Subpontic osseous hyperplasia: A case series and literature review

Abstract

A subpontic osseous hyperplasia (SOH) is a slow-growinxg, non-neoplastic bone growth that uniquely affects mandibular posterior edentulous ridges underneath pontics of fixed partial dentures. An SOH can result in significant periodontal and restorative complications, however, it is usually corrected by surgical excision. This report presents a series of SOH cases, illustrates SOH management approaches, and reviews the literature on SOH clinical presentations. Published with permission of the Academy of General Dentistry. © Copyright 2014 by the Academy of General Dentistry. All rights reserved.

Full text

Subpontic osseous hyperplasia: a case series
and literature review
Connie A. Lee, DDS, MS n Michael B. Lee, DDS, MS n Chad R. Matthews, DMD, MS n Dimitris N. Tatakis, DDS, PhD
A subpontic osseous hyperplasia (SOH) is a slow-growing, non-neoplastic
bone growth that uniquely affects mandibular posterior edentulous
ridges underneath pontics of fixed partial dentures. An SOH can result in
significant periodontal and restorative complications, however, it is usually
corrected by surgical excision. This report presents a series of SOH cases,
illustrates SOH management approaches, and reviews the literature on
SOH clinical presentations.
Received: August 25, 2012
Accepted: January 28, 2013
Only a limited number of condi-
tions and deformities manifest
themselves on edentulous ridges. In
fact, the pertinent subcategory introduced
in a classification scheme includes only 6
clinical entities: vertical and/or horizontal
ridge deficiency, lack of gingiva/keratin-
ized tissue, gingival/soft tissue enlarge-
ment, aberrant frenum/muscle position,
decreased vestibular depth, and abnormal
color.1 Of these, only the first (ridge
deficiency) can be considered specific to
edentulous ridges. Another condition/
deformity specific to edentulous ridges is
the subpontic osseous hyperplasia (SOH).
SOH, first described in 1971 by Calman
et al, is a non-neoplastic growth of bone
underneath pontics of fixed partial den-
tures (FPDs); therefore, SOH uniquely
affects edentulous ridges bound by FPD
abutment teeth.2
SOH is relatively uncommon, usu-
ally asymptomatic, and can occur from
several months to many years after FPD
insertion.3 The lesion typically presents
unilaterally, even in the presence of
bilateral FPDs, and has a predilection for
the mandible, particularly the first molar
region.4-6 Routinely, both the radiographic
and histologic features of SOH are con-
sistent with normal, compact, lamellar
bone, similar to other exostoses.2 ,5-7 The
size and shape of an SOH lesion depends
on its growth stage, the dimension of the
edentulous space, and the position and
shape of the inferior border of the associ-
ated pontic.6 Various etiologic factors have
been suggested, but the exact etiology of
SOH remains unknown.3,5,6
Fig. 1.
(Case No. 1)
Periapical radiographic images of the fixed partial denture ( FPD) . A. Eleven years prior to treatment. B. Six years prior to treatment.
C. Fourteen months prior to treatment. Note the progressive increase in lesion dimensions, the obliteration of the space under the pontic, and the
increasing proportion of the radiopaque, cor tical bone-like, coronal aspect of the lesion.
A B C
Fig. 2.
(Case No. 1)
Buccal views of the FPD. A. Preoperative. B. Following flap elevation with bony lesion exposed (note the correspondence with
Fig. 1C.). C. Following resection. D. At 6 weeks postoperative.
Prosthodontics/Fixed
46 July/August 2014 General Dentistry www.agd.org
A B C D

Although SOH lesions per se may go
unnoticed by patients, increasing difficulty
in oral hygiene practices under the FPD
is often reported.3,5,6 Few reported cases
include patients that reported discomfort/
sensitivity or pain in the area.6,8-11 The
growing size of an SOH may impinge on
the FPD pontic(s), leading to loosening or
dislodgement of the FPD.3,5,6 Progressively
increasing limitation of access to the FPD
abutment teeth could result in caries
development.5 The impaired oral hygiene
around SOH-associated teeth may also
lead to localized gingival inflammation
and periodontal attachment loss.5,7,8 The
periodontal and restorative complications
of SOH constitute the main indications
for treatment, which routinely consist of
surgical excision.5,6 The purpose of this
article is to present a series of SOH cases,
illustrate SOH treatment approaches, and
review the literature on the clinical presen-
tation of SOH.
Case No. 1
A 79-year-old woman presented to one
of the authors with a medical history
including hearing loss, frequent urination,
chronic obstructive pulmonary disease,
arthritis, stroke, and congestive heart
failure. She was taking several medications,
including atenolol, quinidine, captopril,
coumadin, oxycodone, furosemide, and
lovastatin. She reported a 45- to 50-year
smoking history, quitting at age 69. She
also reported receiving dental prophylaxis
every 6 months. She denied any history of
parafunctional habits or any oral pain.
Oral examination revealed the space
under the bar-like pontic of the patient’s
full gold FPD (replacing tooth No. 30)
was obliterated (Fig. 1 and 2). Radiographs
obtained from the patient’s general dentist
indicated that the lesion—already pres-
ent 11 years prior to presentation to the
author—had grown substantially over the
years. The lesion was clinically diagnosed
as SOH. The radiographs also showed
evidence of remaining extraction socket
lining, suggesting a slow remodeling of
the extraction socket cortical walls. Deep
(6-8 mm) probing depths were present on
teeth No. 29 and 31. There was also evi-
dence of attachment loss in other localized
areas. No tori were present. The patient
received nonsurgical mechanical therapy,
and maintenance care was recommended.
The patient presented again 14 months
after the initial therapy and the probing
depths around teeth No. 29 and 31 had
increased by 1-2 mm. Surgical removal
of the SOH was recommended. At the
time of surgery, buccal and lingual full
thickness flaps were elevated, the SOH
was removed using rotary and hand
instruments, flaps were closed with 4-0
silk sutures, and periodontal dressing was
applied. Analgesic medication (acetamin-
ophen) and antimicrobial rinse (chlorhexi-
dine) were prescribed. Postoperative
follow-ups at 1, 3, and 6 weeks revealed
healing within normal limits. The patient
did not return for any appointments
beyond the 6-week postoperative visit,
despite repeated invitations to do so.
Case No. 2
A 47-year-old man presented to the
Graduate Periodontology clinic, The Ohio
State University, for consultation regarding
gingival recession on his maxillary central
incisors. Following a clinical examination,
and upon further discussion, the patient
related increasing difficulty in performing
oral hygiene procedures under an FPD
that had replaced tooth No. 30. The space
under the pontic had been obliterated.
Previous radiographs were obtained from
the patient’s general dentist. Seventeen
years prior to the patient’s presentation
to the authors, tooth No. 30 had been
extracted due to caries and pulpal involve-
ment. A 3-unit gold FPD was inserted,
and 10 years later, during a visit to his gen-
eral dentist, a subpontic lesion was noted.
Radiographically, the extraction socket
lining was still evident and the subpontic
osseous mass appeared somewhat less radi-
opaque than the adjacent alveolar bone.
Subsequent radiographs revealed that the
lesion had increased in density and mesio-
distal length under the pontic (Fig. 3). The
lesion was clinically diagnosed as SOH.
The patient, who did not have any tori,
declined both a proposed removal of the
lesion and a proposed treatment for his
maxillary central incisors, and did not
return to the clinic.
Case No. 3
A 64-year-old woman was referred to the
Graduate Periodontology clinic due to
localized increased pocketing (5-6 mm).
She was systemically healthy and took
multivitamin tablets daily. Upon examina-
tion, it was noted that the space under her
mandibular left full gold bar-like pontic
(replacing tooth No. 19) was obliter-
ated; the patient was not able to perform
proper hygiene measures in the area. Tooth
No. 19 was extracted approximately 30
years prior to presentation. An FPD was
inserted approximately 15 years after the
Fig. 3.
(Case No. 2)
Periapical radiographic images of the FPD. A. Seven years prior to initial visit. B. Four years prior to initial visit. C. At initial visit. Note
the progressive increase in lesion dimensions and the increasing proportion of the radiopaque, cortical bone-like, coronal aspec t of the lesion.
A B C
www.agd.org General Dentistry July/August 2014 47

extraction and replaced after 7 years for
unknown reasons. Neither discomfort
nor pain was reported by the patient.
Gingiva was erythematous with some areas
of bleeding on dental probing. Probing
depths were ≤4 mm, except for tooth
No. 17 (mesial, 6 mm) and tooth No. 18
(mesial, 5 mm). There was also a Grade
II furcation involvement on tooth No. 18
(lingual). No mobility was noted. Wear
facets on all teeth suggested bruxism. The
patient’s overall hygiene was good and she
had a midpalatal torus.
The radiographically evident bony mass
was hemispherical in shape and filled the
entire subpontic space. Previous radio-
graphs were retrieved, which indicated
that the size of the bony mass—clinically
diagnosed as SOH—had grown in size
during the 3 years prior to presentation.
The radiographic appearance of the central
portion of the alveolar bone suggested the
presence of a benign fibro-osseous lesion,
most consistent with focal cemento-osseous
dysplasia, which was apparently unchanged
during the same period (Fig. 4).
The proposed treatment plan included
surgical removal of the SOH, osseous sur-
gery on tooth No. 17, and bone grafting
(lingual furcation of tooth No. 18), while
Fig. 5.
(Case No. 3)
Buccal views of the FPD. A. Preoperative. B. Following flap elevation with bony lesion exposed. C. Resection using piezosurgical tip.
D. Flaps sutured. E. Nine days postoperative. F. Eighteen months postoperative.
A B C
D E F
Prosthodontics/Fixed Subpontic osseous hyperplasia: a case series and literature review
48 July/August 2014 General Dentistry www.agd.org
Fig. 4.
(Case No. 3)
Periapical radiographic images of the FPD. A. Three years prior to initial visit. B. At initial visit (note the increase in lesion dimensions
and the increased proportion of the radiopaque, cortical bone-like, coronal aspect of the lesion, which corresponds with Fig. 5B). C. Nine months
postoperative. D. Eighteen months postoperative, which corresponds with Fig. 5F (note the mixed radiolucent /opaque area of alveolar bone, consistent
with focal cemento-osseous dysplasia ).
A B C D

Table. Summary of case reports of subpontic osseous hyperplasia (SOH).
Author
Case
No. Gender
Age
(yrs) Race
Affected
areaa
FPD
units Material Design
U/Bi
lesion Timeb (yrs)
Periodontal
complicationsc
Tori or
exostoses?
Calman et al 19712 1 F 45 - - - - - U - - -
Stafne & Gibilisco 197512 2 - - - - - - - U - - -
Strassler 198113 3 M 58 C19/ 30 3 - Bar Bi 14 - -
Burkes et al 19853 4 M 64 -19/30 3Gold Bar Bi 20 Y Y
5 M - - 19 3Gold Hygienic U<1 - Y
6 F 58 -30 3 - - U - - N
7 F 46 -30 3Gold - U several - Y
8 F 42 -20 - - Bar U 9 - N
9 M 65 -30 - - - U 7 Y N
10 F59 -19/ 30 5/3 - Saddle /
Hygienic
Bi - - Y
11 F49 -20 3 - - U several - Y
12 M68 -19 3 - Hygienic U - - Y
Render 198515 13 - - - 19 3Gold Hygienic U - - -
Savage & Young 19874 14 M47 C30 3Gold Hygienic U20 N -
15 F60 C19 - - - U - - -
Takeda et al 19887 16 F42 A19/ 30 -Silver Bar Bi 20 Y N
Morton & Natkin 19906 17 F42 C19 / 30 - - - Bi - - -
18 M 79 C L 2PM-2M - - - U - - -
19 M54 CR 2PM -1M 3 - - U - - -
20 F56 C30 - - Bar U - - -
21 M53 C19 - - - U - - Y
22 M42 C30 - - - U - - Y
23 M81 C19 3 - Hygienic U - - -
24 F29 A30 - - Bar U - - -
25 M68 CR 2PM-2M,
L 1M-2M
4c- - Bi 5 - Y
26 M45 C19 3 - Bar U 5 - Y
27 M55 C19 - - - U - - -
28 M46 C30 - - - U - - -
29 F68 C19 3 - - U - - -
30 F51 C R/L
2PM-1M
3 - Bar Bi - - -
31 F53 CL 1M-2M 3 - Bar U - - -
32 M35 C19 - - - U 3 - Y
Appleby 199116 33 F52 C30 3 - - U 7 - Y
Abramovitch 199318 34 - - - 19 - - Hygienic U - Y -
Ruffin et al 199322 35 F 67 C 19 3Gold Bar U35 Y Y
Cataldo & Santis 199339 36 F55 -2PM-1PM 4c-Hygienic U 7 - -
Mesaros & Evans 199423 37 F46 -19 3Gold Hygienic U>20 Y Y
www.agd.org General Dentistry July/August 2014 49

retaining the existing FPD. At the time of
surgery, full-thickness flaps were elevated,
the area was debrided, and the teeth were
root planed. A piezoelectric instrument
was used to resect the SOH. The remain-
ing alveolar ridge, which was clinically
normal, was smoothed and recontoured
parallel to the pontic. The removed SOH
was ground with a bone mill and used as
an autogenous particulate bone graft in
the treatment of tooth No. 18. Primary
flap closure was obtained with polyglycolic
acid sutures. The patient was prescribed
chlorhexidine gluconate oral rinse 0.12%
BID, acetaminophen 500 mg (5-6 times
daily, or as needed for pain), and amoxicil-
lin 250 mg TID/7 days. Postoperative
healing was uneventful (Fig. 5).
The patient was placed on regular
maintenance recalls every 3 months. She
reported much easier hygiene practice in
the area. Six months postsurgery, all prob-
ing depths were ≤4 mm. Furcation involve-
ment on tooth No. 18 was improved, but
not eliminated. At 18 months posttreat-
ment, a radiographic assessment suggested
the possibility of SOH recurrence (Fig. 4).
Table continued. Summary of case reports of subpontic osseous hyperplasia (SOH).
Author
Case
No. Gender
Age
(yrs) Race
Affected
areaa
FPD
units Material Design
U/Bi
lesion Timeb (yrs)
Periodontal
complicationsc
Tori or
exostoses?
Cailleteau 199617 38 M64 A30 3Gold - U 40 Y Y
39 F 79 - 19/ 30 3/4c- - Bi - - -
Daniels 19975 40 M30 C19 3Gold Hygienic U11 N N
41 F38 C19 3Gold Hygienic U13 Y Y
42 M44 C2PM-1M 3Gold Bar U24 - N
43 M47 B30 -PFM Mod
ridge-lap
U 9 Y Y
44 M73 C30 3PFM - U 10 - N
Beaumont 199714 45 -61 -19/ 30 - - - Bi >22 - -
Bouquot & LaMarche
199940
46 - - - 30 -PFM - - - - -
Lorenzana & Hallmon
20008
47 F56 -19 3Gold Hygienic U25 Y N
Frazier et al 20009 48 M65 C 3 3 - - U 10 Y -
Ide et al 200320 49 F65 A19 3 - Hygienic U15 Y -
Kessler & Phillips 200610 50 M - - 19/30 3 - - Bi 3 Y -
Islam et al 201021 51 F65 -19 - - Hygienic U - - -
52 M 78 - 30 - - - U - Y -
53 F80 -19 3Gold Hygienic U - Y -
Kato et al 201011 54 F73 A19 Cant PFM - U 18 - N
Present study 55 F 79 C 30 3Gold Bar U>10 Y N
56 M47 C30 3Gold Hygienic U17 Y N
57 F64 A19 3Gold Bar U 8 Y Y
Summary 57 52% Fd
48% Md
Mean
56.6e
18% Af
3% Bf
79% Cf
18% Big
82% Ug
62% Yh
38% Nh
Abbreviations: -, indicates missing o r unknown data; A , Asian; B, Black; C, Caucasian; F, female; M, male; FPD, fixed par tial denture; Cant, cantilever; M, molar; PM premolar; PFM,
porcelain-fused-to-metal; U, unilateral ; Bi, bilateral;Y, yes; N, no.
aTime since FPD insertion
bOral hygiene difficulty; increased probing depth and/or gingival inflammation around abutment teeth.
cFPD with 2 pontics and 2 abutments
dBased onl y on those s tudies w ho repor ted this information (n = 52)
eBased onl y on those s tudies w ho repor ted this information (n = 51)
fBased onl y on those s tudies w ho repor ted this information (n = 34)
gBased onl y on those s tudies w ho repor ted this information (n = 56)
hBased onl y on those s tudies w ho repor ted this information (n = 29)
Prosthodontics/Fixed Subpontic osseous hyperplasia: a case series and literature review
50 July/August 2014 General Dentistry www.agd.org

Discussion and literature review
The present report documented a series
of radiopaque lesions that occurred under
FPD pontics. The lesions were clinically
diagnosed as SOH, and all occurred in
the mandibular first molar area. The
management of this slow-growing, benign
lesion is by surgical excision, using hand,
rotary, or piezoelectric instruments.
The bone excised during the treatment
of this exostosis-like tissue growth can
be a source of autogenous bone graft, as
reported in the third case.
SOH, first described by Calman in
1971, has been reported in the literature
under various names, including osteoma,
hyperostosis, plateauization, subpontic
osseous proliferation, subpontic bony
deposition, reactive subpontine exostosis,
subpontic hyperostosis, pontic hyperostosis,
hyperostosis alveolaris externa, and subpon-
tic tissue enlargement.2-4,6-18
The Table summarizes the limited
number of reported SOH cases in chrono-
logical order. Among those cases that
reported age and race, the average patient
diagnosed with SOH was Caucasian
(~80%) and 56.6 years of age. SOH
manifests equally in both genders, mostly
as a unilateral lesion (82% of the cases in
the Table that reported on lesions) and
overwhelmingly in the mandibular first
molar area, under an FPD that is typi-
cally 3 units with a bar/hygienic pontic
design, and made of gold. Although on
rare occasions, SOH has been reported as
early as within the first year of FPD place-
ment, the majority of cases have an FPD
history >7 years.3
Many reports, the present one included,
have noted that the radiographic appear-
ance of SOH is more radiopaque than the
underlying ridge, with a tendency for the
radiopacity to increase with time. Others
have noted a mixed radiopaque/radiolu-
cent appearance, while some have reported
a thin radiolucent line separating the ridge
from the growth.3,4,6-8,18-21
The typical approach to SOH manage-
ment has been to excise the bony growth,
as was performed in this report.3,5,7-9,16
Recurrence after excision is rare, as is
spontaneous regression.3,5 ,16 As part of
SOH management, some authors have
suggested removal of the FPD and
replacement of the missing teeth with
implants.3,5 ,8, 9,16
The etiology of OH has not been
definitively established. The most com-
monly suggested etiologic factors have been
functional/occlusal stress, chronic localized
inflammation/tissue irritation, or a combi-
nation thereof.2-7,11,12,20,21 The possible role
of genetics has also been suggested.3,6,11,17,21
Soft tissue impingement, a functionally cre-
ated vacuum under the pontic, trauma from
oral hygiene practices under the pontic,
generation of electric currents, and muscle
insertion or hyperactivity have also been
suggested as etiologic factors.6,8,11,15,17,22,23
Among the potential etiologic/contrib-
uting factors mentioned above, functional
stress and genetics appear to be the ones
supported by suggestive findings.24 -26 The
shape and dimensions of the mandible
change during opening and closing, pos-
sibly resulting in additional functional
stresses in the FPD area, thus becoming
the trigger for bone growth.24, 25 Ralph
& Caputo showed that stress patterns
become concentrated on the cortical
plates when vertical loads are applied
in the mandible.26 These facts, along
with the differences between maxilla
and mandible with respect to cortical
bone content, cortical plate thickness,
and shape changes during mouth move-
ment could explain the almost exclusive
presentation of SOH in the mandible.
Most SOH cases occur under bar-like or
hygienic pontics; it is possible that such
pontic designs allow for higher bending
stress distribution on the edentulous
ridge, due to connectors that are thinner
in comparison to other pontics. To date,
SOH has not been reported under short-
span FPDs supported by implants placed
in the posterior mandible. However, bone
growth in the molar region of the man-
dible has been reported under the canti-
lever portion of fixed full arch prostheses
supported by interforaminal implants.2 7, 2 8
This coincident bone growth suggests
that the molar region of the mandible
may be particularly susceptible to reactive
bone formation in response to functional
stresses, regardless of whether the stress
originates from tooth-supported posterior
FPDs, as in the case of SOH, or implant-
supported fixed full arch prostheses.
Of the cases in the Table that reported
on tori/exotosis incidence, 62% reported
tori/extosis and 38% did not. In subjects
>20 years of age, the reported clinical
prevalence of tori from various large-scale
studies ranged from <10% to 15%-25%,
and as high as 40% occasionally in select
populations.19,29-33 Therefore, there appears
to be a strong association between SOH
and tori/exostoses, as previously suggested.3
One of the 3 cases presented in this report
was associated with a palatal torus. In this
context, it should be noted that presence
of tori has been associated with other oral
exostoses and a greater height of interden-
tal alveolar bone, regardless of the presence
or absence of occlusal stress (parafunctional
habits).34-36 It is possible that SOH shares
the same genetic predisposing factors
implicated in tori development.37,38 The
strong association between SOH and tori/
exostoses is also reflected in the similar
complications they present under FPDs,
such as hyperostosis and chronic pain.39,40
In summary, SOH is a slow-growing,
benign, osseous lesion distinctly associated
with mandibular posterior edentulous ridges
bounded by FPD abutment teeth. SOH
can result in significant periodontal and
restorative complications, therefore patients
presenting with SOH should be appropri-
ately and promptly managed.
Author information
Dr. C. Lee is in private practice in Maple
Grove, Minnesota. Dr. M. Lee is in
private practice in Redlands, California.
Dr. Matthews is in private practice in Rock
Hill, South Carolina. Drs. C. Lee and
Matthews are former residents, Division of
Periodontology, College of Dentistry, The
Ohio State University, Columbus, where Dr.
Tatakis is a professor and program director.
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