and maxillary sinusitis) must be discriminated against. False negatives are rarer because, in general, the patient recognizes his tooth by light vertical percussion (pulp necrosis with chronic apical periodontitis).

3-3 Intraoral palpation test : “technique see 3rd Year diagnostic driving course”

• A very painful apical palpation indicates the presence of a suppurative collection, while a sensitive palpation provides more information on an inflammatory state.
• The differential diagnosis should be made with a “septum syndrome” (pain when pressure is exerted on the interdental papilla), a dental fracture and, more rarely, a problem of fracture of the jaws (jumping) or a muscular problem (contracture).

4. Additional tests:
   • The gutta-percha cone test:

• the presence of a fistulous orifice indicates the existence of a deep infectious focus whose location and origin are unknown. The introduction of a gutta-percha cone (accessory cone, fine caliber) into the ostium makes it possible to follow the

fistulous path to its source.

• An X-ray taken in this way will allow this source to be located: the causative tooth and the affected root or a periodontal pocket.
• Anesthesia is not necessary to perform this test.

• The cavity test:
  • In the case of crowned teeth, a drill sensitivity test, known as a cavity test, may be useful if there is still doubt about pulp vitality.
• Periodontal probing:
• sulcular probing of a tooth, on its proximal, vestibular and lingual surfaces, using a graduated periodontal probe is necessary

when seeking to differentiate between periodontal and endodontic damage, in hybrid forms of endo-periodontal lesions.

• A probe that “dives” into a specific point along the root

indicates the presence of a fistula of apical origin emerging, at the level of the sulcus, into the periodontal pocket.

• Transillumination:
  • The search for a crack that could explain the presence of an apical lesion on an apparently intact tooth can be done using the transillumination test.
  • In the case of a vertical fracture, the light is blocked by the gap between the fragments: one side is illuminated, the opposite side remains dark. The test can also be performed after removal of a restoration, which will sometimes directly reveal the crack line.
• The X-ray examination:

The presence of a periapical radiolucent bone image detected by means of a retroalveolar image constitutes the third key criterion for the diagnosis of PA.

10. Classic criteria for radiological diagnosis of apical lesions:
    • Desmodontal thickening: Considered the first pathological sign reflecting early apical periodontitis.
    • The interruption of the lamina lasts.
    • Presence of radiolucent image which indicates obvious bone destruction.
11.  Differential diagnosis :

Endodontic lesions are the subject of a 5th year course.

• However, here is a summary table which includes the essential signs allowing the difference to be made between: lesion of origin

endodontic; endoperiodontal; and mixed.

XII-Clinical forms:

1. Symptomatic apical periodontitis:
   1.  Acute periodontitis linked to occlusal trauma:

Typically, this is a tooth with a recent restoration and premature contact.

• The tooth is sensitive to touch and chewing, but vitality tests are normal.

1.  Initial apical periodontitis:
   • At an early stage, commonly referred to as pulpodesmodontitis, it corresponds to the initial passage of pulp inflammation in the periapex.
   • The pain is spontaneous (acute pupitus), caused by simple contact with the tooth, and always recognized by percussion.
   • There is not necessarily a radiographically visible image of desmodontal enlargement.
   • The pulp is vital, and the response to sensitivity tests is positive, particularly on multi-rooted pulps (persistence of vital radicular pulp tissue despite coronal necrosis).
   • At this early stage, changes in the periapex are not necessarily visible radiographically.
   • This condition can be classified as acute irreversible pulpitis or acute onset PA.
2.  Acute apical periodontitis (AAP):
   • Acute apical periodontitis corresponds to a patent inflammation, established in the periapex,
   • following the extension of the endodontic infection towards the apical region.
   • The periapical connective tissue is inflamed and infected by pulp necrosis or septic repression with failed endodontic treatment.
   • At an advanced stage, the inflammation sets in in the periapex and corresponds to a severe exudative inflammation, related to the penetration of germs into the pulp cavity.
   • The pulp is necrotic and pulp sensitivity tests are negative.
   • The pain is spontaneous and exacerbated by percussion or pressure.
   • Palpation, in relation to the apex, is positive.
   • Changes in the periapex become visible radiographically as a radiolucent area.
3. Acute apical abscess (AAA):
   • Acute apical abscess is a common diagnosis of periapical emergency. When it is not accompanied by swelling, it is confined to the bone.
   • Acute apical abscess corresponds to a disruption of the balance between intracanal bacteria and the periapical defenses of the host with passage of pathogenic agents into the periapex and formation of a suppurative collection.
   • This abscess can be primary or secondary (Phoenix abscess) in the event of a pre-existing inflammatory lesion and subsequently fistulize.

 **Primary acute apical abscessed periodontitis:

• Also called acute apical abscess, it corresponds to a localized suppuration of the periapex. The pulp is necrotic, and the response to pulp sensitivity tests is negative. The pain is spontaneous and permanent.
• This is the most painful stage. Contact with the tooth is intolerable and percussion should be avoided.
• Periodontal signs are usually present.
• Palpation at the apex is painful, suggesting the presence of pus.
• Subperiosteal or submucosal swelling is possible.
• A primary acute periapical abscess is not necessarily visible radiographically (entirely intraosseous abscess, without involvement of the cortical bones).

**Secondary acute apical abscessed periodontitis:

• It corresponds to a recurrent periapical abscess or Phoenix abscess. It is an exacerbation of a chronic (granulomatous) lesion.
• The symptoms are very similar to those of a primary abscess.
• The diagnostic criteria are identical to those of the previous stage with one characteristic: a clear radiographic image is always detectable due to pre-existing bone destruction.

Summary table of signs of acute apical periodontitis:

2. Chronic apical periodontitis:

• The lineage of chronic apical periodontitis corresponds to pulpo-periodontal pathologies without pain (or with minimal pain).
• This is an inflammatory defense response of the periapical tissues, in which the proliferative component (granulation tissue) prevails over the

exudative component (abscess). The absence of pain is explained by the absence of excess pressure due to the peripheral bone reaction.

• Lesions are generally discovered following a change in the color of the crown or during radiographic assessments to search for infectious foci.
• Pulp sensitivity tests are negative, as are responses to percussion and palpation, except in cases of secondary acute exacerbation.

1-2 Condensing osteitis or periapical osteosclerosis:

• This is a reaction related to an asymptomatic vital pulp to be attached to the category of chronic pulpitis.
• This reaction reflects the hyperactivity of the irritated bone tissue. Diagnosable radiographically (radiation-dense periapical image), it slowly disappears after adequate root canal therapy.

2.  Chronic apical periodontitis:

• The positive diagnosis of periapical granulomas and cysts is primarily

radiographic and should be correlated with the absence of response to pulp sensitivity tests.

• As the lesions increase in size, contiguity relationships are established with the apices of neighboring roots, sometimes making it difficult to determine the apex of the

causal tooth, which involves testing the sensitivity of all teeth in the region in question.

• The growth of lesions can lead to dental versions/migrations, or even mobility, which can be detected clinically.
• When the lesion is large, a hard bulge on digital palpation may be present in the vestibule.
• Only a biopsy sample can make the differential diagnosis between cyst and granuloma.
• However, this is not necessary since endodontic treatment is indicated as a first-line treatment in both cases.

3-2 Apical periodontitis with fistula:

• A fistula is an externalized drainage pathway for apical inflammatory fluids. Over time, the fistulous tract may become epithelialized.
• Although its appearance is often ignored by the patient, the fistula is created following acute primary or secondary episodes: drainage of the abscess through the fistula leads to the disappearance of the overpressure phenomena and the pain and swelling then regress.
• The path and emergence of the fistula are random; this is why the origin of the lesion must be located using an X-ray taken after

introduction of a gutta percha cone into the fistula.

• Usually, elimination of the ductal infection causes the fistula to disappear, which is a sign of ongoing healing that can predict the healing of the lesion.
• The differential diagnosis between an endodontic fistula and a marginal periodontal defect requires a precise diagnostic approach. “5th Year COURSE”

Conclusion :

The PA sequelae of endodontic infection are inflammatory in nature; they reflect the dynamic combat between intracanal bacterial factors and periapical defense factors.

The concept of PA treatment lies in the preservation of the causative tooth after disinfection of the endodontium.

Appendix:

Periapical inflammatory lesions of endodontic origin

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Periapical inflammatory lesions of endodontic origin