Apical periodontitis
I/ Reminder on the physiology of the periodontium
Endo-periodontal communication pathways;
Apical foramen
Accessory channels
Exposure of dentinal tubules
Apical periodontitis
Apical periodontitis
II/ Definition ; Apical periodontitis is an inflammatory lesion of the deep periradicular periodontium, mainly in the periapical region.
They are the consequence of various attacks that can alter the dental pulp and lead to bacterial infection of the endodontium, including caries, trauma and iatrogenic surgical procedures.
This inflammatory reaction is favored by the anatomical and connective continuity that exists at the level of the natural foraminal passageways, between the root canal on the one hand and the desmodontal space on the other.
III) Terminology and classification
Apical periodontitis
Acute apical periodontitis
PAA is an acute inflammation of pulpal origin initiated in a healthy periapex.
Primary, it corresponds to a short-term, incipient inflammation. It can transform directly into a primary periapical abscess if the pulp infection is sudden, or more often develop into chronic apical periodontitis.
Secondary, it corresponds to a phase of exacerbation of a pre-existing chronic lesion and results in the formation of secondary abscesses or micro-abscesses called “phoenix” due to a resurgence of activity of polymorphonuclear leukocytes within the apical granulation tissue.
Chronic apical periodontitis
Chronic apical periodontitis is a slow and long-lasting inflammatory reaction, linked to lymphoplasmacytic infiltration of the periapex, accompanied by underlying bone destruction.
This form can evolve into secondary abscess, fistulization or transformation into a cyst depending on the virulence and pathogenicity of the intraductal bacterial flora
IV/ Etiologies
1- Pulpopathies
The bacterial pulp infection causing PA is of exogenous origin and comes mainly from caries, non-watertight restorations, chronic aggression by erosion-abrasion-attrition and trauma which lead to pulpitis, then necrosis from the outset or secondarily septic.
Besides direct contamination of the pulp by the progression of dentin infection, the routes of penetration of bacteria into the canals are:
– cracks,
– the side channels,
– microcracks that expose the dentinal tubules in the cervical area
– Erosions which lead to dissolution of the mineral matrix of the tooth,
– Deep periodontal pockets with terminal alveolysis exposing the apical and lateral canals
Apical periodontitis
2- Dental trauma
Trauma can lead to septic necrosis through direct (fracture) or indirect (crack) exposure of the pulp to oral bacteria.
Furthermore, these traumas cause dislocations or simple dental shocks which damage the vascular-nervous bundle.
pulpoperiodontal and deprives the pulp of its vascularization.
This is followed by necrosis due to ischemia, which is initially asymptomatic and aseptic. Bacterial contamination occurs secondarily.
The longer the time between the trauma and the endodontic treatment, the greater the risk of developing a root infection.
Apical periodontitis
3- Iatrogenic causes
– All poorly conducted and non-watertight restorative dentistry procedures can cause irreversible damage to the pulp through heating or infiltration, which can lead to necrosis.
Similarly, the protrusion of root canal filling materials beyond the apical limits is a major cause of apical periodontitis.
Iatrogenic inoculation of bacteria into the periapex by apical over-instrumentation is also a cause of the appearance or non-healing of PA during endodontic treatments.
V/ Immunological characteristics
The dynamics of the periapical inflammatory reaction essentially reproduce the pulp reactions to infection, with the only difference being the destruction of the periapical bone.
Apical lesions are reactive in nature; they reflect a dynamic struggle between the aggressive agents from the infected canal and the host’s defense reactions in the periapex.
Apical periodontitis
1: Aggression factors
Bacteria generate several deleterious effects depending on the pathogenicity and virulence of the species involved. Bacterial by-products released into the canal migrating into the periapex are strongly involved:
Proteolytic enzymes: promote tissue penetration of microorganisms. Some enzymes destroy immune complexes and make the antibodies necessary for humoral and cellular defense unavailable.
Exotoxins: are highly antigenic toxoid molecules, such as leukotaxin which lyses leukocyte membranes.
Endotoxins: (lipopolysaccharides) are pyretic macromolecules originating in particular from the disintegration of the membranes of gram-negative bacteria.
Lipopolysaccharides (LPS) exert direct and indirect pathogenic effects involving the production of cytokines, prostanoids, and other mediators.
2: Host defense factors
Cells: Defense cells constitute half of the cell population of periapical lesions:
Neutrophils predominate in the acute phases; whereas
B and T lymphocytes and macrophages accumulate in chronic phases.
The presence of Malassez epithelial cells proliferating in cystic and granulomatous lesions is also noted, as well as the differentiation of osteoclasts on the adjacent alveolar wall.
Molecular mediators and effectors: Cells activated during the inflammatory reaction produce a multitude of intercellular messengers with the mission of inactivating and destroying pathogenic agents.
VI) Pathogenesis and structure of lesions;
VI/1: The initial acute response and primary exacerbation
This is an intense and short-lived host response. This initial acute response is characterized by hyperemia, vascular congestion, periodontal edema, and limited bone resorption.
Histologically, tissue changes are limited to the periapical desmodontal space. At this initial acute stage, several pathways are possible:
Spontaneous healing (aseptic inflammations)
Primary abscess formation
Abscess and fistulization
Evolution towards chronicity (granulomas and cysts)
Apical periodontitis
VI/ 2: Chronic transformation and secondary exacerbation:
The continued presence of intracanal irritants gradually promotes the passage of the initial inflammation towards a lesion encapsulated by collagenous connective tissue containing more and more macrophages and lymphocytes, producing antibodies and cytokines.
During this transformation, these cytokines will sometimes stimulate the osteoclast activation factors (bone resorption), and sometimes promote the growth factors stimulating the proliferation of fibroblasts and angiogenesis. Thus the granuloma reflects a stage of balance between the aggressors confined in the canal and a self-controlled defense.
At any time this fragile balance can be disrupted, with bacteria advancing to the edge of the periapex and triggering an acute exacerbation in the form of secondary abscesses.
(phoenix or recurring abscesses)
Apical periodontitis
VI/3: Transformation into a cyst
Not all granulomas develop into cysts, but cysts are considered a direct sequela of granulomas. Only 20% of epithelialized lesions are cysts, and of these, half are pocket cysts opening into the duct and not true cysts.
The pathogenesis of a true cyst involves three stages:
Quiescent Malassez epithelial debris begins to proliferate under the influence of growth factors,
A cavity lined by epithelium develops
The cyst increases in volume through the molecular agents of bone resorption which diffuse towards the bone periphery (cytokines and metalloproteinases).
A true cyst is defined by four main histological elements, from the center to the periphery:
A cystic cavity that contains necrotic debris and erythrocytes left over from hemorrhages. The presence of cholesterol crystals in certain cystic cavities results from the precipitation of lipids from disintegrated cells (erythrocytes, lymphocytes, etc.) and circulating lipids.
A continuous epithelium lining the cystic cavity. This is a stratified squamous epithelium
Peripheral tissue containing vessels and infiltrated by macrophages
A collagenous fibrous capsule containing all of the above elements
Apical periodontitis
In the case of pocket cysts, the formation of the lesion is different:
A neutrophil barrier is established at the apex to contain intracanal germs. Over time, these neutrophils accumulate and form an apical plug,
Epithelial cords proliferate at the periphery and make epithelial attachment to the root walls
The plug continues to grow and as it disintegrates a micro-pocket forms, then widens forming a sac-like diverticulum of the canal.
VII) Specific periapical manifestations
Transient apical pathology: Corresponds to a localized and reversible alteration of the periapex whose resolution does not require endodontic treatment. This is an inflammation linked to a moderate and “sterile” aggression whose return to normal occurs gradually after the stimulus disappears.
Condensing apical periodontitis: This is a chronic inflammation of the periapex with a characteristic picture of apical radiopacity. Resolution occurs after endodontic treatment of the causative tooth.
Foreign body granuloma: The inclusion in the periapex of foreign materials, most often infected, can initiate and/or perpetuate certain periapical lesions refractory to endodontic treatment.
Periapical actinomycotic infection: It is a sequela of carious infection, it is linked to the endodontic penetration of Actinomyces Israelii and Proprionibacterium proprionicum, which have the ability to form typical filamentous colonies, which allows them to escape the phagocytic defenses of the host and survive in an extra-radicular situation.
VIII) Clinical diagnosis of apical periodontitis
8-1: Means of diagnosis
Assessment of symptoms: We will focus on characterizing the pain felt by the patient, by asking specific questions aimed at assessing the causal tooth, the irreversible nature of the process and the strictly pulpal or pulpo-periodontal origin.
Assessment of objective signs: The exo-oral examination will look for signs of dental infection by visualization and palpation:
(facial asymmetry, swelling, skin fistula, etc.)
The endo-oral examination will allow the objective clinical signs of the pathology to be recognized:
* Dental signs: Deep cavities, cracks, fractures, dental dyschromia and other anomalies.
* Mucosal signs: Inflammatory appearance of soft tissues, ulceration.
* Functional signs: Occlusal interferences, abnormal mobility.
8-2: Clinical diagnostic tests
The tests are therapeutic trials, which aim to reproduce the symptoms described by the patient:
Pulp sensitivity tests: These will include thermal and electrical tests. A negative response to all three of these tests indicates that the pulp is necrotic.
Periradicular tests:
* Percussion tests: The tooth is lightly percussed axially with the handle of a mirror: a painful response can detect periodontal inflammation.
* Intraoral palpation tests: Intraoral palpation is carried out in the vestibule with the pulp of the gloved index finger, moved along the alveolar processes at the apices in search of a sensitive or painful inflammatory area. A very painful apical palpation indicates the presence of a purulent collection, while a sensitive palpation indicates an inflammatory state.
Palpation also allows the disappearance of the external bony cortex to be diagnosed by the Crane sign known as the bucket sign.
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 fine gutta cone into the ostium allows the fistulous path to be followed to its source. An X-ray taken in this way will allow this source to be located.
Cavity test: In the case of crowned teeth, a drill sensitivity test , known as a cavity test, may be useful if there is any 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 to differentiate between periodontal and endodontic damage.
Transillumination: The search for a crack that could explain the presence of an apical lesion on an apparently healthy tooth can be done with the transillumination test. In the case of a vertical fracture, the light is stopped by the hiatus between the fragments: one face is illuminated, the opposite face remains dark.
Apical periodontitis
8-3: The X-ray examination
The presence of a periapical radiolucent bone image detected by means of a retroalveolar radiograph constitutes another key criterion for the diagnosis of apical periodontitis.
IX) Clinical forms,
9-1: Symptomatic apical periodontitis
The main signs of symptomatic apical periodontitis are pain of periapical origin (from discomfort to intolerable pain), swelling (inconstant), positive palpation of the vestibule opposite the apex, lack of response to pulp vitality tests (except for initial reactions of the periapex), radiography (from desmodontal enlargement to extensive radiolucent image).
9-1-1: Primary PAA; At an early stage, commonly called pulpodesmodontitis, it corresponds to the initial passage of pulp inflammation in the periapex. The pain is spontaneous, caused by simple contact with the tooth, and always recognized by percussion. The pulp is vital and the response to vitality tests is positive, particularly on multi-rooted ones.
At a more advanced stage, inflammation occurs in the periapex and corresponds to severe exudative inflammation with the penetration of germs into the pulp cavity. The pulp becomes necrotic and vitality tests are then negative. The pain is spontaneous and exacerbated by percussion or pressure. Palpation at the apex is positive.
9-1-2: Primary abscessed PAA; Also called acute apical abscess, it corresponds to a localized suppuration of the periapex. The pulp is necrotic, the pain is spontaneous and permanent. This is the most painful stage. Contact with the tooth is unbearable and percussion must be avoided. Periodontal signs are generally present. Palpation in relation to the apex is painful, suggesting the presence of pus. A subperiosteal or submucosal swelling is possible
9-1-3: Secondary abscessed PAA; This corresponds to the recurrent periapical abscess also called Phoenix abscess. It is an exacerbation of a chronic lesion (granulomatous). The symptoms are substantially similar to those of the primary abscess. On X-ray, a radiolucent image is always detectable due to the pre-existing bone destruction.
9-2: Asymptomatic apical periodontitis;
These painless periodontal pathologies correspond to the lineage of chronic apical periodontitis. This is an inflammatory response of defense of the periapical tissues, in which the proliferative component prevails over the exudative component
9-2-1: Condensing osteitis; 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 (radiopaque periapical image), it slowly disappears after adequate root canal therapy.
Apical periodontitis
9-2-2: PAChronic; The positive diagnosis of granulomas and cysts is primarily radiographic. When 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 tooth in question; which implies testing the vitality of all the teeth in the region considered. The growth of the lesions can lead to dental versions/migrations or even clinically identifiable mobilities.
Only a biopsy sample can make the differential diagnosis between cyst and granuloma.
Apical periodontitis
9-2-3: PA with fistula; A fistula corresponds to an externalized drainage pathway for apical inflammatory fluids. Over time, the fistulous tract can become epithelialized. The fistula is created following primary or secondary acute episodes: drainage of the abscess through the fistula results in the disappearance of the overpressure phenomena and the pain and swelling then regress .
Usually, elimination of the ductal infection allows the fistula to disappear.
In some cases (extra-radicular infections of endodontic origin, combined endo-periodontal lesions), the fistula may persist despite adequate endodontic treatment. The differential diagnosis between the fistula of endodontic origin and a marginal periodontal defect is made by intrasulcular periodontal probing which allows to characterize the narrow/wide and mixed apical/marginal defect
Apical periodontitis
Conclusion ; Establishing a clear and precise diagnosis of PA involves knowing the etiopathogenic mechanisms of the acute and chronic lines of pulpo-periodontal diseases. A relevant approach consists in identifying during the interview with the patient the symptoms making the existence of a periapical pathology probable or improbable, then to confront this diagnostic hypothesis with the data of clinical observation.
The key criteria for the diagnosis of apical periodontitis are:
Presence of an endo-periodontal bacterial contamination pathway
Lack of response to pulp vitality tests
Presence of a periapical radiolucent bone image.