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Radicular cyst – Pathogenesis

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Author: Sanketh DS, MDS


“A cyst is defined as a pathological cavity, lined by epithelium, having fluid, semifluid or gaseous contents that are not created by the accumulation of pus”.

A cyst consists of 3 components – 1) the central cavity (lumen), 2) the epithelial lining and 3) the cyst wall/capsule

The lumen or the cavity contains fluid or semifluid material, like cellular debris or mucus. The epithelial lining could be any of the different types like stratified squamous which could be keratinized or non-keratinized, pseudo-stratified, columnar or cuboidal. The capsule or the wall is the connective tissue comprising of collagen, ground substance, fibroblasts and blood vessels.

Cysts are frequent lesions occurring in the oral cavity and are of much significance because they may be destructive and cause significant signs and symptoms.

Radicular or periapical cyst, is the most common inflammatory cyst arising due to the proliferation of the epithelial rests in the periodontal ligament. This proliferation is a result of the inflammation induced by bacteria and necrotic products seeping into the periapex through the infected pulp. Hence radicular cysts are most often found in the apices of infected teeth or sometimes in the lateral aspects of roots, when the inflammation spreads through the lateral canals.


Once the tooth is infected and not adequately treated, the cavitation extends, with the infection advancing to the pulp. The infection could elicit an inflammatory response and assuming treatment is not initiated, could cause necrosis of the pulp. Alternatively, necrosis of pulp could also be caused if the tooth is severely traumatized.

The bacterial components could seep through the dead pulp to the underlying periapex, further eliciting a periapical bone inflammation. The body’s immune system responds with a periapical granuloma formation ( tissue tries to heal itself). Periapical granuloma is basically composed of granulation tissue and a lot of inflammatory cells.

Do not confuse periapical granuloma to a tuberculous granuloma or a granuloma due to any other granulomatous infection. The “granuloma” in periapical granuloma is a misnomer and is only composed of granulation tissue! 

The pathogenesis of a radicular cyst could be spaced into 3 phases namely, a phase of initiation, a phase of cyst formation and a phase of cyst expansion.

Phase of initiation

This phase involves proliferation of the epithelial rests of Malassez. These epithelial rests in the periodontal ligament, come to lie in the periapical granuloma of the infected tooth with a necrotic pulp.

1. Bacterial components/antigens may initiate an inflammatory response by being presented to the effector T helper(Th) (CD 4+) cells by macrophages. The effector Th cells after recognition release cytokines IL-2 and IFN γ. IL-2 further helps in proliferation of other Th cells and IFN γ activates macrophages. Activated macrophages release pro-inflammatory cytokines like TNF α, IL-1 and IL-6 of which IL-1 and 6 may help in proliferation of the epithelial rests of malassez.

2. IL-2 released by Th cells also activates B cells which become plasma cells producing antibodies.  Antigen-Antibody complexes formed may elicit a complement response leading to increased vascular permeability and a leucotactic response further fuelling inflammation and epithelial proliferation.

3. Another key reason for inflammation and direct induction of proliferation of the epithelial rests are the bacterial endotoxins!  These endotoxins may also indirectly initiate a complement response.

4. Local changes in the connective tissue like an increase in CO2 tension and decrease in oxygen concentration have also been speculated to activate proliferation of epithelial rests.

Phase of cyst formation

This phase involves the cavity/lumen being lined by the proliferating odontogenic epithelium. There are two possibilities for this to happen, both of which could be feasible.

1. One concept postulates that the epithelium proliferates and lines an already existing cavity which may have been formed by the connective tissue breakdown due to proteolytic enzyme activity.

2. Another proposes that epithelium proliferates first and then undergoes degeneration at the centre to form a cavity. This process is further subdivided into two schools of thought.

a) One proposes that as the cells proliferate, the cells in the centre move away from the nutrients provided by the connective tissue and as a result undergo ischaemic liquefactive necrosis. This creates a central cavity surrounded by a viable epithelium.
b) The other proposes the degeneration of the cells to be due to an immunologic reaction or autolysis as opposed to ischaemic necrosis due to lack of blood supply.

Such degenerations happening in the epithelial islands in different parts of the connective tissue may coalesce to form a larger cavity!

Phase of cyst expansion

This phase contributes to the expansion of the radicular cyst and there are many reasons postulated:

1. It has been hypothesised that osmosis contributes to the expansion of radicular cyst. The inflammatory exudate, high protein content, cell breakdown products and hyaluronic acid in the cystic fluid  increase the osmotic pressure causing fluid accumulation in the lumen leading to expansion.

2. The internal hydrostatic pressure of radicular cysts have shown to be higher than capillary blood pressure leading to bone resorption on expansion.

3. Also cytokines like IL-1 and 6 and prostaglandins released by plasma cells and fibroblasts help in resorption of bone helping expansion.

4. Collagenases breakdown connective tissue components and this also contribute to cyst expansion!

As long as inflammation persists, there is epithelial proliferation and this has been suggested to contribute to cyst expansion.


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Sapp JP, Eversole LR, Wysocki GP. Contemporary Oral and Maxillofacial Pathology. 2 nd ed. Mosby; 2004.

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