Abstract
While radiolucent periapical lesions have been extensively studied to avoid misdiagnosis of apical periodontitis with non-endodontic lesions, radiopaque lesions in the periapical region are equally significant in dental practice. The diagnosis and management of these radiopaque or hyperdense lesions present a considerable challenge for clinicians. These osseous alterations can stem from neoplastic, dysplastic, or metabolic origins. With the increasing utilization of cone-beam CT in dentistry, a thorough review of radiopaque lesions, both inflammatory and non-inflammatory, is crucial. Such a review aids clinicians in formulating a robust differential diagnosis. Distinguishing between inflammatory and non-inflammatory lesions is paramount for accurate diagnosis and appropriate treatment planning. This article provides a detailed review of the current literature, encompassing clinical, radiographic, histological, and management aspects of radiopaque and hyperdense jaw lesions, with a focus on their differential diagnosis.
Keywords: Radiopaque Lesions of the Jaw, Differential Diagnosis, Periapical Periodontitis, Cone Beam Computed Tomography, Oral Pathology
Introduction
Accurate diagnosis is the cornerstone of effective therapeutic protocols for root canal infections and associated periapical conditions.[1] Periapical changes, frequently encountered in dental practice, include dental granulomas, radicular cysts, and periapical abscesses.[2] These conditions are typically associated with bone resorption, manifesting as radiolucencies on radiographic examinations.[3] However, radiopaque lesions also occur in the periapical region and warrant careful consideration as they may originate from both endodontic and non-endodontic causes.[4] Low-grade chronic periapical inflammation can induce both osteoblastic and osteoclastic activity, leading to varied radiographic presentations.[5]
Advanced imaging techniques play a vital role in diagnosing radiopaque lesions, providing essential information on lesion margins, relationships with adjacent teeth, and internal content, particularly in lesions with calcified components.[6] While considerable research has focused on radiolucent periapical lesions to prevent misdiagnosis of apical periodontitis with other radiolucent entities,[4, 7] radiopaque lesions in the periapical area are equally relevant to endodontic practice and demand thorough investigation.[8, 9, 10, 11]
Endodontic diagnosis relies heavily on both clinical and radiographic examinations. Periapical radiographs and cone beam computed tomography (CBCT) are indispensable tools for detecting and diagnosing inflammatory, dysplastic, and neoplastic periapical diseases.[12, 13, 14] For many clinicians, the diagnosis and management of radiopaque and hyperdense lesions can be particularly complex. Bender and Mori highlighted the diagnostic considerations of periapical and periodontal radiopacities of endodontic and periodontal origin as early as 1985.[15] A contemporary and detailed review of radiopaque lesions, encompassing both inflammatory and non-inflammatory types, is highly relevant and can significantly assist endodontists and general dental practitioners in establishing accurate differential diagnoses.
This review aims to provide an in-depth analysis of the existing literature concerning the clinical, radiographic, histological, and management aspects of radiopaque and hyperdense lesions of the jaws. It further explores the differential diagnoses of these lesions, offering a practical guide for clinicians.
Methodology
This review employed a comprehensive search strategy using the PubMed online database to identify relevant studies, reviews, and case reports on radiopaque and hyperdense lesions of the jaws, with a particular focus on those occurring in the periapical region. The search was limited to articles published in English in indexed dental and medical journals, focusing on the following aspects of radiopaque lesions: etiology, clinical presentation, radiographic characteristics, histological features, and management strategies. Manual searches were also conducted in key journals including the Journal of Endodontics, Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, Oral Oncology, International Endodontic Journal, and Head and Neck Pathology. Article selection was based on the authors’ expert judgment regarding the relevance and pertinence of the information, representing diverse dental specialties (endodontics, oral pathology, oral radiology, and oral medicine). The World Health Organization (WHO) Classification of Head and Neck Tumours[16] and the widely recognized textbook “Oral and Maxillofacial Pathology” by Neville et al.[2] were utilized as authoritative references, particularly to resolve any discrepancies or information gaps found in the selected articles. This comprehensive approach identified 22 distinct entities described in the literature, which were broadly categorized as inflammatory, non-inflammatory, neoplastic, and metabolic in nature (Table 1). The subsequent sections detail the clinical and radiographic features of specific diseases within these four categories, aiding in the differential diagnosis of radiopaque lesions of the jaw.
[Table 1: Clinical, radiographic and epidemiological features of radiopaque/hyperdense lesions.]
Results
Inflammatory Lesions
Reactional Osteogenesis
Reactional osteogenesis (RO) is a recently characterized asymptomatic, localized radiopaque lesion found within the maxillary sinus, often associated with a molar apex compromised by secondary root canal infection. RO is postulated to be a reactive bone formation of the sinus mucosa in response to chronic, low-grade inflammatory stimuli originating from an infected root canal. This reaction results in new bone apposition on the superficial cortical bone of the maxillary sinus.[12] Radiographically, RO is typically an incidental finding, presenting as an ill-defined, dome-shaped radiopaque thickening, mimicking a retention pseudocyst on conventional radiographs. CBCT imaging reveals RO as a hyperdense, well-defined lesion, ranging in shape from irregular to round or ovoid (Figure 1, A–C). Currently, only four cases, described by Estrela et al., have been reported in the literature, highlighting the rarity of this entity.[12] In their study, all cases were observed in female patients within the fifth to seventh decades of life. Histologically, RO exhibits bone tissue at various stages of maturation, including concentric lamellae, organized Haversian systems, mature bone tissue, marrow, and inflammatory cell infiltrates. Treatment strategies for RO focus on eradicating the causative root canal infection, thereby resolving the maxillary sinus inflammation and associated bone reaction. Endodontic treatment is the primary approach; however, surgical intervention may be necessary if the apical infection persists.
Condensing Osteitis (Focal Sclerosing Osteomyelitis)
Condensing osteitis (CO), also known as focal sclerosing osteomyelitis, is an asymptomatic, pathological alteration in bone structure considered to be a response to prolonged, low-grade inflammatory stimuli from an inflamed or necrotic dental pulp.[17] CO manifests on periapical radiographs as a diffuse radiopaque bone lesion in the alveolar process, predominantly associated with the apex of a mandibular premolar or molar, or at a tooth extraction site. Clinically, CO is typically associated with teeth exhibiting signs of pulp disease, such as deep caries or extensive restorations.[18, 19] CO may also present adjacent to radiolucent inflammatory periapical lesions (granulomas, cysts, and abscesses) (Figure 1, D) or an enlarged periodontal ligament space.[6] CBCT imaging reveals CO as an ill-defined, non-expanding sclerotic lesion associated with an infected tooth (Figure 1, E). Epidemiological studies on CO show considerable variability; however, it is commonly detected between the third and seventh decades of life, with no significant gender predilection.[20] Biopsy is generally not required for CO diagnosis, and its histological characteristics have only recently been comprehensively described. Microscopically, CO demonstrates dense layers of compact bone replacing bone marrow and cancellous bone. Fibrosis and inflammation may be occasionally observed in the bone marrow region.[18] Diagnosis of condensing osteitis is primarily based on clinical and radiographic findings. The recommended treatment is root canal therapy to eliminate the source of infection.[19]
Osteomyelitis of the Jaw
Osteomyelitis is defined as an inflammatory condition affecting the medullary and cancellous portions of bone, extending to the Haversian systems and potentially involving the periosteum of the affected area.[20] Osteomyelitis predominantly affects the mandible, with maxillary involvement being less frequent, likely due to the maxilla’s richer vascular supply.[6] Odontogenic infections are the most common etiological factor; however, in some cases, the cause remains undetermined.[21] The diverse clinical and pathological presentations of jaw osteomyelitis have led to numerous classifications. This review focuses on stages of osteomyelitis that may induce radiopaque changes visible on imaging.
Chronic osteomyelitis (COS) is characterized by bone infection persisting for at least one month.[22, 23, 24] The etiology of chronic osteomyelitis can be non-specific, and its clinical presentation varies from localized lesions to extensive involvement of the hemi-mandible.[23] Symptoms of chronic osteomyelitis are also variable, ranging from mild to severe, and may include limited jaw opening. Patients in this stage may not present with systemic signs of infection such as fever, leukocytosis, or suppuration, but may exhibit mandibular enlargement without overt soft tissue involvement. Chronic osteomyelitis affects all age groups, with incidence peaks in adolescence and after 50 years of age. In some cases, chronic osteomyelitis presents with more pronounced infectious foci, suppuration, intra- and extraoral fistulae, and soft tissue involvement. Sequestration and pathological fractures may occur in later stages.[21] Imaging exams are crucial for differentiating chronic osteomyelitis from malignant tumors; however, biopsy is indicated when radiographic findings are inconclusive regarding the inflammatory nature of the lesion.[23] Early chronic osteomyelitis may present as a mixed radiolucent/radiopaque area with varying degrees of periosteal reaction and subperiosteal bone formation, often progressing to sclerotic changes in later stages (Figure 1, F–G).[23] Treatment for both acute and chronic osteomyelitis involves eradicating the causative microorganisms with broad-spectrum antibiotics, surgical removal of infected teeth, debridement of infected bone, and sequestrectomy of necrotic bone fragments.[26] Decortication of cortical plates to access infected medullary bone or surgical resection may be required for chronic refractory osteomyelitis.[24]
Osteomyelitis with proliferative periostitis (OSPP) represents a specific type of chronic osteomyelitis characterized by an inflammatory reaction leading to periosteal new bone formation. This condition has been described using various terms, including proliferative periostitis, periostitis ossificans, and Garre’s osteomyelitis. While some consider OSPP synonymous with Garre’s osteomyelitis, Garre’s osteomyelitis may be more accurately defined as acute osteomyelitis with inflammatory periosteal new bone formation. OSPP is typically associated with odontogenic infections, often of endodontic origin, and usually presents as a localized, slow-growing swelling along the inferior border and buccal cortex of the mandible in the molar region.[27] Radiographically, OSPP is characterized by radiopaque concentric parallel layers of new bone deposition in the periosteal region, giving an “onion skin” appearance, without cortical perforation. Histologically, all types of chronic osteomyelitis primarily show irregular, reactive woven bone or sclerotic bone with occluded Haversian systems and varying degrees of marrow fibrosis. Marked osteoblastic rimming and inflammatory cells (both acute and chronic) may be present in chronic osteomyelitis specimens.[23] Treatment for OSPP involves removing the source of infection, which may include endodontic treatment or tooth extraction. Resolution of the infection typically promotes bone remodeling. Surgical remodeling may be indicated in cases of extensive lamellar bone growth.[27]
Non-Inflammatory Lesions
Idiopathic Osteosclerosis
Idiopathic osteosclerosis (IO) is an asymptomatic, non-expansile, localized radiopaque lesion observed in the alveolar process, primarily in posterior regions, with no identifiable etiological factor.[28] IO most frequently occurs in the periapical region of the mandibular first molar, followed by the mandibular first and second premolars.[29] IO lesions can be positioned in several ways: superimposed over the root of a tooth with a less distinct periodontal membrane, underlying the apex of a tooth but separated from the root by a visible periodontal membrane, or further away from a tooth, closer to the inferior border.[30] Radiographically, IO is characterized by a well-defined bony radiopaque or hyperdense lesion, which can appear as a round, elliptical, or irregular mass with a ground-glass appearance (Figure 1, G–H).[28, 31] Diagnosis of IO is usually based on radiographic and clinical findings, such as radiopaque areas subjacent to the apices of asymptomatic teeth with minimal or no restorations, and without any other apparent cause.[30] Long-term studies have indicated that IO is a stable condition requiring no intervention for either the lesion or the adjacent tooth.[28] Although biopsy is typically unnecessary, the microscopic features of IO include dense lamellar bone and small marrow channels without inflammatory cell infiltration.
Cemento-Osseous Dysplasia
Cemento-osseous dysplasia (COD) is the most prevalent fibro-osseous lesion of the jaws. COD encompasses a group of benign lesions of unknown etiology characterized by the replacement of normal bone with fibrous tissue and newly formed mineralized structures.[32] COD lesions exhibit a spectrum of radiographic appearances, ranging from entirely radiolucent to radiopaque, depending on the lesion’s stage of maturation. COD is categorized into three subtypes based on radiographic presentation: focal COD, periapical COD, and florid COD. All three subtypes are usually discovered incidentally on routine radiographs.[16]
Focal COD is an asymptomatic, solitary lesion typically found in the posterior quadrants of the jaws, either near a tooth root or in an edentulous area.[18] It is more commonly observed in the posterior mandible of women, with a mean age of 30-40 years, and shows a higher prevalence among Black individuals.[33] Periapical COD is also asymptomatic and occurs adjacent to tooth-bearing areas, specifically associated with one or more vital mandibular anterior teeth. It predominantly affects middle-aged women and also demonstrates a strong predilection for Black patients.[34] Florid COD is diagnosed when the lesion involves two or more quadrants of the jaw, usually affecting the mandible bilaterally and sometimes extending to the maxilla. Florid COD is more common in middle-aged Black women, although it can affect other age, racial, and gender groups.[18]
Radiographically, COD typically progresses through different phases, from a completely radiolucent lesion to mixed or radiopaque lesions near the apices of mandibular teeth or at extraction sites. The radiolucent phase may resemble periapical endodontic infections; however, pulp vitality tests are positive. Mixed and radiopaque lesions are generally round, with a well-defined radiolucent rim surrounding the radiopaque area, and are distinctly separated from the tooth root (Figure 2, A–D).[18]
Histopathologically, COD exhibits diverse patterns of calcified structures. Early-stage COD shows a vascular fibrous stroma with osteoid and some basophilic cementoid structures. In later stages, the stroma becomes more fibrotic, with more defined osteoid trabeculae, thicker curvilinear bony trabeculae, and potentially prominent cementoid masses. When clinical and radiographic features are clearly indicative of COD, biopsy and surgical intervention are generally unnecessary.[18] However, periodic radiographic follow-up is recommended to confirm the diagnosis[34] and to monitor for potential odontogenic infections in overlying teeth. Due to the avascular and dysplastic nature of COD bone, odontogenic infections can lead to widespread contamination, potentially progressing to osteomyelitis and bone sequestration (Figure 2, C).[18]
Fibrous Dysplasia
Fibrous dysplasia (FD) is a benign developmental disorder characterized by dysplastic osteogenesis, resulting in the replacement of normal bone with fibrous tissue that undergoes abnormal mineralization. Its pathogenesis is linked to mutations in the gene encoding the G protein alpha-subunit (Gs-alpha), disrupting guanosine triphosphatase function and increasing cyclic adenosine monophosphate (cAMP) levels, which stimulate endocrine receptors. Elevated intracellular cAMP levels in bone marrow osteoprogenitor cells are believed to affect preosteoblast proliferation and differentiation.[18, 35] FD can present as a single bone lesion (monostotic form) or multiple bone lesions (polyostotic form). The polyostotic form is less common and may be associated with McCune-Albright syndrome, characterized by hormonal changes, precocious puberty, skin pigmentation, and other endocrine disturbances.[36] The monostotic form is more frequent and can affect craniofacial bones, with the maxilla being more commonly involved than the mandible. FD lesions typically occur in the first to third decades of life, with no gender or racial predilection. Clinically, monostotic FD presents as asymptomatic bone swelling, potentially causing buccolingual and inferior cortical bone expansion, maxillary sinus obliteration, root and tooth displacement, root resorption, inferior mandibular canal dislocation,[35] and malocclusion.[37] Radiographically, FD can range from radiolucent to entirely radiopaque, with most cases exhibiting mixed or radiopaque images that blend into normal bone margins, creating a ground-glass appearance (Figure 3, A and C). Conventional radiographs may also show narrowing of the periodontal ligament space and ill-defined lamina dura merging with the lesional bone.[2] Biopsy is necessary for definitive FD diagnosis; however, clinical and radiographic features, along with microscopic characteristics, are crucial for diagnosis.[18] Due to clinical and histological similarities to other benign fibro-osseous lesions, GNAS mutational analysis may be a valuable adjunct diagnostic tool.[38]
Histopathological examination of FD reveals marked osteogenesis with thin, anastomosing osteoid trabeculae within a hypercellular fibroblastic stroma. Osteoblasts may be observed lining the trabeculae. In advanced stages, osteoid trabeculae thicken and assume “Chinese figure” characteristics (Figure 3, B). Management of FD primarily involves conservative surgical treatment, including cosmetic recontouring surgery, typically after skeletal maturity is reached, and long-term follow-up. Recurrence is infrequent but possible, albeit slow.[2, 18]
Benign Neoplastic Lesions
Osteoma
Osteoma is a benign neoplasm composed of mature bone tissue, resembling cancellous or compact bone. Osteomas can occur throughout the skeleton and even in soft tissues;[39, 40] however, they are most frequently found in craniofacial bones, including the mandible and maxilla. Three types of osteomas are recognized: central osteoma (endosteal origin), peripheral osteoma (periosteal origin), and extraskeletal soft-tissue osteoma. Multiple osteomas of the jaws should raise suspicion for Gardner’s Syndrome. Solitary jaw osteomas are predominantly of the peripheral type,[41] most commonly affecting the posterior mandible and condyle.[5] Central osteoma, while rare, is characterized as a persistent, slow-growing expansive lesion, more frequently found in the mandible, especially in the premolar region, and can be asymptomatic or symptomatic.[41] Central osteomas may be unrelated to teeth or associated with root displacement or resorption.[42] Radiographically, central osteoma presents as a round radiopaque mass with well-defined borders and no apparent radiolucent halo between the lesion and normal bone (Figure 3, D).[5] All three osteoma types share similar histological features, comprising mature bone with compact lamellae or trabecular bone with sparse fibrovascular tissue channels (Figure 3, E).[2]
Diagnosis of central osteoma requires correlation of histological and radiographic findings with evidence of growth, expansion, and tooth displacement, as it can resemble other bone lesions.[41] Biopsy is necessary for confirmation, and surgical excision is the recommended treatment. Recurrence after surgical removal is rare.[42]
Osteoblastoma
Osteoblastomas are benign, slow-growing bone tumors, accounting for approximately 1% of all primary bone tumors.[43] Most are diagnosed in the second and third decades of life, and commonly affect the axial skeleton; the mandible is the second most frequent location. While more prevalent in the mandible, the maxilla can also be affected. Osteoblastomas are typically centrally located within bone, but periosteal lesions have also been reported. Male predilection is suggested, though gender distribution varies across studies.[44] Osteoblastomas can be asymptomatic or present with significant pain, swelling, and tenderness. Pain associated with osteoblastoma may or may not be relieved by nonsteroidal anti-inflammatory drugs or salicylates. Radiographic features include a solitary round or oval radiolucent lesion with radiopaque foci and a demarcated sclerotic margin. Mature lesions may exhibit a radiolucent rim with dense radiopaque structures centrally.[41] Some osteoblastomas may be located near tooth apices, but are not related to pulp necrosis.[44] They are considered to have significant growth potential and are typically larger than 1.5 cm in diameter radiographically.[43] Histopathologically, osteoblastoma features osteoid and bone trabeculae within a well-vascularized connective tissue stroma. Bone trabeculae and osteoid tissue are surrounded by plump osteoblasts with typical morphology. Variable mineralization with basophilic reversal lines may be observed within the osteoid tissue. Incisional biopsy is essential for diagnosis, especially in enlarged and painful lesions. Surgical treatment, ranging from en bloc resection (treatment of choice) to aggressive curettage for tumors in tooth-bearing areas, is recommended following histopathological confirmation.[44] Aggressive osteoblastoma cases may exhibit local invasion and recurrence potential.[45, 46]
Osteoid Osteoma
Osteoid osteoma (OO) is an uncommon benign bone tumor, considered rare in the jaws.[47] It most commonly affects long bones, particularly the proximal femur and tibia, and is usually diagnosed in the second and third decades of life, with a male-to-female ratio of 3:1.[48] In the jaws, mandibular OO is slightly more common, with few cases occurring in tooth-bearing areas. Mohammed et al. reported a rare case of OO associated with the apices of a mandibular second premolar and first molar, where associated teeth tested vital.[47] Craniofacial OO lesions may present with tenderness and swelling, typically ranging from 1-2 cm in size. OO exhibits lower growth potential than osteoblastoma. Severe pain, often worsening at night and relieved by non-steroidal anti-inflammatory drugs, is characteristic.[44] This pain is hypothesized to be due to OO’s rich vascularity, leading to innervation of free nerve endings and prostaglandin production, explaining the pain relief from non-steroidal anti-inflammatory drugs.[49] Radiographically, OO is characterized by a round lytic lesion with a central nidus less than 1 cm in size, surrounded by a sclerotic bony margin.[44] While OO may resemble cemento-osseous dysplasia, biopsy is necessary for diagnosis when bone expansion or pain is present.[47] Histologically, OO is similar to osteoblastoma, with osteoid, fused trabeculae in vascularized stromal tissue, and prominent osteoblast rimming. Surgical excision is the treatment of choice,[47] potentially including affected teeth. Prognosis is generally favorable, with rare recurrence after surgery.
Cementoblastoma
Cementoblastoma is a rare benign odontogenic tumor of mesenchymal/ectomesenchymal origin. It primarily affects adults in the second and third decades of life, with no apparent gender predilection. Cementoblastoma is associated with a tooth root, predominantly mandibular permanent first molars;[50] however, it can occur in other quadrants.[51] Clinically, it presents with pain and swelling of the buccal and lingual alveolar ridges. Affected teeth may test vital but are often painful to percussion.[52] Radiographically, cementoblastoma appears as a round, well-demarcated radiopaque mass surrounded by a thin radiolucent rim, attached to a tooth (Figure 3, F-G). Root resorption, root canal invasion, tooth displacement, and periodontal ligament space obliteration may also be associated features.[50] Microscopically, cementoblastoma shows dense masses of acellular cementum-like material with basophilic reversal lines within a fibrous stroma. The lesion mass merges with the tooth root.[16]
Biopsy is required for diagnosis; correlation with clinical and radiographic findings is crucial to differentiate cementoblastoma from other mineralized tumors. Surgical excision and tooth extraction are typically recommended due to lesion fusion with root cementum. Recurrence risk is low.[52] Early diagnosis may allow for root canal therapy and apicoectomy to save the tooth.[53]
Central Ossifying Fibroma
Central ossifying fibroma (COF) is a benign fibro-osseous lesion with neoplastic behavior, composed of fibrocellular tissue and mineralized material.[16, 54] COF arises in tooth-bearing areas, usually the mandible, often presenting with swelling and cortical expansion. Pain is typically absent, and some cases are incidental radiographic findings.[36] Conventional COF typically occurs in the second to fourth decades of life, with a reported female predilection.[16] Juvenile variants, juvenile trabecular ossifying fibroma (JTOF) and juvenile psammomatoid ossifying fibroma (JPOF), develop mainly in children and have distinct histological patterns.[36] Juvenile OF variants show a predilection for craniofacial bones, particularly paranasal sinuses and gnathic bones. Sinonasal juvenile OF tends to be clinically aggressive, with rapid growth, significant bone expansion, and high recurrence rates. Maxillary sinus lesions can extend into paranasal sinuses and the orbit, demonstrating aggressive behavior. Radiographic presentation of OF varies with lesion maturity. Early lesions may appear as a round unilocular radiolucency with well-defined borders. Mature lesions may show demarcated mixed radiolucent-radiopaque content or be entirely radiopaque.[55] Cortical bone displacement, tooth displacement, and root resorption may occur.[36] Ramos-Perez et al. reported a case of OF mimicking chronic apical periodontitis, presenting as a well-defined unilocular radiolucent lesion in the apical region of an endodontically treated mandibular canine on conventional radiographs. They suggested OF as a differential diagnosis for unusual or persistent apical radiolucencies post-root canal treatment, noting this resemblance is rare.[56] Clinical and radiographic characteristics are essential for OF diagnosis; however, histopathological correlation is crucial for definitive identification. Biopsy is fundamental for OF diagnosis.[57] Histologically, conventional OF shows spindled fibroblast-like cells with cementicle, osteoid, and woven bone deposition. Prominent osteoblastic rimming is often seen adjacent to mineralized material. Fibrous capsule fragments may be present peripherally. Curettage and enucleation are recommended for conventional OF, with low recurrence rates. Juvenile OF may require surgical resection. Sinus involvement may lead to incomplete excision and higher recurrence rates.[58]
Odontoma
Odontoma is the most common odontogenic tumor-like malformation (hamartoma) of unknown etiology, occurring in tooth-bearing areas.[16] These lesions exhibit complete differentiation of epithelial and mesenchymal odontogenic cells, with enamel, dentin, and sometimes cementum formation.[59] Odontomas have no gender predilection and are primarily diagnosed in children and adolescents.[16]
Compound and complex odontomas are two types, differentiated by histologic development and mineralized content development.[59] Compound odontoma presents as numerous tooth-like structures in tooth-bearing areas, mainly the anterior maxilla. Complex odontoma is characterized by amorphous calcification with dysplastic dentin covered by enamel, in tooth-bearing areas, often the posterior mandible.[16, 60] Clinically, both types are slow-growing and rarely symptomatic. Jaw odontomas are often incidental radiographic findings, sometimes discovered during investigations of delayed tooth eruption.[57] Bone expansion, pain, and swelling related to infected odontomas have been reported with larger lesions.[61, 62] Radiographically, compound odontomas show multiple radiopaque tooth-like structures surrounded by a thin radiolucent line, clearly separated from adjacent bone (Figure 4, A–B). Size typically ranges from 1-2 cm in diameter. Complex odontomas present a distinct radiographic pattern with an amorphous radiopaque structure, a fine radiopaque periphery, and a surrounding radiolucent zone (Figure 4, C–D). Histologically, odontomas consist of a connective tissue capsule with odontogenic epithelium strands or islands, tubular dentin formation, and an enamel matrix.[16] Treatment is typically local surgical excision, with rare recurrences.[2]
Calcifying Cystic Odontogenic Tumor (Calcifying Odontogenic Cyst)
Calcifying cystic odontogenic tumor (CCOT), also known as Gorlin cyst, is a rare benign odontogenic neoplasm reclassified in the 2005 WHO classification of odontogenic tumors.[16] First described by Gorlin et al. in 1962,[63] CCOT primarily affects individuals in the second and third decades of life, with no apparent gender predilection. It can occur in the maxilla and mandible, with a predilection for the anterior region,[64] especially the incisor and canine areas.[2] Clinically, CCOT is typically a painless, slow-growing lesion that may cause bone expansion and can be associated with unerupted teeth due to occasional involvement of the crown. Radiographically, CCOT appears as a well-defined unilocular radiolucent lesion, sometimes with irregular radiopaque material of varying density, described as a “salt and pepper” pattern (Figure 4, E–F).[64]
In some cases, CCOT can mimic apical periodontitis, presenting as a well-defined radiolucent round lesion in the periapical region. Unlike apical periodontitis, CCOT is not related to pulp necrosis,[65] but may be associated with infected root canals.[66] Multilocular CCOT presentation is rare.[16] CBCT is valuable for CCOT diagnosis, revealing mineralized content in the lesion periphery.[64] Biopsy is essential for CCOT diagnosis. Histopathology shows a cyst wall of connective tissue lined by thin odontogenic epithelial cells with ameloblastomatous features, frequently associated with ghost cell formation and calcification. Eosinophilic dentinoid or dysplastic dentin may be present. Enucleation is the recommended treatment, with rare recurrence reported.[16]
Adenomatoid Odontogenic Tumor
Adenomatoid odontogenic tumor (AOT) is a rare, benign, slow-growing odontogenic tumor composed of odontogenic epithelium.[16] AOT is usually asymptomatic and diagnosed mainly in the second decade of life, with half of cases in teenagers, and a slight female predilection.[67, 68] Symptoms range from subtle to obvious swelling, tooth impaction, or displacement. Three clinicopathologic variants exist: follicular, extrafollicular, and peripheral AOT (extraosseous type). Follicular AOT is associated with the crown of an unerupted tooth, especially a maxillary canine. Extrafollicular AOT may be in the periapical region of the anterior mandible, sometimes with tooth displacement. Radiographically, early AOT can be a well-defined unilocular radiolucency related to the crown, interradicular region, lateral root, or apex, mimicking apical periodontitis.[67, 68] Despite similarity to apical periodontitis, AOT typically preserves the periodontal ligament space and lamina dura, unlike inflammatory periapical lesions which usually cause periapical alterations.[68] Fine calcifications within the radiolucent lesion may be visible, depending on calcified deposits and radiographic technique (Figure 4, G–H).[14] Biopsy is needed for suspected cases. Clinical, radiographic, and histological correlation aids AOT diagnosis. Histologically, AOT consists of odontogenic epithelial cells with cuboidal or columnar features, forming nests or rosette-like structures. Some tumors may be partially cystic with a solid epithelial lining. Duct-like spaces lined by columnar cells with polarized nuclei, and amorphous nodules with amyloid-like and calcified substances may be seen. Dysplastic structures or calcified osteodentin may be present.[16] Conservative surgical excision is the treatment for AOT, with excellent prognosis.[69]
Ameloblastic Fibro-Odontoma
Ameloblastic fibro-odontoma (AFO) is a rare, slow-growing benign tumor of odontogenic ectomesenchyme resembling dental papilla, containing epithelial strands and nests resembling dental lamina, enamel organ, dentine, and enamel.[70] AFO typically affects young patients aged 5-17, with no gender predilection. Clinically, it presents as painless swelling causing delayed tooth eruption, displacement, or loosening. AFO usually affects the posterior mandible or maxilla, causing evident bony expansion.[71] Conventional radiographs show a well-defined radiolucent area with variable radiopaque material, mainly affecting the crown of unerupted teeth or the periapical region. Radiopaque material can be abundant, making AFO similar to odontoma. Diagnosis is based on histopathological examination, revealing cell-rich primitive ectomesenchyme resembling dental papilla, permeated cords, and nests of odontogenic epithelium with ameloblastic differentiation. Mesenchymal cells are stellate or spindle-shaped. Dentinoid and enamel matrix structures of varying maturation are observed.[72] Treatment varies due to AFO rarity. Curettage of the involved tooth may suffice for small tumors. Curettage or enucleation may be indicated for larger tumors, especially when basal cortical bone can be preserved. Recurrence is infrequent.[71]
Malignant Neoplastic Lesions
Osteosarcoma
Osteosarcoma is a primary malignant bone tumor characterized by osteoid or bone matrix production. Typically affecting long bones, 5-13% occur in the jaws. Maxilla and mandible are equally affected, predominantly in patients aged 10-20, with slight male predilection.[16] Jaw osteosarcomas tend to occur one to two decades later than long bone osteosarcomas, with mandibular tumors more frequent in the molar region.[73] Clinically, these lesions present with evident swelling, sometimes pain, tooth loosening,[16, 74] or paresthesia. Some patients report increased tumor growth post-extraction,[73] or have pre-existing conditions like prior radiation, fibrous dysplasia, Paget’s disease, and chronic osteomyelitis.[16] Radiographically, osteosarcoma can be sclerotic to mixed radiolucent/radiopaque (Figure 4, I), with density varying by tumor differentiation or disease stage. A case of osteosarcoma mimicking benign cementoblastoma, with a well-defined high-density change around a mandibular molar root, has been reported.[8] Radiographic features are variable. Early signs may be widened periodontal ligament space, but some osteosarcomas show periodontal space loss and cortical plate destruction. A sunray pattern, representing parosteal osteogenic reaction to tumor spread,[8, 73, 74] may be seen, but is not pathognomonic.[73] Histopathological examination is essential due to variable radiographic features. Microscopically, osteosarcomas are categorized as osteoblastic, chondroblastic, and fibroblastic subtypes. Osteoblastic osteosarcoma comprises osteoid surrounded by irregularly arranged fibroblast-like cells. Chondroblastic subtype shows lobules of tumor cells with a feathery appearance and atypical chondrocytes in lacunae. Fibroblastic osteosarcoma displays spindle-shaped tumor cells in a herring bone pattern and osteoid formation areas.[2] Treatment protocols are not standardized for jaw osteosarcoma;[73] however, surgical resection with tumor-free margins appears to be the primary modality for better survival rates. Radiotherapy and chemotherapy benefits are controversial.[75] Overall, survival rates are significantly higher in jaw osteosarcoma compared to long bone osteosarcoma, and distant metastases are less frequent.
Chondrosarcoma
Chondrosarcoma is a malignant cartilaginous tumor, representing 10-20% of primary malignant bone tumors, and is among the most common after osteosarcoma.[76] Less than 1% of chondrosarcomas affect the jaws. It is more common in males, typically in the fourth decade of life.[2, 4] Clinically, jaw chondrosarcoma presents as a slow-growing painless swelling, most commonly in the anterior maxilla and mandible, especially symphysis, coronoid, and condylar processes.[76] Radiographic characteristics vary from complete osteolytic lesions to poorly defined radiolucent areas with calcified radiopaque foci. Calcified areas may have a mottled appearance with varied density. Ill-defined borders are consistent with malignancy. In tooth-bearing areas, early cases may show widened periodontal space, mimicking periapical inflammatory conditions or osteosarcoma.[4, 76] CT scans are useful for evaluating tumor extension and cortical and soft tissue involvement.[16] Histopathological examination, via biopsy, is crucial for chondrosarcoma diagnosis. Microscopically, conventional chondrosarcomas are graded I, II, or III based on cell density and nuclear changes in neoplastic chondrocytes. They consist of round to oval cells in lacunae permeating a chondroid matrix, possibly with myxoid changes. Conventional and mesenchymal subtypes are most frequent in the jaws. Mesenchymal chondrosarcomas are a mixture of hyaline cartilage and small round to oval cells, often in a pericytomatous vascular configuration.[16] Surgical resection with wide tumor-free margins is the most effective treatment. Radiotherapy and chemotherapy are used for high-grade cases but may not significantly improve survival rates.[76]
Metabolism-Related Lesions
Renal Osteodystrophy
Renal osteodystrophy (osteitis fibrosa cystica) is a bone pathology resulting from mineral and bone disorders in end-stage renal disease, associated with secondary hyperparathyroidism and calcitriol deficiency. These metabolic alterations lead to a broad clinical syndrome with abnormalities in calcium, phosphorus, PTH, and vitamin D metabolism, and bone turnover and mineralization. Jaw involvement is relatively frequent and can be an early sign of renal disease. Clinically, renal osteodystrophy presents as painless, diffuse or localized enlargement of the maxilla and mandible. Radiographically, it appears as a mixed radiolucent/radiopaque lesion with altered trabecular configuration. A diffuse ground-glass pattern and lamina dura loss are also noted.[77, 78] Diagnosis requires clinical, radiographic, and histopathological correlation. Histologically, renal osteodystrophy comprises variably sized woven bone trabeculae, numerous osteoblasts on bone surfaces, and abundant osteoclastic resorption lacunae. Prominent fibrous tissue surrounds trabecular woven bone. Surgical recontouring is the primary management for renal osteodystrophy.[77] Parathyroidectomy has also been reported as successful treatment.[79]
Discussion
Successful root canal treatment is defined by pain relief, periapical lesion resolution or reduction, and functional tooth restoration. Diagnosing periapical lesions in endodontic practice is challenging,[1] as many lesions can mimic endodontic lesions despite diverse origins.[6]
Inflammatory changes in periapical bone structure can result from root canal system infections, leading to osteoclastic or osteoblastic activity. These alterations manifest as radiolucent or radiopaque images on radiographs.[15] Similarly, bone alterations can occur in lesions of inflammatory, neoplastic, dysplastic, and metabolic origins.[8, 9, 10, 11, 77, 80] While radiolucent lesions are more commonly associated with root canal infection, radiopaque lesions present equally complex diagnostic challenges and require similar attention to avoid misdiagnosis.
Clinical assessments, including pulp sensibility and vitality tests, are typically helpful in differentiating inflammatory from non-inflammatory periapical alterations.[81] Comprehensive clinical examination, combined with clinical and radiographic assessments, is crucial for diagnosing periapical lesions. While lack of pulp response suggests endodontic origin, non-endodontic lesions can present similarly. In cases where clinical and radiographic findings are insufficient, biopsy followed by histopathological examination is necessary to determine lesion origin.
CBCT is a valuable diagnostic tool in dentistry,[82, 83, 84, 85] offering high accuracy in detecting periapical lesions compared to periapical and panoramic radiography.[85] CBCT’s characteristics and multi-dimensional imaging allow thorough examination, clarifying periapical lesion location, bone resorption or formation characteristics, and lesion presence, absence, or regression.[86]
Conclusion
In conclusion, endodontists and dental clinicians must be proficient in diagnosing both radiolucent and radiopaque periapical lesions. The ability to differentiate between inflammatory and non-inflammatory lesions streamlines diagnosis and ensures the selection of appropriate therapeutic interventions for optimal patient care. Understanding the differential diagnosis of radiopaque lesions of the jaw is crucial for accurate diagnosis and effective treatment planning in endodontic and general dental practice.
Acknowledgments
The authors declare no conflicts of interest related to this study. This research was partially supported by grants from the National Council for Scientific and Technological Development (CNPq, #306394/2011-1, to C.E.).
References
[List of references as in the original article]
Publication Dates
- Publication in this collection2017
History
- Received03 Mar 2017
- Reviewed27 Apr 2017
- Accepted21 May 2017
