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ŠThe Maxillofacial Center for Diagnostics & Research
* Dedicated to Thomas Bond Jr., MD, of
Baltimore, Maryland -- Father of Oral Pathology
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Subpontic osseous hyperplasia is a benign proliferation of cortical bone beneath a fixed bridge. Presumably it results from unknown pressures of the bridgework on the underlying and surrounding bone, as it is never seen outside this scenario. Poor oral hygiene does not seem to be a factor. The lesion slowly enlarges and eventually presses against the overlying pontic (false tooth), causing a potential infection or irritation because the patient cannot properly clean to area under the bridge. Conservative surgical removal is the treatment in this situation, but smaller lesions need not be treated, merely followed. There is no malignant transformation potential. |
Note: click on underlined words for more detail or photos.
The subpontic osseous hyperplasia (SOH) is the least common of the benign "developmental" bony masses (tori and buccal exostoses). It seems to be unique in that it is related to intimately to prosthetic dentistry -- it only occurs on the crest of the ridge beneath the pontic of a fixed partial prosthesis. Since Calman et al first introduced this unusual anomaly in 1971 only 39 examples have been reported, although it is described in standard textbooks and there may be many more cases out there which are simply not written up in the journals. The name may be artificial, because a bony submucosal mass not found beneath a pontic will naturally be given a different diagnostic name. Other diagnostic terms used for the lesion include: reactive subpontic exostosis, subpontic osseous proliferation, subpontic osseous hyperplasia, subpontic hyperostosis, subpontic osteoma, subpontic hyperostosis and hyperostosis alveolaris externa.
Early authors suggested that SOH was an atypical mandibular torus or hereditary bony hyperplasia, but recent pathoetiologic concepts center around the combination of chronic gingival irritation and periosteal response to mechanical stresses transferred from to teeth to the bone via fixed partial denture abutments. Histopathologic evaluation of the bony masses has been to sparse to contribute to speculation as to the cause of the SOH, usually indicating merely that the bone is "viable." Viability, however, is not defined and photomicrographs published with some reports have actually shown considerable loss and pyknosis of osteocytes, i.e. the classic feature of dead bone, while others have shown atrophic fatty marrow and ischemic myelofibrosis without commenting on the significance of these changes. A recently published series of cases of subpontic osteonecrosis included a single case of SOH with microscopic evidence of ischemic damage to the bone and the marrow. These features led to speculation that this bony alteration is, in fact, influenced by underlying ischemic alteration of the marrow, probably secondarily induced by the mechanical stresses of the associated partial fixed denture.
Clinical Features: This entity is found almost universally in the posterior mandible and shows strong white race and male gender predilections, although this may easily result from unknowable case-selection biases in this very small number of reported cases. Several bilateral examples have been reported and a recent report finally has identified a maxillary example. Typically this lesion occurs many years after placement of the overlying fixed partial prosthesis. It exhibits a progressive but very slow enlargement which eventuates in tissue irritation and subpontic mucositis because of the inability of the patient to keep the subpontic space clean.
Subpontic osseous hyperplasia presents as a sessile cortical dome-shaped or flat-topped enlargement of the superior cortex beneath a pontic (Figures 1-4). Larger lesions will show a concavity on the surface, corresponding to the contour of the overlying pontic. Usually the mass is radiopaque, but often there is a focal radiolucency of the subcortical marrow, possibly indicative of regional ischemic osteoporosis. It is not unusual to find the outlines of extractions sockets remaining years after the tooth has been extracted and the space restored, probably a sign of a chronic ischemic or other low-grade phenomenon capable of interfering with good healing. Occasional cases with develop osteomyelitis of the superficial region after ischemic or inflammatory ulceration of the overlying mucosa. The mucosa is usually normal in color but may be erythematous and edematous when closely contacting the overlying pontic. Some cases will be bilobed, and at surgery the bony surface is usually smooth and not perforated, unless there has been an overlying inflammatory ulceration of the mucosa (Figure 6).
Pathology and Differential Diagnosis: Almost all cases with show a thick cortical proliferation of lamellar bone with abundant or focal loss of osteocytes (from ischemia). There may be prominent or excessive cement lines, another sign of chronic ischemia. Rarely, the lesional covering is only a thin cortex, with most of the mass comprised of fatty marrow showing areas of wispy fibrosis and vessel dilation, signs of regional ischemic osteoporosis. When infected, the marrow spaces with contain more dense fibrosis and variable numbers of chronic and acute inflammatory cells. These are all features of tori and other exostoses, but there is no difficulty in making an appropriate diagnosis because the SOH is so site-specific a diagnosis.
Treatment and Prognosis: Conservative surgical removal with bony recontouring and with relief of prosthesis-induced mechanical stresses is the treatment of choice, with occasional recurrences expected. Simple removal of the pontic irritation does not result in shrinkage of the bony mass.
Note: Click on underlined author's names for additional detail.
Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. Philadelphia, W. B. Saunders; 1995.
Elder D, Elenitsas R, Jaworsky C, Johnson B Jr. Lever's Histopathology of the skin, 8th edition. Philadelphia; Lippincott-Raven, 1997.
Sapp JP, Eversole LR, Wysocki GP. Contemporary oral and maxillofacial pathology. Mosby; St. Louis, 1997.
Odell EW, Morgan PR. Biopsy pathology of the oral tissues. London; Chapman & hall Medical, 1998.
Tinker ET. Sanitary dummies. Dent Rev 1918; 32:401-408.
Rumpel C. Prophylaktische und Functionelle Prothese. Deutsche Zahnartsliche Wochenschrift 1925; 226-234.
Reichenbach E. Untersuchungen zur Frage Ciner Zweckmassigen Gestaltung des Bruckendoppers. Vierteljahrschrift fuer Zahnheilkund. 1931; 47:125-138.
Stein RS. Pontic-residual ridge relationship: a research report. J Prosthet Dent 1966; 16:251-285. {mild stimulation under pontic may initiate a cascade that leads to activation of osteogenic growth factors]
Calman HI, Eisenberg M, Grodjesk JE, Szerlip L. Shades of white interpretations of radiopacities. Dent Radiogr Photogr 1971; 44:3-10.
Stafne EC, Gibilisco JA. Oral roentgenographic diagnosis, 4th edition. Philadelphia: WB Saunders; 1975, p. 133-134.
Strassler HE. Bilateral plateauization. Oral Surg Oral Med Oral Pathol 1981; 52:222.
Burkes EJ, Marbry DL, Brooks RE. Subpontic osseous proliferation. J Prosthet Dent 1985; 53:780-785.
Savage NW, Young WG. Reactive subpontine exostoses. Oral Surg Oral Med Oral Pathol 1987; 63:498-499.
Takeda Y, Itagaki M, Ishibashi K. Bilateral subpontic osseous hyperplasia: a case report. J Periodontol 1988; 59:311-314.
Morton TH, Natkin E. Hyperostosis and fixed partial denture pontics: report of 16 patients and review of literature. J Prosthet Dent 1990; 64:539-547.
Appleby DC. Investigating incidental remission of subpontic hyperostosis. JADA 1991; 122:61-62.
Wasson DJ, Rapley JW, Cronin RJ. Subpontic osseous hyperplasia: a literature review. J Prosthet Dent 1991; 66:638-641.
Ruffin SA, Waldrop TC, Aufdemorte TB. Diagnosis and treatment of subpontic osseous hyperplasia. Oral Surg Oral Med Oral Pathol 1993; 76:68-72.
Mesaros AJ Jr, Evans DB. Subpontic osseous hyperplasia. Gen Dent 1994; May/June:264-266.
Neville B, Damm D, Allen C, et al. Oral and Maxillofacial Pathology. Philadelphia: W. B. Saunders, 1995:17.
Frazier KB, Baker PS, Abdelsayed R. A case report of subpontic osseous hyperplasia in the maxillary arch. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000; 89:73-76.
Figure 1: Cortical mass beneath pontic overlying areas of ischemic osteonecrosis (bone marrow edema) with scalloped margins and focal sclerosis. Another area of ischemic marrow damage is seen distally (arrow). From: Bouquot JE, LaMarche, J Prosthet Dent, 1999; 81:148-158. [return to text] |
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Figure 2: Cortical proliferation is located eccentrically beneath the pontic, with a small focus of radiolucency immediately beneath its surface, representing focus of acute osteomyelitis. The mucosal surface was ulcerated and the area was painful. [return to text] |
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Figure 3: Broad based expansion of the superior cortex has occurred, with a fairly well demarcated oval radiolucency in deeper medullary area. The latter area was histologically consistent with regional ischemic osteoporosis. [return to text] |
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Figure 4: A thick, sclerotic cortical
elevation or mass is seen to have a superior concavity, corresponding to
the contour of the overlying pontic, which has been removed in the
photo. Notice the residual socket outline of the long-extracted
root (chronic ischemic problem?)
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Figure 6: Appearance of bony mass at surgery. With thanks from Dr. Brad Neville, Charleston, SC [return to text] | |
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