SUB-PONTIC TISSUE ENLARGEMENT BENEATH THE IMPLANT SUPPORTED FIXED PARTIAL DENTURE: PART 1

Subpontic tissue enlargement (STE), the cause of which is still unclear, is known by many names: osteoma,1 subpontic hyperostosis,2–5 plateauization,6 subpontic osseous proliferation,7 subpontic bony deposition,8 reactive subpontine exostoses,9 and subpontic osseous hyperplasia.10–14 The characteristic feature of STE is slow and spontaneous bone growth, which is in most cases found in the posterior region of the mandible under the pontic of a fixed partial denture (FPD). The present report illustrates a case of STE under-neath a implant-supported FPD that had been for 11 years. 

Other case of STE under IS-FPD, which appeared eight years later.

Surgically excised bone tissue emerged as STE.

The authors believe that the cause of STE in the present case was not only biomechanical loading to the mandible, but also included other factors such as chronic irritation and genetic predisposition. Implants loading in the posterior mandible might affect bone tissue structure at cellar level.  Hypertrophic action based on functional loading of the implants under the periosteum may be created and substantially born the remodeling and modeling around the IS-FPD to occlusal direction for many years.

 References

1. Calman HI, Eisenberg M, Grodjesk JE, Szerlip L. Shades of white. Interpretation of radiopacities. Dent Radiogr Photogr 1971;44:3–10. 2. Gibilisco JA. Condensing osteitis and osteosclerosis. In: Gibilisco JA (ed). Stafne’s Oral Radiographic Diagnosis, ed 5. Philadelphia,
WB Saunders, 1985:140–249.
3. Morton TH Jr, Natkin E. Hyperostosis and fixed partial denture
pontics: Report of 16 patients and review of literature. J Prosthet
Dent 1990;64:539–547.
4. Appleby DC. Investigating incidental remission of subpontic hy-
perostosis. J Am Dent Assoc 1991;122:61–62.
5. Cailleteau JG. Subpontic hyperostosis. J Endod 1996;22:147–149. 6. Strassler HE. Bilateral plateauization. Oral Surg Oral Med Oral
Pathol 1981;52:222.
7. Burkes EJ Jr, Marbry DL, Brooks RE. Subpontic osseous prolifer-
ation. J Prosthet Dent 1985;53:780–785.
8. Render PJ. Bony deposition under a fixed partial denture.
J Prosthet Dent 1985;54:524–525.
9. Savage NW, Young WG. Reactive subpontine exostoses. Oral
Surg Oral Med Oral Pathol 1987;63:498–499.
10. Takeda Y, Itagaki M, Ishibashi K. Bilateral subpontic osseous
hyperplasia. A case report. J Periodontol 1988;59:311–314.
11. Ruffin SA, Waldrop TC, Aufdemorte TB. Diagnosis and treatment of subpontic osseous hyperplasia. Report of a case. Oral Surg Oral
Med Oral Pathol 1993;76:68–72.
12. Daniels WC. Subpontic osseous hyperplasia: A five-patient report.
J Prosthodont 1997;6:137–143.
13. Frazier KB, Baker PS, Abdelsayed R, Potter B. A case report of sub-
pontic osseous hyperplasia in the maxillary arch. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod 2000;89:73–76.
14. Wasson DJ, Rapley JW, Cronin RJ. Subpontic osseous hyper-
plasia: A literature review. J Prosthet Dent 1991;66:638–641.
15. Nakai H, Niimi A, Ueda M. Osseous proliferation of the mandible after placement of endosseous implants. Int J Oral Maxillofac
Implants 2000;15:41–-424.
16. Taylor TD. Osteogenesis of the mandible associated with implant
reconstruction: A patient report. Int J Oral Maxillofac Implants
1989;4:227–231.
17. Oikarinen VJ, Siirilä HS. Reparative bone growth in an extremely
atrophied edentulous mandible stimulated by an osseointegrated implant-supported fixed prosthesis: A case report. Int J Oral Maxillofac Implants 1992;7:541-544.
18. Powers MP, Bosker H, Van Pelt H, Dunbar N. The transmandibu- lar implant: From progressive bone loss to controlled bone growth. J Oral Maxillofac Surg 1994;52:904-910.
19. Murphy WM. Clinical and experimental bone changes after intra- osseous implantation. J Prosthet Dent 1995;73:31-35.

 Citation From Kato S,Kato M, and Hanamoto H. 

Subpontic Tissue Enlargement of the Mandible Following Cross-Arch Fixed Partial Denture Reconstruction: An 18-Year Follow-up J Prosthodont 2010;23:243–245.

 

Further reading
*Modeling and Remodeling
Unique mechanisms of bone adaptation maintain skeletal integrity, repair fatigue damage, and provide a continuous stream of metabolic calcium.
Modeling involves individual and uncoupled sites of bone formation  or resorption that change the shape or form of a bone. this is the principal mechanism for adapting osseous structure to functional loading.
Remodeling is the mechanism of bone turnover . It involves coupled sequences of cell activation (A), bone resorption (R), and bone formation (F). The duration of ARF remodeling cycle (sigma) for humans is about 4 months for trabecular bone and approximately 6 months for cortical bone.

Modeling  is the principal means of skeletal adaptation to functional and therapeutic loads. Relatively modest changes in the distribution of osseous tissue along cortical bone surfaces dramatically affect the overall load-bearing capability. Similar to other structural materials, the stiffness of long bone,  such as body of the mandible, is related to the fourth power of the diameter, e.g., doubling the diameter of a bone increases its stiffness 16 times. Thus, even modest layers of mineralized tissue deposited on the outer surface of a bone can substantially increase its stiffness and strength. Skeletally atrophic patients may experience a substantial increase in skeletal mass of the mandible following a functional restoration of occlusion with implants. This is an example of the hypertrophic mechanism for increasing bone strength by adding osseous tissue at the periosteal surface.

All bones are able to adept by modeling mechanisms. Focused bone resorption and formation events are the means of trabecular "micro modeling" to optimally resist functional loads. A good example of this process is the network of secondary trusses that forms in the marrow cavity to support an integrated implants.The internal loading of the maxilla and mandible via osseointegrated implants can produce marked changes in external and internal skeletal architecture. Bone mass and geometry reflect the distribution of stress associated with dynamic loading.

Cortical bone remodeling (internal turnover) is accomplished by paravascular cutting-filling cones. The later is a functional unit of osteoclasts and osteoblasts organized around a proliferating, dedicated blood vessel. Trabecular bone (spongiosa) remodels in a similar manner vis "hemicutting-filling cones" that selectively remove and replace a set volume of bone at a specific site. The principal difference in trabecular remodeling is the lack of an internal, dedicated blood supply. The hemi-cutting-filling cone depends on the vascularity of the marrow.

Trabecular bone remodels at about 20% to 30% per year.  From a metabolic perspective, the spongiosa is the most important calcium reservoir in the body. Virtually all trabecular bone is within the metabolic fraction. Remodeling can be accomplished without compromising skeletal integrity because (1) only a small portion of supporting osseous tissue is turning over at ant time, and (2) the remodeling process preferentially attacks the metabolic fraction. The later is at least structurally important aspect of the bone.

Under most circumstances, cortical bone remodels at about 2% to 10% per year. Since only a portion of the cortex is in the metabolic fraction, the remodeling rate for cortical bone is usually 3 to 10 times less than for adjacent trabecular bone. Because all of it is in the metabolic fraction, trabecular bone usually has a remodeling rate of 20% to 30% per year.

(Citation from Orthodontic Applications of Osseointegrated  Implants: in KW Higuchi ed. Roberts WE. Bone physiology, metabolism, and biomechanics. 161-190.) 

*sigma“: The gaggle of cell phenotypes (or cell packet) responsible for
remodeling is the basic multicellur unit (BMU), and temporal duration ( i.e. , life span) of a BMU is called sigma.” Holinger JO. Bone Dynamics: Morphogenics, Growth, Modeling, and Remodeling. In; Lieberman JR, Friedlaender GE. (eds.) Bone regeneration and repair, Biology and clinical application. Totowa, New Jersey, Humana Press 2005: 1-19.