Hard tissue lumps of the oral and maxillofacial region are frequently encountered in dental and oral surgery practice. These lesions may arise from bone, cartilage, or calcified tissues and range from benign developmental anomalies to metabolic bone disorders. While many of these conditions are non-neoplastic and asymptomatic, their clinical and radiographic appearance may mimic tumours, leading to diagnostic uncertainty. A sound understanding of these conditions is essential for accurate diagnosis, appropriate management, and patient reassurance.
Table of Contents
ToggleClassification of Non-Tumour Hard Tissue Lumps
Non-tumour hard tissue lumps can broadly be classified into:
- Developmental anomalies (e.g. tori)
- Reactive or inflammatory lesions (e.g. giant cell granuloma)
- Metabolic bone disorders (e.g. Paget’s disease, brown tumour)
- Developmental fibro-osseous conditions (e.g. fibrous dysplasia, cherubism)
Understanding this classification helps clinicians differentiate benign conditions from true neoplasms and malignant disease.
Tori
Definition and Types
Tori are benign bony exostoses that arise from cortical bone. They are developmental anomalies rather than true pathological lesions and are commonly found in the oral cavity. The two principal types are:
- Torus palatinus – located along the midline of the hard palate
- Torus mandibularis – located on the lingual aspect of the mandible, typically in the premolar–molar region
These lesions may be unilateral or bilateral and vary significantly in size and shape.
Aetiology
The exact cause of tori is unknown, but several factors have been implicated:
- Genetic predisposition
- Functional stress and occlusal forces
- Environmental influences
Tori are not associated with systemic disease and should not be confused with syndromic conditions such as Gardner syndrome, which involves multiple osteomas and intestinal polyposis.
Clinical Features
- Usually asymptomatic
- Hard, immobile, and covered by normal mucosa
- Slow growing and often detected incidentally
- May become ulcerated due to trauma from food or dentures
Radiographic Features
- Dense radiopaque mass
- Continuous with underlying cortical bone
- No associated bone destruction
Management
In most cases, no treatment is required. Patients should be reassured that tori are benign and harmless. Surgical removal may be indicated when:
- They interfere with denture construction
- They repeatedly ulcerate
- They compromise oral hygiene or speech (rare)
Giant Cell Granuloma
Overview
Giant cell granulomas are benign lesions characterized by the presence of multinucleated giant cells. In the oral cavity, they may occur as:
- Peripheral giant cell granuloma – arising from gingiva or alveolar mucosa
- Central (intra-osseous) giant cell granuloma – occurring within bone
The extracted text primarily refers to the intra-osseous presentation.
Aetiology and Pathogenesis
The exact cause is uncertain, but these lesions are thought to represent a reactive process rather than a true neoplasm. Possible triggers include:
- Trauma
- Local irritation
- Inflammatory stimuli
Clinical Presentation
- May present as a painless bony swelling
- Sometimes discovered incidentally on radiographs
- More common in younger individuals
- Can cause tooth displacement or root resorption in aggressive cases
Radiographic Features
- Radiolucent lesion
- Unilocular or multilocular
- Well-defined or poorly defined margins depending on activity
Histology
- Numerous multinucleated giant cells
- Background of spindle-shaped mesenchymal cells
- Areas of haemorrhage and hemosiderin deposition
Management
- Careful surgical enucleation is the treatment of choice
- Recurrence is possible, especially with aggressive lesions
- Adjunctive treatments (e.g. corticosteroid injections) may be used in selected cases
Brown Tumour
Definition
A brown tumour is not a true neoplasm but a reactive bone lesion associated with hyperparathyroidism. It represents localized bone resorption caused by excessive osteoclastic activity.
Pathophysiology
In hyperparathyroidism, elevated parathyroid hormone levels lead to:
- Increased bone resorption
- Replacement of bone with fibrous tissue
- Accumulation of hemosiderin, giving the lesion its characteristic brown colour
Clinical Features
- May involve jaws, ribs, pelvis, or long bones
- Jaw lesions may present as painless swelling
- Can cause tooth mobility or malocclusion
Radiographic Appearance
- Radiolucent lesions
- Similar in appearance to giant cell granulomas
- May be multiple
Histology
- Indistinguishable from giant cell granuloma
- Diagnosis relies on biochemical findings, not histology alone
Diagnosis
Diagnosis is confirmed by laboratory tests showing:
- Elevated parathyroid hormone
- Altered calcium and phosphate levels
Management
- Treatment focuses on correcting hyperparathyroidism
- Surgical excision of the bone lesion is rarely required
- Lesions often regress once hormone levels normalize
Paget’s Disease of Bone
Overview
Paget’s disease of bone is a chronic metabolic disorder characterized by abnormal bone remodeling. It typically affects individuals over the age of 55 and may involve multiple skeletal sites, including the jaws.
Aetiology
The cause remains uncertain, but factors implicated include:
- Genetic susceptibility
- Viral infections (e.g. measles virus, respiratory syncytial virus)
Pathogenesis
Normal bone remodeling is replaced by a chaotic process involving:
- Excessive bone resorption
- Compensatory but disorganized bone formation
This results in structurally weak, enlarged, and deformed bone.
Clinical Features
- Bone pain
- Enlargement of affected bones
- Cranial neuropathies due to nerve compression
- In the jaws, the maxilla is more commonly affected than the mandible
Dental implications include:
- Hypercementosis of tooth roots
- Difficulty with extractions
- Poor healing following surgery
Radiographic Features
- Classic “cotton wool” appearance
- Mixed radiolucent and radiopaque areas
- Loss of normal trabecular pattern
Biochemical Findings
- Elevated alkaline phosphatase
- Increased urinary hydroxyproline
Management
- Avoid general anaesthesia where possible
- Use prophylactic antibiotics for dental procedures
- Plan extractions surgically due to risk of fracture and bleeding
- Medical management includes: Bisphosphonates and Calcitonin
Fibrous Dysplasia
Definition
Fibrous dysplasia is a developmental fibro-osseous disorder in which normal bone is replaced by fibrous connective tissue and immature bone.
Epidemiology
- Onset typically in childhood
- May be monostotic (single bone) or polyostotic (multiple bones)
- Jaw involvement is common in craniofacial forms
Pathogenesis
The condition arises from a post-zygotic mutation affecting bone-forming cells, leading to abnormal bone maturation.
Clinical Features
- Painless, slow-growing bony swelling
- Facial asymmetry when jaws are involved
- Lesions tend to stabilize after puberty
Radiographic Appearance
- Characteristic “ground-glass” appearance
- Poorly defined margins
- Loss of normal bone trabeculation
Histology
- Fibrous stroma replacing normal bone
- Irregular trabeculae of woven bone
- Trabeculae resemble “Chinese characters”
Management
Conservative management is preferred
Surgical intervention is delayed until growth stabilizes
Options include:
Skeletal resculpting
Orthognathic surgery
Orthodontic treatment
Cherubism
Definition
Cherubism is a rare, hereditary fibro-osseous condition considered a bilateral variant of fibrous dysplasia.
Genetics and Onset
- Autosomal dominant inheritance
- Presents in early childhood, typically between 2 and 4 years of age
Clinical Features
- Bilateral expansion of the mandible and/or maxilla
- Full, rounded cheeks giving a “cherubic” facial appearance
- Dental displacement and delayed eruption
- Often painless
Radiographic Features
- Bilateral, multilocular radiolucencies
- Symmetrical jaw involvement
Histology
- Similar to fibrous dysplasia
- Presence of multinucleated giant cells
Natural History and Management
- Disease activity often decreases after puberty
- Lesions may regress or “burn out”
- Surgical resculpting may be required after growth cessation
- Early aggressive surgery is generally avoided
Conclusion
Non-tumour hard tissue lumps of the oral and maxillofacial region encompass a diverse group of conditions with varying aetiologies, clinical behaviour, and management strategies. While many are benign and self-limiting, their resemblance to neoplastic disease underscores the importance of thorough clinical assessment, radiographic evaluation, and, where necessary, histological and biochemical investigation.
For dental professionals and oral surgeons, recognizing these conditions is critical to:
- Avoid unnecessary intervention
- Provide appropriate reassurance
- Plan safe and effective treatment
A systematic approach ensures optimal patient outcomes and reinforces the importance of multidisciplinary collaboration when managing complex bone disorders.
References
- Cawson, R. A., Odell, E. W., & Porter, S. R.
Cawson’s Essentials of Oral Pathology and Oral Medicine. 9th ed. London: Elsevier; 2017.
– Comprehensive reference for tori, giant cell lesions, fibrous dysplasia, and Paget’s disease affecting the jaws. - Scully, C.
Oral and Maxillofacial Medicine: The Basis of Diagnosis and Treatment. 4th ed. London: Elsevier; 2019.
– Authoritative source on non-neoplastic oral and maxillofacial bone disorders. - Neville, B. W., Damm, D. D., Allen, C. M., & Chi, A. C.
Oral and Maxillofacial Pathology. 4th ed. St. Louis: Elsevier; 2016.
– Detailed histopathology and clinical correlation of giant cell granuloma, brown tumour, fibrous dysplasia, and cherubism. - Peterson, L. J., Ellis, E., Hupp, J. R., & Tucker, M. R.
Contemporary Oral and Maxillofacial Surgery. 7th ed. St. Louis: Elsevier; 2019.
– Surgical management principles and dental implications of metabolic and developmental bone disorders. - Regezi, J. A., Sciubba, J. J., & Jordan, R. C. K.
Oral Pathology: Clinical Pathologic Correlations. 7th ed. St. Louis: Elsevier; 2017.
– Classic reference for differential diagnosis of fibro-osseous lesions. - Marx, R. E., & Stern, D.
Oral and Maxillofacial Pathology: A Rationale for Diagnosis and Treatment. 3rd ed. Hanover Park: Quintessence; 2012.
– In-depth discussion of metabolic bone diseases including Paget’s disease and hyperparathyroidism. - Whyte, M. P.
Paget’s disease of bone. New England Journal of Medicine. 2006;355(6):593–600.
– Seminal review on pathogenesis, clinical features, and management of Paget’s disease. - Chapurlat, R. D., & Orcel, P.
Paget’s disease of bone. The Lancet. 2008;372(9633):155–163.
– Evidence-based overview including biochemical markers and bisphosphonate therapy. - Triantafillidou, K., Venetis, G., Karakinaris, G., & Iordanidis, F.
Central giant cell granuloma of the jaws: A clinical study of 17 cases. Journal of Oral and Maxillofacial Surgery. 2011;69(6):e60–e65.
– Clinical behaviour and management of central giant cell granulomas. - Kaban, L. B., Troulis, M. J., & Ebb, D.
Fibrous dysplasia of the craniofacial bones. Oral and Maxillofacial Surgery Clinics of North America. 2006;18(4):507–524.
– Definitive reference for fibrous dysplasia and cherubism. - Papadaki, M. E., et al.
Cherubism: Best clinical practice. Orphanet Journal of Rare Diseases. 2012;7(Suppl 1):S6.
– Modern consensus on diagnosis, natural history, and management of cherubism.
