Hypercementosis

Hypercementosis is a non-neoplastic dental condition characterized by the excessive deposition of cementum on the roots of one or more teeth, resulting in abnormal thickening and alteration of root morphology, often presenting as a bulbous or club-shaped enlargement, particularly at the apical third.^[1] This overproduction of cementum, which is the mineralized tissue covering the tooth root, extends beyond normal physiological limits and can affect the entire root surface or specific regions, leading to a nodular, diffuse, or mixed pattern of hyperplasia.^[2] Typically asymptomatic and discovered incidentally through radiographic examination, hypercementosis does not usually cause pain or functional impairment but may complicate dental procedures such as extractions due to the enlarged root size and ankylosis potential.^[3] The etiology of hypercementosis remains incompletely understood but can be classified as idiopathic, localized, or associated with systemic factors; localized forms often arise from mechanical stimuli like excessive occlusal forces, tooth repair following trauma or fracture, or periapical inflammation, while systemic associations include conditions such as Paget's disease of bone, acromegaly, hyperparathyroidism, and certain genetic mutations affecting mineralization pathways.^[2] Prevalence increases with age, most commonly affecting mandibular molars and premolars, and it may occur unilaterally or bilaterally without gender predilection.^[1] Radiographically, it appears as a radiopaque thickening around the root with preservation of the periodontal ligament space and lamina dura, distinguishing it from other root alterations like osteomas or tumors.^[3] Although benign and requiring no specific treatment in most cases, management focuses on addressing any underlying causes or associated pathologies, with periodic radiographic monitoring recommended to track progression and prevent complications during endodontic or surgical interventions.^[2] In rare instances linked to systemic diseases, hypercementosis serves as a diagnostic clue, prompting further medical evaluation.^[4]

Introduction

Definition

Hypercementosis is a non-neoplastic condition characterized by the excessive deposition of normal cementum on the roots of one or more teeth, which may be idiopathic or secondary to various stimuli, leading to thickened, bulbous, or distorted root morphology.^[1]^[5] Cementum is the calcified connective tissue that covers the tooth roots, serving primarily to anchor the periodontal ligament fibers to the root surface and thereby attaching the tooth to the alveolar bone.^[6] In hypercementosis, this excessive cementum accumulation alters the root shape but does not primarily affect the enamel or dentin.^[7] The condition involves hyperplasia primarily of cellular (radicular) cementum, which is layered over the primary acellular (coronal) cementum and contains cementocytes within its matrix.^[8] Hypercementosis can manifest as focal involvement of a single tooth, multifocal affecting several teeth, or generalized across multiple teeth, often resulting in a bulbous enlargement particularly at the apical region.^[1]^[7] It is frequently associated with aging, where continued cementum apposition occurs as a physiologic response to functional demands.^[9]

Classification

Hypercementosis is classified etiologically into primary (idiopathic) and secondary (reactive) forms, where primary hypercementosis lacks an identifiable cause and typically presents as a generalized condition.^[10] Secondary hypercementosis arises as a reactive response to various stimuli, such as local trauma or systemic disorders.^[11] This distinction aids in differentiating idiopathic cases, often seen in older adults as an age-related phenomenon, from those linked to specific conditions like Paget's disease of bone, which commonly manifests as generalized secondary hypercementosis.^[10] In terms of extent, hypercementosis is categorized as focal or generalized. Focal hypercementosis is confined to one or a few teeth, often limited to specific root surfaces, whereas generalized hypercementosis involves multiple teeth or the entire dentition.^[12] This classification reflects the distribution and helps in assessing the potential underlying factors, with focal forms more frequently tied to localized irritants.^[13] Morphologically, hypercementosis exhibits distinct subtypes based on the pattern of cementum deposition: concentric, eccentric, or excrescence. Concentric hypercementosis involves uniform thickening around the root, resulting in a diffuse, even apposition of cementum.^[13] Eccentric hypercementosis features asymmetric bulging or irregular deposition on one side of the root, often associated with mechanical stress.^[13] Excrescence-type hypercementosis presents as nodular outgrowths or localized masses, resembling structures like cementoma, typically occurring at the apex or along the root.^[14] These morphological variations provide insights into the adaptive or pathological nature of the condition.^[13]

Clinical Presentation

Signs and Symptoms

Hypercementosis is typically asymptomatic and is most often discovered incidentally during routine dental examinations or radiographic imaging performed for unrelated conditions.^[5] Patients generally report no discomfort, and the condition does not alter the appearance or function of the tooth crown or surrounding gingiva.^[2] In some cases, symptoms may arise if hypercementosis is associated with inflammation, trauma, or secondary conditions such as periodontitis or periapical pathology. These can include tooth mobility, tenderness to percussion, or localized pain, particularly during chewing or biting.^[10] Rarely, excessive root thickening or elongation in teeth lacking an opposing occlusal surface may lead to occlusal interference, causing discomfort or uneven bite.^[7] Clinically, advanced hypercementosis may present with enlarged, bulbous roots that can be detected through careful probing or palpation, though such findings are uncommon and usually require significant cementum deposition.^[15] The condition progresses slowly and non-painfully over years, with gradual enlargement of the root structure, and is more frequently observed in mandibular molars compared to other teeth.^[16] This insidious development often goes unnoticed until extraction is attempted, where the altered root morphology can complicate the procedure.^[5]

Complications

Hypercementosis significantly complicates dental procedures, particularly tooth extraction, due to the excessive cementum deposition that enlarges and often fuses roots to surrounding bone, mimicking ankylosis and increasing the risk of root fracture or mandibular jaw fracture during removal.^[17] This fusion can prolong surgical time and necessitate specialized techniques to avoid iatrogenic damage to adjacent structures.^[2] Such irregularities may be associated with periodontal disease, though the relationship is complex and often involves inflammation contributing to cementum deposition.^[10] Endodontic treatment of teeth with hypercementosis is challenged by altered root canal anatomy, including narrowed or obliterated canals and an increased distance from the cementodentinal junction to the apex, which complicates instrumentation, shaping, and obturation.^[18] These changes often require advanced imaging and techniques to achieve adequate apical limits without perforation.^[19]

Etiology

Local Factors

Local factors contributing to hypercementosis encompass mechanical stresses and inflammatory processes within the oral environment that provoke excessive cementum apposition on tooth roots. These triggers are distinct from systemic influences and primarily involve localized responses to physical or pathological stimuli in the periodontal tissues.^[13] Occlusal trauma and excessive masticatory forces, such as those arising from bruxism or malocclusion, stimulate cementoblast hyperactivity by subjecting the periodontal ligament to repetitive biomechanical loading. This response often manifests as apical or focal cementum thickening, particularly in posterior teeth under sustained pressure. For example, molars in individuals with habits involving heavy chewing exhibit hypercementosis as an adaptive mechanism to distribute forces more effectively.^[13]^[1] Periapical inflammation or infection, commonly resulting from pulp necrosis or post-traumatic repair, induces reactive cementum deposition to stabilize the affected root and seal defects. Such cases frequently occur in endodontically involved teeth where chronic inflammatory mediators persist, leading to nodular or diffuse apposition along the root surface.^[13]^[20] Localized hypercementosis is exemplified in teeth adjacent to edentulous areas, where loss of neighboring or opposing dentition alters occlusal balance and amplifies masticatory loads on the remaining roots. Similarly, following periodontal interventions like root planing, residual inflammatory resolution can trigger compensatory cementum formation in affected sites.^[13]^[3]

Systemic Factors

Systemic factors contributing to hypercementosis involve various whole-body conditions that disrupt normal cementum formation and remodeling, often leading to generalized or multifocal excessive deposition. These etiologies are typically identified through case reports and systematic reviews, highlighting their role in altering periodontal and skeletal homeostasis.^[13] Endocrine disorders, particularly those affecting growth hormone and thyroid function, have been associated with hypercementosis. Acromegaly, characterized by excess growth hormone secretion, can result in thickening of dental roots due to accelerated cementum apposition, often affecting multiple teeth in a diffuse manner. This association is supported by early radiographic observations in affected patients, where hypercementosis contributes to occlusal discrepancies alongside other craniofacial changes.^[13]^[21] Similarly, hyperthyroidism, including toxic goiter, has been linked to marked cementum overgrowth, potentially through heightened metabolic activity influencing mineral deposition on roots, with cases showing pronounced involvement of premolars and molars.^[13]^[22] Skeletal diseases represent another key category, with Paget's disease of bone being a prominent example. This condition involves chaotic bone remodeling driven by osteoclastic and osteoblastic hyperactivity, extending to the jaws and causing excessive, generalized hypercementosis across all teeth. Histological analyses reveal irregular cementum layers mirroring the disorganized bone patterns, often complicating dental extractions due to root ankylosis.^[13]^[23] Hyperparathyroidism, especially secondary forms linked to chronic kidney disease, can also promote hypercementosis alongside jaw bone alterations like ground-glass opacities, attributed to parathyroid hormone-mediated increases in calcium mobilization and cementoblast activity.^[13] Genetic predispositions play a role in rare familial instances of hypercementosis, sometimes exhibiting autosomal dominant inheritance without an identified specific gene mutation. For example, mutations in the ENPP1 gene, associated with generalized arterial calcification of infancy, have been documented to cause significant root hypercementosis in affected individuals, likely due to impaired pyrophosphate regulation affecting mineralization.^[13]^[24] Additionally, conditions like Gardner's syndrome feature generalized hypercementosis as part of broader odontogenic anomalies, underscoring hereditary influences on cementum hypertrophy.^[13] These systemic and genetic factors often interact with local dental stressors, amplifying cementum deposition.

Pathophysiology

Cellular Mechanisms

Hypercementosis involves the excessive deposition of cellular cementum on tooth roots, driven primarily by the hyperactivity of cementoblasts, the specialized cells responsible for cementum formation. These cementoblasts, derived from mesenchymal cells in the periodontal ligament, become activated in response to various stimuli, including mechanical stress from occlusal forces and inflammatory cytokines released during localized inflammation. This activation leads to increased production of cementum matrix, resulting in accelerated apposition of cementum layers. Periodontal ligament fibroblasts play a supportive role in this process by secreting signaling molecules that modulate cementoblast activity. These fibroblasts respond to environmental cues by releasing growth factors that promote cementoblast differentiation and proliferation. In general cementogenesis, factors such as bone morphogenetic proteins (BMPs) and transforming growth factor-beta (TGF-β) have been shown to enhance markers of mineralization in cementoblasts.^[25] At the core of hypercementosis lies dysregulated mineralization, characterized by overproduction of extracellular matrix components. Normally, cementoblasts undergo apoptosis to balance deposition, but in hypercementosis, this regulation may be altered, leading to persistent matrix synthesis and the formation of thick, layered cellular cementum containing embedded cementocytes. The precise molecular pathways, such as potential involvement of Wnt/β-catenin signaling in promoting mineralization, remain incompletely understood but have been implicated in experimental models of cementum formation. These cellular processes may establish feedback loops that perpetuate cementum overproduction. The expanding root-cementum interface alters the distribution of occlusal forces across the periodontal ligament, generating additional mechanical signals that further stimulate cementoblasts and fibroblasts. Cementocytes express connexin 43, a gap junction protein, which may contribute to intercellular communication in response to stress.^[26] Such interactions highlight the adaptive nature of cementum homeostasis at the cellular level, though the exact mechanisms in hypercementosis require further research.^[27]

Tissue Changes

Hypercementosis manifests as excessive deposition of cementum on the tooth root, resulting in significant root enlargement characterized by thickening that can extend up to several millimeters, often forming bulbous apices or circumferential layers that alter the overall root morphology. This enlargement typically occurs diffusely or focally, with examples including up to 3.2 mm of additional thickness in premolars, and is more commonly observed in the apical third of the root. The process involves continuous apposition of cementum layers, which can give the root a club-shaped or drumstick-like appearance in severe cases.^[28] Histologically, the excess tissue consists of laminated cellular cementum, a post-eruptive structure formed by cementoblasts that become entrapped as cementocytes within the matrix, providing functions such as root repair and periodontal attachment. Sharpey's fibers, the collagenous insertions anchoring the periodontal ligament to the cementum, are prominently embedded in these layers, particularly in areas of mechanical stress. Importantly, this cementum lacks any neoplastic characteristics, distinguishing it from pathological proliferations, and maintains a normal mineralized composition without inflammatory or dysplastic features.^[29] The surrounding periodontal tissues may exhibit impacts such as potential ankylosis, involving direct fusion of the hyperplastic cementum to the alveolar bone, which obliterates the intervening periodontal ligament space in affected areas. Alternatively, the ligament space can widen due to the expansive cementum growth, altering the normal architecture without necessarily leading to resorption. These changes arise from prolonged stimuli that initiate cellular signals for cementum formation, as explored in related mechanisms.^[28] Progression of these tissue alterations is gradual, occurring over decades throughout the tooth's lifespan, with apposition intensifying in response to local or systemic factors and becoming more pronounced in posterior teeth like molars and premolars due to their functional demands.^[28]

Diagnosis

Radiographic Features

Hypercementosis is typically identified on panoramic or periapical radiographs as excessive thickening of the tooth root, particularly at the apical third, resulting in a loss of the normal tapered outline and often presenting as bulbous, club-shaped, or spiked apices.^[3]^[30] The excess cementum appears radiopaque with a uniform density slightly less than that of dentin but comparable to bone, and it is contained within the lamina dura without associated radiolucent areas unless secondary inflammation is present.^[3]^[10] This root widening is commonly observed in mandibular first molars, where the affected roots may exhibit a smooth or irregular outline while maintaining the periodontal ligament space.^[31]^[10] Advanced imaging such as cone-beam computed tomography (CBCT) provides a three-dimensional assessment, revealing the precise extent of cementum deposition, hyperdense morphology without cortical bone expansion, and intact lamina dura surrounding the thickened root.^[30] In CBCT views, the excess cementum shows no root resorption or fusion with adjacent structures, allowing for detailed evaluation of involvement in multi-rooted teeth like molars.^[32] These radiographic hallmarks enable early detection, correlating with clinical findings of asymptomatic root enlargement.^[3]

Differential Diagnosis

Hypercementosis must be differentiated from other conditions presenting with root-associated radiopacities or alterations in root morphology on radiographs, as misdiagnosis can lead to unnecessary interventions.^[33] Periapical cemento-osseous dysplasia (also known as periapical cemental dysplasia) appears as focal radiopacities at the tooth apex, typically involving the anterior teeth, particularly mandibular incisors, and is more prevalent in females.^[33]^[34] Unlike hypercementosis, which involves continuous thickening of the root cementum with preservation of the periodontal ligament (PDL) space, periapical cemento-osseous dysplasia manifests as a distinct fibro-osseous lesion with stages of osteolytic, cementoblastic, and osteogenic changes, often showing mixed radiodensities surrounded by a radiolucent rim and no disruption to the lamina dura.^[33] Odontoma and cementoblastoma, both neoplastic lesions, can mimic hypercementosis due to their radiopaque nature near roots but exhibit distinct borders and are frequently associated with pain or swelling.^[35] Cementoblastoma specifically fuses directly to the root, obliterating the PDL space and presenting as a well-defined radiopacity with a radiolucent rim, whereas odontoma forms a hamartomatous mass with tooth-like structures that may displace adjacent teeth.^[33] In contrast, hypercementosis lacks neoplastic features, maintains PDL integrity, and is asymptomatic.^[35] Root resorption and idiopathic osteosclerosis represent additional mimics, though they differ fundamentally in tissue involvement. Root resorption displays loss of root structure with irregular, mottled margins often linked to trauma, inflammation, or orthodontic forces, directly opposing the additive cementum deposition in hypercementosis.^[33] Idiopathic osteosclerosis, a benign bony radiopacity, lacks association with the PDL or cementum and appears as a well-circumscribed dense area without root alteration or systemic ties.^[35] Key discriminators for hypercementosis include its seamless continuity with the normal radicular cementum, absence of symptoms such as pain or cortical expansion, and maintenance of a normal PDL space and lamina dura on imaging.^[33] These features, often confirmed via panoramic or periapical radiographs, help distinguish it from the discrete lesions or structural losses seen in the differentials.^[35]

Management

Treatment Approaches

Hypercementosis is typically asymptomatic and requires no active intervention unless it complicates other dental conditions or extraction is necessary.^[1] In such cases, regular monitoring through periodic radiographic examinations is recommended to assess progression and detect any associated pathology.^[1] When extraction is indicated, surgical approaches are employed due to the altered root morphology and increased bulk, which can complicate standard procedures. Techniques include tooth sectioning to reduce resistance, followed by interseptal bone removal and conservative buccal bone guttering to facilitate root retrieval without excessive force, minimizing risks such as jaw fracture. Preoperative radiographic evaluation, such as orthopantomograms, is essential to plan the extent of hypercementosis and inform patient consent regarding potential complications. For teeth with periapical involvement, surgical endodontic management may be performed to address lesions while preserving the tooth, particularly when non-surgical access is hindered by root fusion or excessive cementum. Endodontic therapy in hypercementosis-affected teeth demands modified techniques to navigate altered canal anatomy, often guided by cone-beam computed tomography (CBCT) for precise identification of root structure and periapical pathology prior to instrumentation and obturation. Adjunctive measures focus on mitigating contributing factors. No specific pharmacologic treatments target hypercementosis itself, with management emphasizing mechanical and procedural interventions tailored to individual cases.^[1]

Prognosis

Hypercementosis typically follows a benign course in most cases, with no further progression of cementum deposition occurring in the absence of ongoing stimuli such as occlusal trauma or inflammation.^[2] As a non-neoplastic condition, it generally requires no active intervention beyond periodic monitoring to assess for any associated dental issues, yielding an excellent long-term prognosis for affected teeth that remain asymptomatic and functional.^[1]^[36] The outlook may worsen in the presence of underlying systemic conditions, such as Paget's disease of bone, where hypercementosis serves as a localized manifestation.^[37] Following extraction, which may be necessitated by unrelated pathology, the procedure is typically successful when employing appropriate techniques to address the enlarged root morphology, though it carries a risk of intraoperative challenges such as root fracture.^[5] The impact on quality of life is generally minimal for isolated cases, but severe hypercementosis can pose challenges in orthodontic treatment by reducing tooth movability or in prosthetic planning due to altered root anatomy.^[38]

Epidemiology

Prevalence and Distribution

Hypercementosis exhibits a variable prevalence across populations, with studies reporting rates ranging from approximately 5% to 15% in the general adult population.^[39]^[40]^[41] This condition becomes more common with advancing age, particularly as a response to chronic occlusal stress or functional demands on teeth.^[42]^[2] The distribution of hypercementosis is not uniform across the dentition; it occurs most frequently in mandibular molars and premolars, with mandibular teeth generally showing higher involvement than maxillary ones.^[2]^[12] Prevalence can vary significantly in specific historical populations; for example, rates up to 84% have been reported in 17th- to 19th-century skeletal samples from enslaved individuals in the Caribbean, potentially linked to unique environmental and occupational stresses.^[43] Generalized hypercementosis, involving multiple teeth across the dentition, is rare, with an estimated prevalence of less than 1%, whereas the focal form is more common, particularly in adults over 40 years.^[1]^[2] Recent studies from the 2020s highlight global variations, with higher rates observed in industrialized populations potentially linked to dietary factors and mechanical stresses from prolonged tooth retention. For instance, a 2023 study in a Mexican population reported a prevalence of 16.3%.^[39]^[40]^[40]

Associated Risk Factors

Hypercementosis is progressively more common with advancing age, as cumulative occlusal and functional stresses on the periodontal ligament stimulate excessive cementum deposition over time. Studies indicate that the condition's frequency rises significantly in adults, with mean ages of affected individuals often exceeding 30 years. For mandibular third molars specifically, incidence increases from near zero under 20 years to over 90% in those aged 50 and older. This age-related progression is attributed to lifelong mechanical loading on teeth, particularly molars, which undergo compensatory thickening of root cementum. No gender predilection has been observed.^[2]^[12]^[44]^[3] Occupational factors involving high masticatory or manual demands elevate the risk of hypercementosis through sustained occlusal overloads. Individuals in professions requiring repetitive use of teeth as tools—such as fish net mending or basket weaving in traditional labor-intensive settings—exhibit higher rates due to functional stress akin to using teeth as a "third hand." Similarly, bruxism, often exacerbated in occupations with chronic jaw clenching or grinding, correlates with up to 30% of cases. Heavy manual laborers face comparable risks from amplified occlusal trauma during chewing tough or abrasive materials.^[45]^[12]^[46] A history of dental trauma, orthodontic intervention, or periodontal disease substantially increases susceptibility to hypercementosis by disrupting normal periodontal ligament function and triggering reparative cementum overproduction. Trauma, such as from injury or fracture, is documented in a small percentage of cases but often initiates focal thickening as a response to localized stress. Orthodontic treatments, which involve controlled tooth movement, have been associated with altered cementum dynamics in a low percentage of treated patients. Periodontal disease contributes in about 24% of instances, where chronic inflammation around roots—particularly in mandibular molars—promotes excessive deposition as an adaptive measure against mobility.^[2]^[12]^[47] Socioeconomic status indirectly influences hypercementosis detection rates, as lower access to routine dental care in underserved populations delays radiographic identification of the condition. Individuals from lower socioeconomic backgrounds often experience reduced opportunities for preventive screenings, leading to underreporting despite potentially higher underlying risks from unaddressed oral stressors. This disparity highlights how healthcare inequities can skew observed prevalence, with better-resourced groups showing higher diagnosis rates through more frequent imaging.^[45]

Research and History

Historical Development

The earliest descriptions of excessive cementum deposition on tooth roots emerged in the late 19th century, coinciding with advances in microscopy that allowed odontologists to differentiate cementum from other dental tissues. Detailed histological observations were first provided by Jan Purkinje and Anders Retzius in the 1830s, who identified the layered structure of cementum but did not yet address pathological overgrowth. By the end of the century, classifications based on visual examination of isolated teeth were developed, with early reports describing bulbous or nodular enlargements.^[28] In the early 20th century, odontologists explored the condition in the context of periodontal disease and occlusal trauma, with observations on pyorrhea alveolaris suggesting it as a reparative response to functional stress, as noted in Max Karolyi's 1901 work. The terminology evolved from earlier terms like "exostosis" and "hyperostosis" to "excementosis," reflecting confusion with osseous pathologies. The modern term "hypercementosis" gained prominence in the 1930s through dental texts, such as those by Gardner and Goldstein in 1931, who formalized it as excessive, non-neoplastic cementum buildup, distinguishing it from true neoplasms.^[48]^[49]^[28] Key milestones included the radiographic identification of hypercementosis in the 1920s, enabled by emerging dental X-ray techniques, with early descriptions in pathology texts like Endelman and Wagner's 1920 work noting apical thickening on films. By the 1930s, radiologists like Weinberger provided systematic radiographic criteria, highlighting its characteristic bulbous root appearance. A significant association was established in the late 1930s when Rushton in 1938 linked generalized hypercementosis to Paget's disease of bone, first described by Sir James Paget in 1876, observing it as a skeletal manifestation in affected jaws.^[50]^[49]^[23] Early understandings included misconceptions that hypercementosis represented a neoplastic process, akin to tumors, due to its mass-like radiographic presentation; however, by the mid-20th century, histological studies clarified it as a reactive, compensatory phenomenon to stimuli like inflammation or mechanical forces, rather than malignant growth.^[28]

Recent Advances

A 2023 systematic review synthesized evidence from 75 studies on the etiologies of hypercementosis, confirming five key local factors: intensive and repetitive masticatory efforts, carious lesions with apical periodontitis, tooth impaction, periodontal disease, and concrescence.^[13] These factors were associated with localized cementum overgrowth, often on affected roots, while systemic influences like Paget's disease were less consistently linked.^[13] The review highlighted that idiopathic cases, comprising a significant portion without identifiable local or systemic triggers, may involve genetic predispositions, as supported by case reports of familial patterns and early-onset occurrences in young patients. Advances in dental imaging have incorporated artificial intelligence (AI) to enhance early detection of hypercementosis through cone-beam computed tomography (CBCT) analysis. AI platforms, such as Diagnocat, now automatically identify hypercementosis alongside other root abnormalities in 3D scans, improving diagnostic accuracy and efficiency in clinical settings.^[51] Studies from 2022 onward demonstrate that AI-assisted CBCT segmentation achieves high precision in delineating cementum thickness, facilitating earlier intervention before complications like ankylosis arise.^[52] Molecular research in 2024 has elucidated the role of Wnt/β-catenin signaling in driving cementoblast hyperactivity and hypercementosis. Activation of this pathway in Axin2+ periodontal progenitor cells promotes excessive cementum apposition during regeneration, leading to overgrowth as observed in mouse models.^[53] These findings suggest potential therapeutic targets, such as Wnt inhibitors, to modulate cementogenesis in pathological cases.^[53] Emerging evidence links bisphosphonate use in osteoporosis treatment to hypercementosis, particularly in areas affected by medication-related osteonecrosis of the jaw (MRONJ). A 2015 histopathological study of teeth extracted from bisphosphonate users reported hypercementosis in 87.5% of cases, often co-occurring with pulpal alterations.^[54] Recent prevalence studies from 2020 to 2025 indicate rates of 10-16% across diverse populations, with higher detection in urban cohorts possibly due to increased access to advanced imaging.^[39]^[40]