Periradicular Inflammatory Lesions of Endodontic Origin
Introduction :
Bacterial migration and proliferation within the endodontic network as well as the passage of toxins into the periapical tissues promote the occurrence of periradicular inflammatory lesions of endodontic origin (LIPOE) (CNEOC, 2010) also called apical periodontitis (Nair, 2004) or lesions of endodontic origin. The latter are the site of destruction of bone tissue (radiolucent images of alveolysis) and of the attachment system with or without associated root resorptions in favor of pathological granulomatous tissue.
- LIPOE Definition and Terminology:
LIPOE (according to CNEOC2010), commonly called “apical periodontitis”, are inflammatory lesions of the deep periradicular periodontium, mainly of the periapical region, secondary to bacterial infection of the endodontium (Lafargues 2001).
These pathological entities were described by Weine and Hess:
For Weine, these are symptomatic and asymptomatic pulpo-periapical pathologies.
According to Hess, these are acute and chronic desmodontitis.
- Etiology of LIPOE:
Apical lesions can have several causes: infectious, traumatic, iatrogenic or
chemicals.
• Infectious causes: We distinguish between lesions due to a primary infection and those due to a secondary infection.
—Primary infectious causes: are the consequence of pulp necrosis. The bacterial infection develops within the root canal and spreads to the periapex. The bacteria act in synergy and release antigenic endotoxins that cause an inflammatory process involving immune reactions.
—Secondary infectious causes: It should be noted
– defective endodontic treatments (carried out under septic conditions, for example, failure to use a dam and failure to irrigate with sodium hypochlorite).
– Coronary sealing defects, conducive to microbial recolonization.
– apical lesions are the result of periodontal infections. Some periodontal pockets may reach the accessory canals or the apical foramen of a tooth, thus creating an endo-periodontal communication.
• Traumatic causes: These are represented by dislocations, contusions and secondarily by occlusal overloads.
• Iatrogenic causes: These are related to an iatrogenic fault such as:
– An excess of sealing paste.
– A gutta percha cone overflow.
– Incomplete root canal fillings involving the persistence of necrotic tissue.
– Untreated instrumental false routes.
– Fractures of endodontic instruments in the dental canal or beyond the apex.
• Chemical causes: All chemical substances are toxic and can damage the pulp. Moderate or severe inflammation may occur, followed by pulp necrosis and apical lesion.
3) Classifications and pathogenesis of LIPOE:
–According to the CNEOC (2012) we distinguish:
3.1- chronic LIPOE which are most often asymptomatic and discovered incidentally in which the proliferative component (granulation tissue) prevails
on the exudative component (abscess). The absence of pain is explained by the absence of excess pressure due to the peripheral bone reaction. They result from a dynamic balance between, on the one hand, the aggression factors (bacteria and toxins) in the intracanal position and, on the other hand, the immune defenses in the periradicular position which prevent the progression of the aggressors. When the balance is maintained, the defenses organize themselves and form an inflammatory lesion (cyst or granuloma) which aims to prevent the extension of the infectious process to the rest of the body.
3.2- acute LIPOE is very painful and manifests itself through exacerbated clinical signs. It results from the disruption of the balance between the aggression factors (bacteria and toxins) and the immune defense mechanisms. When the balance is disrupted, the defenses are overwhelmed and the aggression factors move into a periradicular situation, which causes an apical or latero-radicular abscess.
The transition from the chronic to the acute phase is essentially based on the disruption of the balance between the pathogenic flora and the host’s immune defenses (Orstavik and Pitt Ford, 1998). It should be noted that in the absence of adequate treatment, the spread of infection to celluloadipose tissues is likely to result in septicemic and thromboembolic complications that can put the patient’s prognosis at risk (Peron and Mangez, 2008).
- Diagnosis of LIPOE
4.1) Means of diagnosis
Assessment of symptoms
Specify the nature of the pain felt by the patient, by asking precise 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
- Exoral examination: by inspection and palpation, we look for facial easemetry, swelling, cutaneous fistula, large and painful lymph nodes, limitation of mouth opening, difficulty swallowing.
- The intraoral examination: we look for deep cavities, cracks and
fractures, abrasions and erosions, extensive and defective restorations, dental dyschromia and other anomalies; inflammatory appearance (redness, edema) of soft tissues, ulcerations, fistulous ostium; occlusal interferences, abnormal mobility.
The practitioner must, at the level of each suspected tooth, look for and analyze the direct and indirect signs which reflect the existence of a bacterial contamination pathway from the endodontium to the periodontium. The presence of this first key criterion is essential to consider the diagnosis of PA.
- Clinical diagnostic tests:
— Pulp sensitivity tests : these 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 APICAL PERIODONTITIS (AP).
Periradicular tests
• Percussion test (axial): a painful response can detect periodontal inflammation. In case of doubt, the response is analyzed in relation to a healthy control tooth.
• Intraoral palpation test: intraoral palpation is performed in the vestibule, looking for a sensitive or painful inflammatory area. A very painful apical palpation indicates the presence of a suppurative collection, while a sensitive palpation provides more information on an inflammatory state.
NB: In the case of PA, palpation also allows the disappearance of the vestibular bone cortex to be diagnosed by the so-called bucket sign of the skull or by the return shock sign. Spontaneous or exacerbated painful responses to these tests are characteristic of the acute lineage of PA.
Additional tests
• The gutta-percha cone test: to follow the fistulous path to its source. An X-ray taken in this way will allow this source to be located.
• The cavity test: if there is still doubt about the vitality of the pulp.
• Periodontal probing: in order to differentiate between periodontal and endodontic damage, in hybrid forms of endo-periodontal lesions.
• Transillumination: the search for a crack that could explain the presence of an apical lesion on an apparently intact tooth.
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.
5) Clinical forms of LIPOE:
5.1- chronic LIPOE
This line includes chronic apical periodontitis, namely:
——chronic periodontitis with granuloma and epithelial granuloma, or with periapical cysts: true or pocket
——chronic apical periodontitis with fistula of endodontic origin
——condensing osteitis.
5.1.1) granuloma and epithelial granuloma,
a) Definition : This is a very common pseudo – tumoral lesion, epithelialized or not, which results from a slow and long-term evolution of the inflammatory process leading to the formation of granulomatous tissue, following a lymphoplasmacytic infiltration of the periapex, accompanied by adjacent bone destruction.
b) Pathogenesis:
The continued presence of intracanal irritants gradually promotes the passage of
initial inflammation towards a lesion encapsulated by collagenous connective tissue rich in macrophages, lymphocytes and plasma cells, producing antibodies and cytokines.
These cytokines will on the one hand stimulate the osteoclast activation factors and therefore promote bone resorption, and on the other hand stimulate the proliferation of fibroblasts, angiogenesis, the reconstruction of the connective tissue and the slowing down of resorption.
c) Clinical signs
Periapical granuloma is an old lesion in which:
–the associated tooth does not respond to electrical and thermal stimuli.
— The patient does not complain of pain.
–percussion tests are only weakly positive.
— palpation is not painful, if chronic apical periodontitis perforates the bony cortex, palpation of the periapical area becomes sensitive.
d) Radiography: on the retro-alveolar image, a radiolucent image with a poorly defined limit at the apical level is observed, synonymous with the destruction of the lamina dura and the apical bone.
e) Phases of the development of the granuloma
Three phases of development of a granuloma are described:
—A phase of endosteal atency during which the discovery of the granuloma can only be made radiologically, no clinical symptoms.
—A phase of bone deformation during which the finger opposite the apex feels a small curvature,
—A phase of externalization during which the lesion then exceeds the thinned bony table and becomes submucosal. Palpation reveals a soft, relentless mass. Opposite the apex, the mucosa takes on a more or less dark tint, often wine-red.
f) Pathological anatomy
Microscopically , the granuloma has the shape of a small fleshy bud, the volume of which is classically described as ranging from that of a millet grain to that of a corn kernel. It is attached to the apex of the dental root, at the level of the apical foramen, or in the inter-radicular region or laterally. The granuloma is whitish or reddish, smooth, rounded, plain or polylobed. Its consistency varies from soft to retinal.
g) Historically , the granuloma is a granulation tissue infiltrated by inflammatory cells and vascularized, limited by a fibrous capsule. This well-defined fibro-connective membrane is composed of dense collagen fibers, firmly attached to the root surface. Cells, originating from the Malassez debris, proliferate to form epithelial trabeculae with irregular arrangement. Sections show that this epithelium is frequently present in granulomas, 50% of the lesions being epithelialized. In some cases, the epithelium can grow and form a plug that seals the foramen. These epithelial trabeculae are surrounded by bundles of fibers infiltrated by chronic inflammatory cells.
Periradicular Inflammatory Lesions of Endodontic Origin
h) Evolution:
It may remain quiescent and symptom-free for several years and without detectable radiographic changes. As it may flare up in the form of a secondary abscess (the phoenix abscess or recurrent abscess), fistulize, or transform into a cyst, bone resorption resumes and a widening of the radiolucent zone is observed.
5.1.2) periapical cysts
a) Definition : A cyst is a closed pathological cavity that does not communicate with the outside and most often contains a liquid or semi-liquid substance.
Chronic cystic apical periodontitis is a transformation of a granuloma into an inflammatory cyst, consisting of a pocket formed by the proliferation of epithelial tissue and cystic degeneration of the connective-epithelial tissue of the tumor center. The cystic fluid of the pocket contains cholesterol crystals.
There are two types of periapical cysts:
–the true periapical cyst : it is an inflammatory apical cyst with a distinct pathological cavity, completely surrounded by an epithelium so that there is no communication with the pulp cavity;
–the pocket cyst : it is an inflammatory apical cyst comprising a cavity, in the form of a sac, surrounded by an open epithelium and in continuity with the dental apex.
b) Pathogenesis
Periapical cysts are generally considered to be a direct sequela of periapical granulomas, but not all granulomas develop into cysts.
The process of cyst formation takes place in 3 phases:
* First phase : proliferation of epithelial debris of Malassezquiescents. These epithelial debris proliferate under the influence of growth factors released by cells residing inside the granuloma.
*Second phase : development of an epithelial cavity . Two hypotheses attempt to explain this cystic formation:
—the theory of nutritional deficiency layer forms, the necrotic tissue liquefies, and the cystic cavity is transformed into the interior of the granuloma.
—the theory of encapsulation of a secondary abscess by peripheral epithelial proliferation.
* Third phase: expansion of the cyst.
The exact mechanism of this cyst expansion process has not been clarified.
c) C linique
Periapical cysts, usually asymptomatic, sometimes become painful when the inflammatory process becomes more severe or when an abscess forms.
The cystic lesion is asymptomatic, however the objective clinical signs of the cyst are:
–an emerging pain on apical palpation, while the “return shock” is perceived on transverse percussion,
–a small regular arch, if the development is vestibular, covered with healthy or poorly vascularized mucosa, and not very painful.
–when a thin bony shell covers the cysteon one can perceive a sensation of crackling of celluloid ball.
Sometimes the cyst wall may become associated with the gingival fibromucosa after destroying the bony cortex. A fluctuating liquid swelling may then be felt under the mucosa, with a thin bony rim surrounding it.
–In the exteriorization phase, a punctiform, intraoral or cutaneous fistulization can be observed, with an inflammatory clinical appearance. When the bulky mass is noticeable, it can cause dental displacements.
Periradicular Inflammatory Lesions of Endodontic Origin
d) Radiologically : the appearance of the cysts is almost identical to that of the granulomas.
periapical, but according to some authors, the lytic image of a cyst is often more voluminous and set with a better defined linear bone condensation.
e) Anatomy pathology:
Macroscopically: the cysts are of variable size (0.5 to several centimeters in diameter) and apical or latero-radicular.
Their lumen contains a citrine, viscous or haematic liquid, often sprinkled with cholesterol flakes.
Histologically: The four components of a true apical cyst are:
–a cystic cavity , which contains necrotic tissue and erythrocytes, remnants of hemorrhage. 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 , which lines this cavity. It is a stratified squamous epithelium whose thickness varies from one to several layers depending on the activity of the inflammatory process: if it is intense, the epithelium is thick, hyperplastic with multiple invaginations in the underlying connective tissue; if it is less intense, the epithelium will be thin, with 3 to 4 cell layers.
–a peripheral tissue , containing vessels, infiltrated by macrophages, lymphocytes and plasma cells, more rarely by polymorphonuclear cells;
–a fibrous , collagenous capsule , containing all of the preceding elements.
f) Evolution
Untreated, the periapical cyst grows only slowly. No ameloblastic proliferation of its lining has ever been reported. As for the occurrence of squamous cell carcinoma, it has only been exceptionally reported.
5.1.3) Apical periodontitis with fistula of endodontic origin or fistulization
Apical periodontitis with fistula of endodontic origin is characterized by
the appearance of a fistula. This is a route of bacterial pulpo-periodontal contamination and corresponds to an externalized drainage route for apical inflammatory fluids. Its appearance is often ignored by the patient, the fistula is created following acute primary or secondary episodes: drainage of the abscess by the fistula Over time, the overpressure phenomena disappear and the pain and swelling regress. The fistulous tract can become epithelialized.
–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.
Clinical signs
– Negative response to pulp sensitivity tests.
– Presence of a fistular ostium: positive gutta-percha test allowing
to objectify the relationship with the causal tooth.
X-ray:
-Periapical radiolucent image of bone destruction.
Evolution: elimination of the canal infection causes the fistula to disappear
5.1.4) Condensing osteitis:
Or sclerosing osteitis is a proliferative response of periapical bone tissue to low-intensity, long-term pulp irritation characterized by an increase in periapical bone density.
The bony trabeculae thicken to such an extent that the marrow spaces disappear or are reduced to small points of fibrous tissue. This reaction is seen in young people around the apices of lower teeth with large carious lesions and a chronically inflamed pulp.
After endodontic treatment, a return to normal trabeculation is estimated.
5.2-acute LIPOE
This lineage includes acute serous and suppurative apical periodontitis: initial serous apical periodontitis, acute apical periodontitis, and acute apical abscess.
Periradicular Inflammatory Lesions of Endodontic Origin
5.2.1-Initial apical periodontitis (IAP) or pulpo-desmodontitis
Definition: Initial apical periodontitis (IAP) corresponds either to an early inflammation of endodontic origin (following acute pulpitis), or to a transient inflammation following trauma to the alveolodental ligament (over-occlusion restoration, intraligamentous anesthesia) (CNEOC 2012).
Clinical signs: Dull, continuous pain, exacerbated by occlusal contact; on clinical examination, a defective restoration, carious lesion, fracture may be observed.
Radiological signs: Slight ligament widening.
Pulp vitality tests (pulp is vital) so responds to tests.
Positive percussion test, pathognomonic sign of passage of inflammation into the periapex.
Differential diagnosis: Pulpitis, Septum syndrome, Flare up.
5.2.2) 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 (CNEOC 2012).
The periapical connective tissue is inflamed and infected by pulp necrosis or septic discharge with failed endodontic treatment.
Clinical signs: spontaneous, continuous, localized pain, exacerbated by chewing, slight dental mobility, sensation of long tooth, overbite.
Radiological signs: Ligamentous widening or periapical radiolucent image with more or less diffuse limits if the lesion is significant.
Vitality tests: the tooth does not respond to the cold test but the patient responds to the hot test.
Axial percussion test is painful (positive).
Differential diagnosis: is made with Pulpitis, Septum Syndrome, Flare-up.
5.2.3) Acute apical abscess (AAA):
Acute apical abscess is a common periapical emergency diagnosis. 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 (CNEOC 2012).
This abscess can be primary or secondary (phoenix abscess) in the event of a pre-existing inflammatory lesion and subsequently fistulize.
Clinical signs: Spontaneous pain, exacerbated by the slightest contact, swelling, redness of the gum, gingival abscess opposite the root in question, palpation of the apex is painful.
General condition altered
More or less significant dental mobility.
Radiological signs: Periapical radiolucent lesion and bone lysis.
Vitality tests: the tooth is mortified so it does not respond to pulp vitality tests .
Axial percussion: is very painful.
Differential diagnosis Pulpitis, Septal syndrome, Pericoronitis, Periodontal abscess and Sinusitis.
- The treatment
–Chronic LIPOE: Treatment of chronic LIPOE consists of eradicating the root canal infection, either by performing initial therapy to eliminate the primary infection of the endodontium, or by endodontic retreatment or apical surgery to eliminate a persistent infection after prior endodontic treatment.
To treat chronic periapical lesions, it is necessary to reduce the microbial population to a tolerable threshold, close the endodontic exit portals and promote healing.
The canal system must be sealed after debridement of the lesion by obturation of the treated canals.
The body then takes charge of repairing the lesion. The quality of disinfection of the root canal system depends mainly on the irrigation solutions. Particular attention must be paid to the disinfection of teeth already treated endodontically due to the presence of resistant bacteria such as Enterococcus faecalis which cause persistent LIPOE.
Acute LIPOE: it is carried out in two stages:
First stage: this is the primary emergency treatment to relieve the patient and eliminate the pain.
Emergency treatment of initial apical periodontitis:
- Disinfection of the endodontium under sodium hypochlorite field.
- and installation of calcium hydroxide.
- Temporary non-compressive, watertight seal.
- Under occlusion.
Emergency treatment of acute apical periodontitis:
- Canal trimming under field, shaping and irrigation with sodium hypochlorite.
- Calcium hydroxide as a temporary filling.
- Temporary non-compressive, watertight seal.
- Put under occlusion.
- Prescription for painkillers.
Emergency treatment of acute apical abscess:
- Drainage (transcanal drainage of pus if non-surgical).
- Rinse with physiological serum.
- Leave the tooth open.
The second stage is the performance of conservative treatment (endodontic treatment followed by a watertight root canal and coronal filling.
Periradicular Inflammatory Lesions of Endodontic Origin
Prediction:
The prognosis for healing a LIPOE ranges from 74 to 86% for correctly performed non-surgical endodontic treatments and retreatments. If we compare the asymptomatic functional maintenance of the tooth on the arch, the prognosis is high (between 91 and 97%). The effectiveness of endodontic therapies is therefore indisputable. Extraction in the case of LIPOE must therefore remain exceptional.
Periradicular Inflammatory Lesions of Endodontic Origin
Conclusion :
It is essential to understand that LIPOE represent an extra-radicular manifestation of an intra-canal pathology (Orstavik and Pitt Ford, 1998). Periradicular inflammation is therefore a response to endodontic infection. Although uncommon, it is however possible to demonstrate the presence of extraradicular bacteria either within the lesion itself (e.g. acute apical abscess) or within cemental lacunae on the root surface (Nair et al., 1993; Nair, 2004). LIPOE can be acute or chronic.
Untreated cavities can damage the pulp.
Orthodontics aligns teeth and jaws.
Implants replace missing teeth permanently.
Dental floss removes debris between teeth.
A visit to the dentist every 6 months is recommended.
Fixed bridges replace one or more missing teeth.