Hubbry Logo
Periapical cystPeriapical cystMain
Open search
Periapical cyst
Community hub
Periapical cyst
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Periapical cyst
Periapical cyst
Periapical cyst
View on Wikipedia
from Wikipedia
Periapical cyst
Other namesRadicular cyst, inflammatory cyst
CT scan through head showing a right periapical cyst
SpecialtyDentistry Edit this on Wikidata

Commonly known as a dental cyst, the periapical cyst is the most common odontogenic cyst. It may develop rapidly from a periapical granuloma, as a consequence of untreated chronic periapical periodontitis.[1]

Periapical is defined as "the tissues surrounding the apex of the root of a tooth" and a cyst is "a pathological cavity lined by epithelium, having fluid or gaseous content that is not created by the accumulation of pus."[2]

Most frequently located in the maxillary anterior region, the cyst is caused by pulpal necrosis secondary to dental caries or trauma. Its lining is derived from the epithelial cell rests of Malassez which proliferate to form the cyst.[2] Such cysts are very common. Although initially asymptomatic, they are clinically significant because secondary infection can cause pain and damage. In radiographs, the cyst appears as a radiolucency (dark area) around the apex of a tooth's root.[3]

Signs and symptoms

[edit]
Visual image of the face of the person shown on the CT scan above. Swelling can be observed in the right cheek.

Periapical cysts begin as asymptomatic and progress slowly. Subsequent infection of the cyst causes swelling and pain. Initially, the cyst swells to a round hard protrusion, but later on the body resorbs some of the cyst wall, leaving a softer accumulation of fluid underneath the mucous membrane.[citation needed]

Secondary[clarification needed] symptoms of periapical cysts include inflammation and infection of the pulp causing dental caries. This infection is what causes necrosis of the pulp.[4]

Larger cysts may cause bone expansion or displace roots. Discoloration of the affected tooth may also occur. Patient will present negative results to electric and ice test of the affected tooth but will be sensitive to percussion. Surrounding gingival tissue may experience lymphadenopathy. The alveolar plate may exhibit crepitus when palpated.

Complications

[edit]

Expansion of the cyst causes erosion of the floor of the maxillary sinus. As soon as it enters the maxillary antrum, the expansion rate increases due to available space for expansion. Performing a percussion test by tapping the affected teeth will cause shooting pain. This is often clinically diagnostic of pulpal infection.[citation needed]

Causes

[edit]

Dental cysts are usually caused due to root infection involving tooth decay. Untreated dental caries then allow bacteria to reach the level of the pulp, causing infection. The bacteria gains access to the periapical region of the tooth through deeper infection of the pulp, traveling through the roots. The resulting pulpal necrosis causes proliferation of epithelial rests of Malassez which release toxins at the apex of the tooth. The body's inflammatory response will attack the source of the toxins, leading to periapical inflammation. The many cells and proteins that rush to an area of infection create osmotic tension in the periapex which is the source of internal pressure increase at the cyst site.

These lesions can grow large because they apply pressure over the bone, causing resorption. The toxins released by the breakdown of granulation tissue are one of the common causes of bone resorption.

There are two schools of thought regarding cyst expansion.[5]

  1. Complementary response to inflammation
  2. Chemical reaction with Interleukin and Prostaglandin

Mechanisms

[edit]

Periapical cysts develop due to an inflammatory stimulus in 3 stages:[4]

  1. Initial stage: Epithelial cells from the rests of Malassez at the apex of the roots of a non-vital tooth (one where the nerve and blood supply in the tooth have degenerated and no longer exist) become stimulated due to the body's inflammatory response to bacterial endotoxins infecting the pulp or as a direct response to necrotic pulp tissue, therefore re-entering the growth phase. Bacterial byproducts then are able to seep into the periapical region through the infected pulp.
  2. Cyst development stage: Epithelial cells form strands and are attracted to the area which contains exposed connective tissue and foreign substances. Several strands from each rest converge and surround the abscess or foreign body.
  3. Cyst growth stage: Fluid flows into the cavity where the forming cyst is growing due to the increased osmolality of the cavity in relation to surrounding serum in capillaries. Pressure and size increase.

The definitive mechanism by which cysts grow is under debate; several theories exist.

Biomechanical theory

[edit]

Pressure and concentration differences between the cystic cavity and the growth surroundings influence fluid movement into the cyst, causing size increase.

Biochemical theories

[edit]

a. Collagenase (breakdown of collagen) in the jaw bone leads to bone degeneration, providing room for cysts to develop. Substances released by the body's immune system as a result of the connective tissue breakdown, such as cytokines and growth factors, contribute to the mobilization and proliferation of epithelial cells in the area.

b. Bone resorption caused by metabolism of acidic substances produced by cysts contributes to cyst growth. Such substances include Prostaglandin-2 and Interleukin-1 which are both produced by the cyst itself.

Nutritional deficiency theory

[edit]

Epithelial cells will form a mass inside the cavity and the innermost cells become deprived of nutrients because they are far from the source of nutrients (the blood vessels). The innermost cells die and form an aggregate of dead tissue. The inner cells undergo ischemic liquefactive necrosis which creates the cavity space surrounded by growing epithelial cells. This theory is unlikely in the absence of malignant transformation of epithelial cells as it does not follow the existing relationship between connective tissue and epithelium.[4]

Abscess theory

[edit]

Epithelial cells have an inherent quality to reproduce and cover any connective tissue that is not already lined with epithelia. Formation of an abscess must precede the epithelial proliferation in order for the cells to carry out this tendency. This theory explains why cysts are lined in epithelia but not why the initial cysts itself forms.[6]

Diagnosis

[edit]

A non-vital tooth is necessary for the diagnosis of a periapical cyst, meaning the nerve has been removed by root canal therapy.[citation needed]

Oral examination

[edit]

The surrounding intraoral anatomical structures should be palpated to identify the presence of bone expansion or displacement of tooth roots as well as crepitus noises during examination, indicating extensive bone damage. Bulging of the buccal or lingual cortical plates[7] may be present. Age of occurrence in the patient, the location of the cyst, the edges of cystic contours, and the impact that the cyst has on adjacent structures must all be considered for proper diagnosis.[3]

Radiology

[edit]

Several lesions can appear similarly in radiographic appearance.[2] Intraoral X-rays or a 3-D cone beam scan of the affected area can be used to obtain radiological images and confirm diagnosis of cysts in the periapical area. Circular or ovoid radiolucency surrounding the root tip of approximately 1-1.5 cm in diameter is indicative of the presence of a periapical cyst.[2] The border of the cyst is seen as a narrow opaque margin contiguous with the lamina dura. In cysts that are actively enlarging, peripheral areas of the margin may not be present. Periapical cysts have a characteristic unilocular[8] shape on radiographs. There is also a severe border of cortication[9] between the cyst and surrounding bone. Pseudocysts, on the other hand, have a fluid filled cavity but are not lined by epithelium, therefore they have a less severe and more blurred border between the fluid and bony surroundings.[10]

Histopathology

[edit]
Histopathology of a periapical cyst, with metaplastic changes of mucus-secreting cells (B), and ciliated cells (C).
Cholesterol clefts of a periapical cyst of the jaw.

In light microscopy, periapical cysts show:[11]

  • Stratified squamous epithelium of variable thickness, except when originating in a maxillary sinus where there is respiratory epithelium (pseudostratified ciliated columnar epithelium).
  • A fibrous capsule of varying thickness, with chronic inflammatory cells, wherein a plasma cells may be abundant

They sometimes have the following features:[11]

  • Rushton hyaline bodies, which are amorphic, eosinophilic, linear to crescent-shaped bodies in the cyst epithelium, present in 10% of periapical cysts.
  • Scattered ciliated cells
  • Cholesterol clefts in the cyst lining.

Classification

[edit]

Periapical cysts exist in two structurally distinct classes:

  1. Periapical true cysts - cysts containing cavities entirely surrounded in epithelial lining. Resolution of this type of cyst requires surgical treatment such as a cystectomy.[10]
  2. Periapical pocket cysts - epithelium lined cavities that have an opening to the root canal of the affected tooth. Resolution may occur after traditional root canal therapy.[10]

Differentiation

[edit]

Radiographically, it is virtually impossible to differentiate granuloma from a cyst.[2] If the lesion is large it is more likely to be a cyst. Radiographically, both granulomas and cysts appear radiolucent. Many lesions of the mandible in particular appear cystlike in appearance. It is often necessary to obtain a biopsy and evaluate the tissue under a microscope to accurately identify the lesion.[2]

Treatment

[edit]

The infected tissue of the periapical cyst must be entirely removed, including the epithelium of the cyst wall; otherwise, a relapse is likely to occur. Root canal treatment should be performed on the tooth if it is determined that previous therapy was unsuccessful. Removal of the necrotic pulp and the inflamed tissue as well as proper sealing of the canals and an appropriately fitting crown will allow the tooth to heal under uninfected conditions.[2]

Surgical options for previously treated teeth that would not benefit from root canal therapy include cystectomy[12] and cystostomy.[12] This route of treatment is recommended upon discovery of the cyst after inadequate root canal treatment. A cystectomy is the removal of a cyst followed by mucosa and wound closure to reduce chances of cyst regeneration. This type of treatment is more ideal for small cysts.[citation needed] A cystostomy is recommended for larger cysts that compromise important adjacent anatomy. The cyst is tamponaded to allow for the cyst contents to escape the bone. Over time, the cyst decreases in size and bone regenerates in the cavity space.

Marsupialization could also be performed, which involves suturing the edges of the gingiva surrounding the cyst to remain open. The cyst then drains its contents and heal without being prematurely closed. The end result is the same as the cystostomy, bone regeneration. For both a cystostomy and marsupialization, root resectioning may also be required in cases where root resorption has occurred.[13]

Epidemiology

[edit]
Relative incidence of odontogenic cysts.[14] Periapical cysts are labeled at left.

Periapical cysts comprise approximately 75% of the types of cysts found in the oral region. The ratio of individuals diagnosed with periapical cysts is 3:2 male to female, as well as individuals between 20 and 60 years old. Periapical cysts occur worldwide.

Types of Periapical cysts:

Apical: 70%

Lateral: 20%

Residual: 10%

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Periapical cyst

View on Grokipedia
from Grokipedia
A periapical cyst, also known as a radicular cyst, is an inflammatory that originates from the proliferation of epithelial remnants of the root sheath of Hertwig (Malassez rests) at the apex of a non-vital , typically resulting from untreated pulpal due to bacterial infection from caries, trauma, or restorative procedures. It represents the most common type of odontogenic cyst, accounting for approximately 50-60% of all odontogenic cysts according to various studies, and is more frequently observed in the anterior of adults aged 20-50 years, with no marked predilection. These cysts develop in the context of chronic apical periodontitis, where persistent microbial infection in the system leads to inflammatory mediators stimulating epithelial cell rests, resulting in cyst formation through increased and hydrostatic forces that expand the lesion. Periapical cysts are classified into true cysts, which are completely enclosed by , and pocket (or bay) cysts, which maintain communication with the ; the latter often respond better to nonsurgical intervention. Clinically, they are usually asymptomatic and discovered incidentally on routine dental radiographs as a well-circumscribed, unilocular radiolucency attached to the root apex, though larger lesions (>10 mm) may cause cortical expansion, swelling, on percussion, , or displacement of adjacent structures if secondarily infected. Diagnosis relies on a of clinical evaluation, including negative pulp vitality testing, and imaging such as periapical radiographs or cone-beam computed tomography (CBCT), which reveals a round or oval radiolucency with corticated borders; definitive confirmation requires histopathological examination showing a fibrous wall lined by non-keratinized , often with and cholesterol clefts. Treatment primarily involves nonsurgical endodontic therapy, such as root canal , with , and , which achieves resolution in 85-95% of cases by eliminating the infectious source and allowing natural cyst involution, particularly for cysts. For persistent, symptomatic, or large cysts (>200 mm²), adjunctive surgical approaches like with enucleation, , or decompression are employed, yielding success rates of 60-91%, while extraction is reserved for non-restorable teeth. Long-term follow-up with serial radiographs is essential to monitor healing, as untreated cysts can lead to or rarely .

Overview and classification

Definition

A periapical cyst, also known as a radicular cyst, apical cyst, or dental cyst, is the most common inflammatory , arising at the apex of a non-vital due to chronic resulting from pulpal . This lesion forms in association with , where persistent infection or trauma leads to the proliferation of epithelial remnants. Historically, it has been referred to by synonyms such as periapical cyst and lateral radicular cyst, reflecting its position relative to the tooth root. Histologically, the periapical cyst is characterized by a lining of non-keratinized derived from the epithelial rests of Malassez, which are remnants of Hertwig's epithelial root sheath entrapped in the alveolar bone. The cyst typically presents as a unilocular, fluid-filled cavity surrounded by a fibrous capsule containing chronic inflammatory cells, such as lymphocytes and plasma cells, with possible inclusions of clefts or rushton bodies. The epithelial lining often exhibits a characteristic arcading or looped pattern due to in response to the inflammatory milieu. Periapical cysts are distinguished from pseudocysts, such as periapical granulomas, by the presence of a complete epithelial lining; granulomas lack this and consist primarily of without a defined cystic cavity. Within cystic lesions, a further distinction exists between true cysts, which are fully enclosed cavities lined entirely by , and pocket cysts (or bay cysts), where the epithelial lining forms an open pouch continuous with the system. This differentiation is crucial for understanding treatment outcomes, as true cysts are self-sustaining and less responsive to non-surgical interventions.

Classification

Periapical cysts, also known as radicular cysts, are classified by the (WHO) as inflammatory odontogenic cysts arising from epithelial remnants in the periodontal ligament due to chronic inflammation from pulpal necrosis. These cysts are subdivided into subtypes based on their anatomical location relative to the tooth root and their persistence following dental intervention. The apical subtype is the most common, typically forming at the apex of a non-vital tooth root and representing the predominant presentation of radicular cysts. The lateral subtype occurs less frequently, developing along the of the , often in association with inflammatory from lateral accessory canals of a non-vital . The residual subtype arises when an existing radicular persists in the after extraction of the involved , remaining unattached to any ; it accounts for approximately 10% of all odontogenic cysts in some analyses. All subtypes are characteristically linked to non-vital teeth with prior pulpal necrosis, though the residual form lacks direct attachment to a current , distinguishing it from active tooth-associated variants.

Epidemiology

Prevalence and incidence

Periapical cysts, also known as radicular cysts, represent the most common odontogenic cysts, accounting for approximately 60% of all odontogenic cysts reported in histopathological analyses. These cysts arise from epithelial remnants in the and are frequently identified in submissions, comprising approximately 60% of odontogenic cysts across various studies. Among all jaw cysts, periapical cysts dominate inflammatory subtypes. Radiographic surveys indicate that true cystic formations occur in about 15-20% of periapical radiolucencies associated with non-vital teeth, highlighting their frequency within endodontic lesions. Global data further underscore this, with radicular cysts making up around 60% of submitted specimens in large cohorts. A 2024 multicenter study reported radicular cysts comprising 58.6% of odontogenic cysts. Prevalence is notably higher in populations with limited access to dental care, where untreated caries contribute to a greater burden of chronic endodontic .

Demographics and distribution

Periapical cysts exhibit a peak incidence between the ages of 20 and 60 years, with the highest frequency occurring in the fourth and fifth decades of life. They are rare in children under 10 years old, as evidenced by limited cases in pediatric cohorts from analyses. A slight male predominance is observed, with male-to-female ratios ranging from 1.2:1 to 2.5:1 across various studies, though no significant is universally reported. This pattern may reflect differences in dental care-seeking behaviors, but direct causation remains unestablished. Anatomically, periapical cysts are most common in the , accounting for approximately 60-70% of cases, particularly in the anterior region involving incisors and canines. The is less frequently affected (30-40%), with lesions often located in the posterior region. In a South Indian cohort (2021-2023), 64% of cases were anterior. Geographic variations correlate with caries and trauma rates, showing higher in regions with elevated dental disease burdens. Ethnic differences are minimal, though registries report relatively higher incidences in Asian and European populations, such as in Iranian, Indian, and cohorts.

Clinical presentation

Signs and symptoms

Periapical cysts, also known as radicular cysts, are frequently and are most commonly discovered incidentally during routine dental radiographs, particularly when investigating unrelated dental issues. In symptomatic cases, patients may experience mild to moderate pain, often elicited by percussion or biting on the affected , along with localized swelling of the gingiva or alveolar mucosa. These symptoms arise due to pressure from the cystic expansion or associated linked to pulpal . Larger cysts exceeding 1 cm in diameter can lead to more noticeable effects, such as facial asymmetry from bone expansion, increased , or the development of a sinus tract with drainage of foul-tasting fluid if the cyst fistulizes to the . The associated consistently tests non-vital on pulp assessments, such as cold or electric pulp testing, reflecting underlying pulpal . Acute symptoms are rare but can occur with superimposed bacterial , manifesting as severe , significant swelling, and potential formation requiring urgent intervention.

Complications

Untreated periapical cysts, also known as radicular cysts, can expand due to continued epithelial proliferation and fluid accumulation, leading to significant and expansion of the surrounding alveolar bone. This expansion may result in thinning and eventual perforation of the cortical plate, particularly in the where proximity to the increases the risk of oroantral communication, allowing oral contents to enter the sinus and potentially causing . In the , growth can displace the roots of adjacent teeth, causing mobility or malposition, and may involve the , compressing the and resulting in or neurosensory disturbances such as numbness in the lower lip or chin. These effects arise from mechanical pressure exerted by the expanding lesion on neural structures. Secondary bacterial infection of the cyst contents can occur, transforming the chronic lesion into an acute periapical abscess characterized by accumulation and severe pain, or progressing to diffuse involving surrounding soft tissues, which may spread to fascial spaces and cause swelling beyond initial cyst-related swelling. Although rare, long-standing periapical cysts carry a risk of into , with an incidence of less than 1% among odontogenic cysts overall, and over 50% of reported primary intraosseous squamous cell carcinomas arising from periapical inflammatory cysts. This transformation is more common in untreated, chronically inflamed lesions. Following tooth extraction without complete cyst removal, residual cysts may form from epithelial remnants of the original persisting in the , leading to recurrent bone destruction and potential expansion years later; recent 2024 reports highlight cases mimicking aggressive neoplasms due to incomplete enucleation during prior procedures.

Etiology and risk factors

Causes

The primary cause of periapical cysts is pulpal resulting from untreated dental caries, which allows bacterial invasion of the pulp chamber and subsequent inflammation at the tooth apex. This process begins with carious lesions breaching the enamel and , leading to pulp exposure and irreversible that progresses to if untreated. Trauma to the , such as fractures or luxation injuries, represents another key initiating factor by disrupting vascular supply to the pulp, thereby promoting and enabling ingress through disrupted pathways. These mechanical injuries often result in immediate or delayed pulpal death, fostering an environment conducive to periapical . Iatrogenic factors, including over-instrumentation during endodontic procedures, can introduce or contaminated beyond the root apex, contributing to persistent and cyst development. Such procedural errors may exacerbate existing infections or initiate new ones in previously treated teeth. The bacterial of periapical cysts is predominantly polymicrobial, with anaerobic species such as and playing dominant roles through spread via the system and formation of biofilms. These organisms thrive in the necrotic pulp environment, perpetuating chronic inflammation. Periapical cysts typically arise as a progression from acute to chronic apical periodontitis, where unresolved pulpal infection leads to periapical and eventual cystic transformation, often involving brief activation of epithelial rests of Malassez in response to the inflammatory stimulus.

Predisposing factors

Poor is a primary predisposing factor for the development of periapical cysts, as it facilitates the accumulation of and , increasing the risk of caries formation and subsequent pulp infection if lesions are not addressed promptly. Individuals with inadequate brushing, flossing, or regular dental check-ups often experience delayed and treatment of carious lesions, allowing progression to irreversible and eventual cyst formation. Systemic conditions such as and significantly heighten susceptibility by impairing immune responses and hindering tissue healing around infected teeth. compromises local and systemic immunity, elevating the odds of persistent periapical lesions by approximately 1.16 times in root-filled teeth compared to non-smokers, due to nicotine's effects on inflammatory mediators and vascular supply. Similarly, disrupts function and production, leading to a higher of chronic apical periodontitis and associated cysts through exacerbated inflammatory responses to endodontic pathogens. Socioeconomic disparities contribute to elevated caries prevalence, thereby predisposing certain populations to periapical cysts through barriers to preventive care and exposure. Low-income groups face higher caries rates due to limited access to dental services, nutritious diets, and fluoridated water, which collectively amplify the untreated progression of dental infections. Areas with suboptimal community water fluoridation further exacerbate this risk by failing to provide protective enamel remineralization, particularly in under-resourced communities. A history of dental trauma, common in sports participants or individuals prone to accidents, predisposes teeth to pulp necrosis and cyst development by directly damaging vascular supply and allowing bacterial ingress. Contact sports like football and account for a substantial portion of traumatic dental injuries, with rates up to 15.5% among young athletes, often leading to delayed and periapical pathology if not managed immediately. Non-athletic accidents, such as falls or vehicular collisions, similarly increase vulnerability in high-risk occupations or environments. Genetic predispositions to periapical cysts are rare but involve variants in immune-related genes that modulate chronic inflammation and host responses to infection. Recent studies have identified polymorphisms in interleukin genes, such as IL-10, IL-12A, and IL-17D, associated with heightened susceptibility to periapical lesions by altering cytokine signaling and prolonging inflammatory cascades. Additionally, WNT pathway gene variants influence bone remodeling and immune tolerance in apical periodontitis, potentially contributing to cyst persistence in genetically prone individuals.

Pathophysiology

Mechanisms of formation

The formation of a periapical cyst begins with an inflammatory stimulus from bacterial invasion associated with necrotic pulp tissue, which activates the epithelial rests of Malassez—residual epithelial cell clusters in the periodontal ligament derived from Hertwig's epithelial root sheath. These rests, normally quiescent, undergo proliferation in response to the chronic inflammatory environment created by microbial products diffusing through the . This initial activation marks the first stage of cyst development, transforming the periapical region from a simple inflammatory focus into a site of epithelial hyperactivity. In the second stage, the proliferating epithelial cells form interconnected strands and networks, eventually coalescing to create a central cavity lined by . This proliferation is driven by inflammatory mediators, including interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α), which are secreted by immune cells such as macrophages and fibroblasts in the inflamed periapical tissues; these cytokines stimulate epithelial and enhance collagenase activity, facilitating tissue remodeling and cavity expansion by degrading the surrounding . The resulting lesion transitions from a solid periapical —characterized by without a distinct cavity—to a true when the epithelial-lined lumen exceeds 0.5 mm in diameter, distinguishing it histologically as a fluid-filled structure independent of direct communication with the in many cases. The third stage involves cyst enlargement through osmotic fluid accumulation and bone resorption. Proteins and cellular debris within the cavity elevate the osmotic pressure of the cystic fluid above that of surrounding tissues, drawing in interstitial fluid and increasing intracystic hydrostatic ; this pressure induces separation of the epithelial lining from the underlying wall, promoting further expansion. Concurrently, bone resorption is mediated by osteoclasts activated via receptor activator of nuclear factor kappa-B ligand () expressed by inflamed stromal cells and immune infiltrates in the periapical tissues, enabling the cyst to grow centrifugally into the alveolar . This process sustains the lesion's progression unless the underlying is addressed.

Theories

The formation of periapical cysts has been explained through several historical and contemporary theories that extend beyond the basic inflammatory response. One early proposal, the nutritional deficiency theory, posits that proliferating epithelial rests of Malassez form a central mass where inner cells undergo due to insufficient supply from surrounding inflamed tissue, creating a cavity lined by viable peripheral . This model, largely outdated in light of subsequent histological evidence showing consistent epithelial proliferation rather than central degeneration as the primary driver, dominated mid-20th-century understandings but has been superseded by more dynamic explanations. Another historical perspective, the abscess theory, suggests that cysts arise when epithelial cells ingress and line a pre-existing abscess cavity formed by in the periapical . This view, which implied cyst development as a secondary organization of an acute suppurative process, gained traction in the late but was discredited by post-2000 studies demonstrating that true form through continuous epithelial proliferation without reliance on prior abscess formation, as evidenced by experimental models and histopathological analyses. The biomechanical theory addresses cyst expansion mechanisms, proposing that hydrostatic pressure gradients within the cyst lumen—arising from osmotic forces due to protein accumulation—and surrounding tissue tension drive progressive enlargement independent of further epithelial growth. This model highlights physical forces as key to the lesion's size, supported by observations of in cystic structures. Biochemical theories emphasize molecular signals stimulating epithelial proliferation, including colony-stimulating factors (CSFs) that regulate hematopoietic and epithelial cell differentiation, as well as proinflammatory cytokines like interleukin-1 and interleukin-6 that act as growth promoters for epithelial rests in the inflamed periapical environment. These factors, released during chronic , foster autonomous cyst wall development by enhancing and survival. Contemporary views integrate these elements into a cohesive model stressing epithelial-mesenchymal interactions, where stromal cells, components, and bone-derived signals interact with epithelial rests to sustain through reciprocal signaling pathways. Recent reviews underscore this holistic approach, noting roles for growth factors and in modulating epithelium-mesenchymal crosstalk to promote persistent formation.

Diagnosis

Clinical examination

Clinical examination of a periapical cyst, also known as a radicular cyst, begins with a thorough patient history to identify potential predisposing factors. Inquiry focuses on previous dental caries, trauma to the affected tooth, or prior endodontic treatments, as these are commonly associated with pulp necrosis leading to cyst formation. Visual inspection reveals possible extraoral or intraoral signs, such as facial asymmetry or gingival swelling over the apex of the involved in larger lesions. Intraorally, one may observe sinus tracts draining from the gingival surface, discoloration indicating pulp , or a bluish hue to the mucosa if the is superficial. Palpation assesses for tenderness or bony expansion at the apical region. Early lesions may present as a smooth, hard prominence without pain, while advanced cases show fluctuance if the cortical bone is thinned or eroded, and tenderness upon digital pressure along the vestibular mucosa. Percussion testing involves tapping the crown of the suspected vertically and horizontally; a positive response, characterized by sharp , suggests periapical , often linked to symptoms like on . Mobility testing may indicate grade 1 or higher tooth displacement if the cyst has caused significant around the root apex. Pulp vitality tests confirm non-vitality of the affected , essential for suspecting a periapical cyst. Thermal tests using cold or heat, or electric pulp testing, typically elicit no response in the involved , distinguishing it from vital pulps in other odontogenic lesions.

Radiographic features

On periapical radiographs, periapical cysts typically appear as well-defined, round or ovoid unilocular radiolucencies centered at the apex of a non-vital , often measuring 0.5 to 1.5 cm in diameter with a sclerotic or corticated border continuous with the . These lesions may show associated findings such as deep carious lesions, periapical , or external root resorption, reflecting the underlying pulpal . Cone-beam computed tomography (CBCT) provides superior three-dimensional assessment of periapical cysts compared to two-dimensional , revealing low-density lesions with precise delineation of size, buccolingual expansion, and involvement of the cortical plates or adjacent structures, alongside loss of the at the root apex. This modality is particularly valuable for evaluating the extent of bone involvement in larger cysts, which may perforate the cortical bone. Magnetic resonance imaging (MRI) of periapical cysts demonstrates low signal intensity on T1-weighted images and high signal intensity on T2-weighted images due to the fluid content, often appearing as well-defined, non-enhancing lesions useful for assessing extension or differentiating from granulomas. In cases of diagnostic uncertainty, MRI highlights homogeneous internal texture and lack of surrounding tissue involvement, aiding in confirmation. Radiographically, lesions exceeding 5-6 mm in diameter are more likely to represent cysts rather than granulomas, though definitive differentiation often requires histopathological correlation.

Histopathological findings

The histopathological diagnosis of a periapical cyst is established by the identification of a cystic cavity completely lined by non-keratinized stratified squamous epithelium, typically measuring 6-20 cells in thickness and often exhibiting a characteristic arcading pattern formed by rete ridges projecting into the fibrous wall. This epithelial lining may show metaplastic changes, including the presence of mucous or ciliated cells, particularly in cysts associated with the maxillary sinus, though such features are not universal. The cyst wall consists of fibrous of variable thickness, infiltrated by a chronic inflammatory response primarily composed of lymphocytes and plasma cells, with occasional foamy macrophages and multinucleated giant cells surrounding cholesterol clefts. The inflammatory infiltrate is typically moderate to dense in the subepithelial zone, reflecting the ongoing to persistent endodontic . The cystic lumen is filled with proteinaceous fluid and desquamated epithelial cells, frequently accompanied by clefts derived from disintegrating inflammatory cells and occasionally bodies known as Rushton bodies, which appear as , crescent-shaped structures within the epithelial lining or lumen. In instances of secondary bacterial , the lumen or wall may contain bacterial colonies, purulent material, and an acute inflammatory component with neutrophilic infiltration and epithelial ulceration. Histopathological evaluation remains the gold standard for distinguishing periapical cysts from periapical granulomas, as the former demonstrate a continuous epithelial lining enclosing a defined lumen, whereas granulomas lack such a complete cystic structure and instead feature with focal epithelial rests amid dense chronic . This differentiation is crucial for confirming the , though both cysts and granulomas often resolve with nonsurgical endodontic .

Differential diagnosis

The differential diagnosis of a periapical cyst primarily involves it from other periapical s that may present with similar radiographic appearances, such as well-defined radiolucencies at the tooth apex. Accurate differentiation is crucial, as it influences management decisions, with histopathological examination often required for confirmation. Periapical granuloma is a common mimic, typically presenting as a smaller (often less than 10 mm in diameter) composed of chronic inflammatory without a complete epithelial lining, in contrast to the true cystic cavity of a periapical cyst. Radiographically, both appear as periapical radiolucencies associated with non-vital teeth, but granulomas tend to show less cortication and respond more reliably to therapy due to their lack of a self-sustaining epithelial barrier. Periapical abscess differs markedly in its acute clinical presentation, featuring accumulation, severe , swelling, and systemic symptoms, whereas periapical cysts are usually chronic lesions. Radiographically, abscesses exhibit ill-defined, diffuse radiolucencies with possible cortical , lacking the well-defined borders typical of cysts, and histologically show purulent inflammation rather than an epithelial-lined cavity. Odontogenic keratocyst may occasionally mimic a periapical cyst radiographically, particularly when inflamed, but is distinguished by its parakeratinized stratified squamous epithelial lining with a uniformly thin, corrugated surface and palisaded basal layer, along with a higher recurrence rate (up to 30%) and potential for multilocular expansion. Unlike periapical cysts, which arise from epithelial remnants in inflamed pulp, odontogenic keratocysts originate from dental lamina and are not directly tied to non-vital teeth. Central giant cell granuloma can resemble a periapical cyst on , especially in unilocular forms near tooth apices, but typically appears multilocular with internal bony and is more aggressive, particularly in young patients under 30 years, leading to cortical expansion or tooth displacement. Histologically, it features multinucleated giant cells in a fibrous stroma without an epithelial lining, differentiating it from the cystic structure of periapical lesions. Malignancies such as must be considered in persistent or periapical radiolucencies, characterized by irregular, ill-defined borders, rapid growth, bone destruction, and possible involvement of vital teeth, unlike the association of periapical cysts with non-vital teeth. Histological evidence of cellular , , or dysplastic changes confirms , which rarely arises de novo but may transform from long-standing odontogenic cysts.

Management

Non-surgical treatment

Non-surgical treatment of periapical cysts primarily involves root canal therapy (RCT), a conservative endodontic procedure that eliminates infection through mechanical , chemical disinfection, and hermetic of the root canal system. This approach targets the necrotic pulp and microbial content responsible for cyst formation, allowing the to resolve via decompression and immune-mediated repair, with higher success for pocket cysts compared to true cysts. RCT is performed in one or multiple visits, often using rotary instrumentation and irrigants such as 1% to disrupt biofilms and remove debris. Indications for RCT include periapical lesions associated with non-vital teeth, though vital pulp preservation is possible but rare in cyst cases due to the underlying pulpal necrosis. For immature permanent teeth with open apices and associated cysts, apexification is integrated, involving placement of calcium hydroxide or mineral trioxide aggregate to induce an apical hard tissue barrier and facilitate obturation. Systemic antibiotics, such as amoxicillin, are reserved for acute symptomatic infections with swelling or fever, while intracanal medicaments like calcium hydroxide paste provide sustained disinfection and alkalinity to inhibit bacterial growth between appointments. Radiographic follow-up is essential, with evaluations at 6-12 months post-treatment to assess resolution through reduction in radiolucency and bone regeneration, using criteria like the Periapical Index. Success rates for resolution via RCT vary by lesion size and criteria; meta-analyses report approximately 87% healing for periapical lesions under loose criteria, with 66-67% under strict criteria for larger cyst-like lesions, and overall rates of 85-90% for associated endodontic infections.

Surgical treatment

Surgical treatment is reserved for periapical cysts that do not resolve with non-surgical endodontic therapy or present as large, symptomatic lesions requiring direct intervention. These procedures aim to remove the cystic tissue, eliminate the infection source, and promote , often using microsurgical techniques for enhanced precision and outcomes. Apicoectomy, also known as root-end resection, is a primary surgical approach for managing persistent periapical cysts associated with vital or previously treated teeth. The procedure involves raising a full-thickness mucoperiosteal flap, performing to access the apex, resecting 3-5 mm of the root tip with a fissure , and preparing a retrograde cavity ultrasonically for sealing with biocompatible materials such as (MTA). This isolates the cyst from the system while preserving the tooth. Microsurgical apicoectomy yields success rates of 86-92% in healing periapical lesions, including cystic ones, based on radiographic and clinical evaluations over 1-4 years. Cystectomy entails complete enucleation of the lining through surgical excision and thorough of the cystic cavity to remove all pathological tissue. It is indicated for isolated periapical not encroaching on vital structures like the or . The procedure is performed via a buccal or palatal flap, with the cyst wall carefully dissected and the bony defect irrigated before closure. When combined with , achieves favorable healing without reported recurrence in case follow-ups up to 1 year. For larger periapical cysts, serves as a decompression technique to reduce size prior to definitive enucleation, thereby protecting adjacent vital structures. The process involves creating a surgical window in the cyst wall, suturing the lining to the , and placing a decompression device or for drainage and gradual shrinkage over weeks to months. This conservative approach promotes osseous regeneration and is particularly useful in infected cases, with radiographic of near-complete resolution in 9 weeks to 1 year. Tooth extraction is considered when the affected tooth is non-restorable due to extensive structural damage or poor , followed by immediate or delayed removal to address residual . Post-extraction, the socket is curetted to excise any cystic remnants, and primary closure is achieved. This method ensures elimination but sacrifices the tooth, making it a last resort in endodontic . Adjunctive regenerative techniques, such as guided tissue regeneration (GTR) with resorbable membranes and grafts (e.g., bovine xenograft), enhance in bony defects following or . These materials are placed into the defect after retrograde filling to support new formation and soft tissue barrier function. Application of GTR in radicular cases has demonstrated complete periapical and cortical regeneration within 6 months, improving long-term outcomes in through-and-through defects.

Prognosis and prevention

Prognosis

With appropriate endodontic treatment, periapical cysts exhibit an excellent , with resolution rates of 90-95% observed on follow-up radiographs at 1 year post-treatment. The recurrence rate is generally low at less than 5%, with rates as low as 1.6% reported for residual cysts resulting from incomplete removal during initial intervention. Several factors influence treatment outcomes, including cyst size, where lesions exceeding 1 cm in diameter are associated with poorer healing rates due to increased complexity and potential for persistent . Patient compliance with follow-up care and protocols is critical for success, as non-adherence can compromise long-term stability. Additionally, comorbidities such as diabetes mellitus negatively impact prognosis by delaying periapical repair and increasing the likelihood of persistent lesions, even after proper treatment. Healing typically manifests as progressive bone fill-in over 6-24 months, monitored via serial radiographs, with complete resolution indicating successful outcome. Persistent radiolucency beyond this period often signals treatment failure, necessitating re-evaluation or surgical intervention. In the long term, the risk of following treatment remains low, with transformation rates estimated at around 0.2% based on recent pathological analyses.

Prevention

Preventing the development of periapical cysts primarily involves strategies to avoid pulpal , which arises from untreated dental caries, trauma, or other insults to the tooth pulp. Regular dental check-ups are essential, allowing for early detection and prompt treatment of caries or other issues that could progress to pulp and . By addressing these problems before they lead to irreversible damage, the risk of cyst formation can be significantly reduced. Maintaining rigorous oral hygiene practices forms the cornerstone of prevention. Brushing teeth at least twice daily with fluoride toothpaste, flossing regularly, and using antimicrobial mouthwashes help minimize plaque accumulation and bacterial load, thereby preventing caries that could invade the pulp. Incorporating , whether through or community , strengthens enamel and reduces caries incidence by approximately 25% in both children and adults. For individuals at risk of dental trauma, such as athletes or those in contact sports, protective measures like custom-fitted mouthguards are highly effective. These devices absorb impact and prevent direct injury to teeth, reducing the incidence of luxations, fractures, or avulsions that might necessitate endodontic intervention and lead to development. Studies indicate that mouthguards can decrease sports-related dental injuries by up to 60 times compared to not wearing one. Patient education plays a vital role in early intervention. Informing individuals about symptoms of , such as sensitivity to temperature or spontaneous pain, encourages timely dental visits to halt progression to and subsequent formation. At the level, initiatives like community and improved access to dental care in underserved populations are crucial. These measures not only promote widespread caries prevention but also address disparities in oral health, indirectly lowering the overall incidence of periapical pathologies.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK574529/
  2. https://pmc.ncbi.nlm.nih.gov/articles/PMC3448196/
  3. https://www.sciencedirect.com/science/article/pii/S1607551X17307659
  4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7398993/
  5. https://pmc.ncbi.nlm.nih.gov/articles/PMC5149102/
  6. https://www.pathologyoutlines.com/topic/mandiblemaxillaperiapicalcyst.html
  7. https://www.aae.org/specialty/a-concise-guide-to-pathology-within-endodontics/
  8. https://suffolkrootcanal.co.uk/wp-content/uploads/2015/04/Non-microbial-etiology-periapical-cysts-sustain-post-treatment-apical-periodontitis-Nair-2003.pdf
  9. https://www.turkjpath.org/doi.php?doi=10.5146/tjpath.2017.01410
  10. https://journals.lww.com/npmj/fulltext/2024/31030/prevalence%2C_characteristics_and_distribution_of.8.aspx
  11. https://www.sciencedirect.com/science/article/pii/0300571288900048
  12. https://onlinelibrary.wiley.com/doi/10.1111/odi.15146
  13. https://pmc.ncbi.nlm.nih.gov/articles/PMC12070580/
  14. https://www.sciencedirect.com/topics/medicine-and-dentistry/periapical-cyst
  15. https://pmc.ncbi.nlm.nih.gov/articles/PMC3532737/
  16. https://pmc.ncbi.nlm.nih.gov/articles/PMC11205176/
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC3125643/
  18. https://journals.lww.com/njcp/fulltext/2023/08000/prevalence_of_odontogenic_cysts_in_a_group_of.16.aspx
  19. https://www.researchgate.net/publication/6868806_The_range_and_demographics_of_odontogenic_cysts_in_a_UK_population
  20. https://www.sciencedirect.com/science/article/pii/S2667147625000445
  21. https://www.researchgate.net/publication/274509942_CLOSURE_OF_FISTULA_OROANTRAL_CAUSED_BY_A_MAXILLARY_EXTENDED_RADICULAR_CYST_USING_A_PALATAL_CONNECTIVE_TISSUE_GRAFT_A_CASE_REPORT
  22. https://jag.journalagent.com/z4/download_fulltext.asp?pdir=tej&plng=eng&un=TEJ-65265
  23. https://www.bibliomed.org/fulltextpdf.php?mno=69559
  24. https://www.cureus.com/articles/423909-unusual-presentation-of-odontogenic-cellulitis-mimicking-drug-induced-angioedema-a-case-report
  25. https://journals.lww.com/cancerjournal/fulltext/2020/16030/primary_intraosseous_squamous_cell_carcinoma.50.aspx
  26. https://www.mdpi.com/2673-6373/4/3/29
  27. https://www.tandfonline.com/doi/full/10.1080/19424396.2024.2413577
  28. https://pmc.ncbi.nlm.nih.gov/articles/PMC7398993/
  29. https://pmc.ncbi.nlm.nih.gov/articles/PMC11835764/
  30. https://www.ncbi.nlm.nih.gov/books/NBK589656/
  31. https://www.sciencexcel.com/articles/uBSMdS6OOQb5q0q4LwJI3y0ODGSo3nJkjh5dRTAt.pdf
  32. https://www.medicoverhospitals.in/diseases/periapical-cyst/
  33. https://pmc.ncbi.nlm.nih.gov/articles/PMC7692336/
  34. https://pmc.ncbi.nlm.nih.gov/articles/PMC3448330/
  35. https://personal.us.es/segurajj/documentos/CV-Art%2520JCR/89-CLOI-Diabetes-AP-2016.pdf
  36. https://pmc.ncbi.nlm.nih.gov/articles/PMC8635037/
  37. https://ajph.aphapublications.org/doi/full/10.2105/AJPH.2013.301699
  38. https://onlinelibrary.wiley.com/doi/10.1111/cdoe.12110
  39. https://jpedres.org/articles/the-prevalence-of-sports-related-dental-injuries-and-the-rate-of-awareness-of-mouthguard-use-among-child-athletes/jpr.galenos.2020.92678
  40. https://endosd.com/traumatic-dental-injuries/
  41. https://www.researchgate.net/publication/354342743_Comparative_Metabolomics_Reveals_the_Microenvironment_of_Common_T-Helper_Cells_and_Differential_Immune_Cells_Linked_to_Unique_Periapical_Lesions
  42. https://www.nature.com/articles/s41598-019-55293-6
  43. https://www.sciencedirect.com/science/article/abs/pii/S0099239907001707
  44. https://pubmed.ncbi.nlm.nih.gov/17878074/
  45. https://www.jscimedcentral.com/jounal-article-info/JSM-Dental-Surgery/Radicular-Cysts-Review-5689
  46. https://bmcoralhealth.biomedcentral.com/articles/10.1186/s12903-018-0586-3
  47. https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1366954/full
  48. https://www.sciencedirect.com/science/article/pii/S0099239987800961
  49. https://pmc.ncbi.nlm.nih.gov/articles/PMC2719712/
  50. https://pubmed.ncbi.nlm.nih.gov/25346864/
  51. https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-2591.1998.00146.x
  52. https://link.springer.com/chapter/10.1007/978-981-15-1346-6_27
  53. https://journals.sagepub.com/doi/10.1177/154411130401500604
  54. https://www.sciencedirect.com/science/article/abs/pii/S0099239915008043
  55. https://pmc.ncbi.nlm.nih.gov/articles/PMC10098462/
  56. https://pmc.ncbi.nlm.nih.gov/articles/PMC10642913/
  57. https://pmc.ncbi.nlm.nih.gov/articles/PMC8336380/
  58. https://www.thieme-connect.de/products/ebooks/pdf/10.1055/b-0034-65757.pdf
  59. https://pmc.ncbi.nlm.nih.gov/articles/PMC11132303/
  60. https://radiopaedia.org/articles/periapical-cyst?lang=us
  61. https://insightsimaging.springeropen.com/articles/10.1007/s13244-013-0298-9
  62. https://pubs.rsna.org/doi/full/10.1148/rg.331125172
  63. https://pmc.ncbi.nlm.nih.gov/articles/PMC10102671/
  64. https://www.cell.com/heliyon/fulltext/S2405-8440%2820%2932037-5
  65. https://ajronline.org/doi/10.2214/AJR.09.7216
  66. https://pmc.ncbi.nlm.nih.gov/articles/PMC5966810/
  67. https://entokey.com/odontogenic-cysts-tumors-and-related-jaw-lesions/
  68. https://suffolkrootcanal.co.uk/wp-content/uploads/2015/04/The-nature-of-the-periapical-lesion-1108-cases-Stockdale-1988.pdf
  69. https://patholines.org/Jaw_cysts
  70. https://bmcoralhealth.biomedcentral.com/articles/10.1186/s12903-024-04110-2
  71. https://www.nature.com/articles/s41598-020-71029-3
  72. https://pubmed.ncbi.nlm.nih.gov/16674747/
  73. https://pmc.ncbi.nlm.nih.gov/articles/PMC10063769/
  74. https://pmc.ncbi.nlm.nih.gov/articles/PMC3010029/
  75. https://pmc.ncbi.nlm.nih.gov/articles/PMC3769875/
  76. https://pmc.ncbi.nlm.nih.gov/articles/PMC5198479/
  77. https://www.jendodon.com/article/S0099-2399%2824%2900441-2/abstract
  78. https://pmc.ncbi.nlm.nih.gov/articles/PMC11188004/
  79. https://pmc.ncbi.nlm.nih.gov/articles/PMC7558840/
  80. https://pmc.ncbi.nlm.nih.gov/articles/PMC2980615/
  81. https://pubmed.ncbi.nlm.nih.gov/26731964/
  82. https://pmc.ncbi.nlm.nih.gov/articles/PMC10955527/
  83. https://pmc.ncbi.nlm.nih.gov/articles/PMC10943812/
  84. https://pmc.ncbi.nlm.nih.gov/articles/PMC3487520/
  85. https://pmc.ncbi.nlm.nih.gov/articles/PMC8916606/
  86. https://pmc.ncbi.nlm.nih.gov/articles/PMC7746164/
  87. https://pmc.ncbi.nlm.nih.gov/articles/PMC4670252/
  88. https://pmc.ncbi.nlm.nih.gov/articles/PMC10907570/
  89. https://pmc.ncbi.nlm.nih.gov/articles/PMC9319780/
  90. https://pmc.ncbi.nlm.nih.gov/articles/PMC11287039/
  91. https://pmc.ncbi.nlm.nih.gov/articles/PMC8156608/
  92. https://pmc.ncbi.nlm.nih.gov/articles/PMC11997300/
  93. https://www.researchgate.net/publication/344316057_Early_Malignant_Transformation_of_Radicular_Cyst_Two_Cases_and_Literature_Review_of_the_Recent_Decade
  94. https://www.merckmanuals.com/professional/dental-disorders/common-dental-disorders/pulpitis
  95. https://my.clevelandclinic.org/health/diseases/24896-periapical-abscess
  96. https://www.profdroguzhangorler.com/dental-and-jaw-cysts
  97. https://www.kin.es/en/patologias/quiste-periapical/
  98. https://lecroydental.com/understanding-periapical-cysts-causes-symptoms-and-effective-treatments/
  99. https://www.rockendony.com/understanding-the-role-of-endodontics-in-treating-oral-cysts/
  100. https://www.cdc.gov/oral-health/data-research/facts-stats/fast-facts-community-water-fluoridation.html
  101. https://www.ada.org/about/press-releases/community-water-fluoridation-prevents-painful-dental-disease
  102. https://www.aapd.org/research/oral-health-policies--recommendations/prevention-of-sports-related-orofacial-injuries/
  103. https://pmc.ncbi.nlm.nih.gov/articles/PMC4148563/
  104. https://www.dentalhealth.org/keeping-your-mouth-safe-while-playing-sport
  105. https://my.clevelandclinic.org/health/diseases/23536-pulpitis
  106. https://promenade-dentist.com/reversible-pulpitis-symptoms/
  107. https://www.cdc.gov/mmwr/preview/mmwrhtml/mm4841a1.htm
  108. https://www.cdc.gov/fluoridation/about/statement-on-the-evidence-supporting-the-safety-and-effectiveness-of-community-water-fluoridation.html
Add your contribution
Related Hubs
User Avatar
No comments yet.