CDR 2006

CDR
Columbia Dental Review 2005-2006

EDITORIAL BOARD
AIM & SCOPE

The Columbia Dental Review is an
annual publication of Columbia University College of Dental Medicine
(CDM). This journal is intended to
be a clinical publication, featuring
case presentations supported by
substantial reviews of the relevant
literature. It is a peer-reviewed
journal, edited by the students of
the school. The editors are selected on the basis of demonstrated
clinical scholarship.
Authors are primarily CDM students
from predoctoral and postdoctoral
programs, CDM faculty and residents, and attendings from afliated hospitals. Peer reviewers are
selected primarily from the CDM
faculty. Instructions for authors
wishing to submit articles for future
editions of the CDR can be found on
the last page of this journal. Opinions expressed by the authors do
not necessarily represent the policies of the Columbia University College of Dental Medicine.
Editors-in-Chief
George Pliakas 06
Christopher Choi 06
Design and Layout
Petar Hinic 06
Editors
Ashi Adamjee 06
Caroline Hocking 06
Tiffany Huang 06
Eleni Michailidis 06
Lavanya Venkateswaran 06
Rishi Verma 06
Assistant Editors
Nicolas Beabeau 07
Sung Cho 07
Evan Christensen 07
Keith Da Silva 07
Sylvia Lin 07
Jae Oh 07
Michael Perrino 07
Mussaad Razouki 07
Faculty Advisor
Letty Moss-Salentijn, DDS, PhD
Faculty Reviewers
Thomas Cangialosi, DDS
Heera Chang, DDS, MD
Steven Chussid, DDS
Martin Davis, DDS
Sidney Eisig, DDS
John Grbic, DMD
Kunal Lal, DDS
Evanthia Lalla, DDS
Louis Mandel, DDS
Tracey Rosenberg, DDS, MD
Letty Moss-Salentijn, DDS, PhD
Margherita Santoro, DDS
George White, DDS
Angela Yoon, DDS
Michael Yuan, DDS
2006 Columbia Dental Review
EDITORS NOTE
The Columbia Dental Review has
served as a voice for students of
the College of Dental Medicine who
have delved into clinical research,
in collaboration with faculty, to explore the signicance of individual
cases within dentistrys various
elds.
Celebrating our tenth volume, we
hope to have continued this long
tradition in a manner worthy of our
predecessors. We were fortunate
to be guided in the inception of this
volume by Andrea Smith 05. Her
devotion to the ninth volume was
integral to its success as recipient
of the Meskin Journalism Award for
excellence in Dental Student Publications.
We extend special thanks to Dr.
Letty Moss-Salentijn and Petar Hinic, whose tireless efforts are representative of the best which CDM
has to offer. Dr. Salentijns guidance
for the CDR has kept this student
publication alive and well, creating
a smooth transition as the torch is
handed down from one class to the
next. Petar Hinics talent and skills
in computer design, as well as dedication, exude from every page of
this volume. We were humbled by
his transformation of the individual
articles into one cohesive collection
unied by his touch.
Finally, we would like to thank the
authors, faculty reviewers, and assistant editors. Certainly, this tenth
volume of the CDR would not have
been possible without their contributions.
CDR

Table of Contents
Keith Da Silva
Sidney Eisig, DDS
Ameloblastoma: A Case Report and Literature Review
David Webb
Stephen Petty
Rick Tsay, DMD, MD
Vincent Carrao, DDS, MD
Spontaneous Mandibular Bone Regeneration
David Koslovsky
Howard Israel, DDS
Stephanie Drew, DMD
Tara Plansky, DMD
C.J. Langevin, DMD, MD
Laike Stewart, DVM
David Behrman, DMD
Reconstruction of the Temporomandibular Joint with

Distraction Osteogenesis in the Minipig Animal Model
15 Paul Li
Tracey Rosenberg, DDS, MD
Hemangioma: A Case Report and Literature Review
19 Candice Zemnick, DMD, MPH Jigs, Guides, Indices, Matrices and Templates in Implant
Dentistry: Prosthodontic Case Control in Implant Dentistry
25 Mussaad Razouki
Parotid Gland Swelling in Patients Seropositive for

Human Immunodeciency Virus
29 Dan Ponce, DDS
A case report of continued tooth development

following traumatic coronal amputation in an 11 month
old boy: Phantom tooth?
Louis Mandel, DDS
Ji Young Kim, DDS

Shantanu Lal, DDS
Front Cover: Eleni Michailidis, Class of 2006, College of Dental

Medicine, working in the lab of Dr. Angela Christiano, Departments of Dermatology, Human Genetics and Development,
Columbia University, New York, NY. Photographed and laid out by
Petar Hinic, Class of 2006, College of Dental Medicine, Columbia
University, New York, NY.
Ameloblastomas are benign, slow-growing odontogenic neoplasms. They are the

most common neoplasms affecting the jaw, yet only constitute approximately 1%
of all cysts and tumors of the maxilla and mandible and 11% of all odontogenic tumors1-3. An ameloblastoma can arise anywhere in the maxilla or mandible, although
the molar region of the mandible and the area surrounding the ascending ramus
appear to be the most common sites4-5. It is an aggressive tumor of epithelial origin
which may arise from the enamel organ, follicle, periodontal ligament, lining of an
odontogenic cyst or marrow of the jaws6-8. Its biological behavior is characterized by
local invasion, resistance to various therapeutic regimens and increased rates of local
recurrence. Ameloblastomas rarely metastasize9-11. We present a case report of a
multicystic ameloblastoma which was treated with surgical resection.
CASE REPORT
Keith Da Silva1
Sidney Eisig, DDS2
1
Class of 2007, College of Dental Medicine,
Columbia University, New York, NY
2
George Guttmann Professor of Clinical Craniofacial Surgery; Division Director, Oral and
Maxillofacial Surgery; Chief, Hospital Dental
Service, New York Presbyterian Hospital,
CDR
A 32 year old woman reported to the department of in the fourth decade2, 4,12. There is some statistical evioral surgery with a lingual swelling in the region of the dence to suggest that ameloblastomas are more comsecond and third mandibular molars on the left side mon in African populations when compared to Cauca(Fig. 1). A panoramic radiograph of the region revealed sians13-14, and there is a predilection for this lesion to
a well circumscribed multilocular radiolucency below occur in males2,4,12. Approximately 80% of ameloblastomas occur in the mandible
the second and third moand are often associated
lar extending beyond the
with unerupted teeth10,15-17.
inferior border of mandiThe remaining 20% occur
ble (Fig. 2). A computed
in the maxilla and are most
tomography (CT) scan
commonly associated with
conrmed the lesion as a
the maxillary tuberosity6.
soft tissue expansion into
Four clinical types of amthe oor of the mouth
eloblastoma have been de(Fig. 3). Aspiration of the
scribed: unicystic amelolesion revealed a viscous,
blastoma, solid multicystic
mucous-like
material.
ameloblastoma, peripheral
A biopsy was then perameloblastoma, and maformed and microscopic
lignant
ameloblastoma.
examination conrmed
The unicystic ameloblasthe diagnosis of multitoma resembles a typical
cystic
ameloblastoma
cystic lesion with either an
(Fig. 4). After extraction
intraluminal or intramural
of the second and third
molars, the patient was Fig. 1. Intraoral photograph depicting a lingual swelling proliferation of the cystic
lining. Diagnosis is based
taken to the operating in the posterior region of the mandible (black arrow)
on the radiological nding
room for radical surgical resection of the ameloblastoma along with 1.5 cm of a well-circumscribed unilocular lesion as well as hisof adjacent healthy bone (Fig. 5). The mandible was tological evidence of an ameloblastoma18. Microscopithen rebuilt with a reconstruction plate (Fig. 6), and cally, unicystic ameloblastomas consist of cystic lesions
the patient was brought to the recovery room in stable in which one or more of the following are present: (1)
a basal cell layer containing columnar cells resembling
condition.
ameloblasts, (2) hyperchromatic nuclei having vacuoDISCUSSION
lated atypical cytoplasm polarized from the basal lamina and (3) a loose stellate reticulum-like epithelium
Ameloblastomas can occur over a wide age range. lining the basilar ameloblast-like cells19-20. Unicystic
However, the average age at the time of diagnosis falls ameloblastomas are clinically less aggressive than the
Volume 10 : 2005-2006
Columbia Dental Review
Fig. 2. Radiograph illustrating a well circumscribed multilocular radiolucency. The lesion appears below the
second and third molar on the left side and borders are
indicated with white arrows
Fig. 3. An Axial CT scan revealed the presence of a soft

tissue lesion originating from the mandible and extending into the oor of the mouth (white arrow)
solid multicystic variety18.

The solid multicystic ameloblastoma is locally aggressive and can grow to an enormous size that may produce marked facial deformity and serious debilitation.
Since it tends to inltrate between the trabeculae of
cancellous bone, the actual margin of the tumor extends beyond the radiographic margins, and high recurrence rates have been reported after curettage. The
radiographic appearance is variable and can be either
unilocular or multilocular21. Many histological patterns
of the lesion have also been described and these include: follicular, plexiform, acanthomatous, granular
cell, desmoplastic, basal cell type, squamous metaplasia and clear cell18-19. The solid multicystic ameloblastoma has a poorer prognosis than the unicystic lesion21.
The peripheral ameloblastoma has been described as
having the histological characteristics of an intraosseous ameloblastoma but occurring in the soft tissue,
primarily the alveolar mucosa. The lesion does not invade underlying bony structures but it may cause local
erosion. This variety of ameloblastoma is a rare entity19. The malignant ameloblastoma is also extremely
rare. It has been dened as an ameloblastoma that
has metastasized but retains its histologically benign
features11,22-23.
An ameloblastoma is usually quiescent for some time

before a patient presents with symptoms24. It often rst
presents as a slow-growing, painless and asymptomatic
swelling. Other signs and symptoms may include, but
are not limited to, facial deformity, malocclusion, tooth
mobility, root resorption, ulcerations and periodontal
disease24-25. Paresthesia is very rare.
Proper diagnosis is essential for treatment planning
and management of an ameloblastoma. Radiology,
histopathology and location are all important factors
for determining the severity and extent of the lesion.
Computed tomographic (CT) scanning and magnetic
resonance imaging (MRI) have also been used as diagnostic aids and are useful for delineating soft tissue
structures and determining the extent of the lesion26.
In the early stages, the lesion may appear cystic, unilocular and may resemble a dentigerous or a residual
cyst. Later it can become multilocular with a characteristic soap bubble or honeycomb appearance, and
expansion of the cortical plates may be seen if the lesion is large.
Ameloblastomas are traditionally managed surgically.
Treatment can range from conservative surgical intervention to radical surgical treatment. Conservative
treatment is generally reserved for smaller lesions and
Fig. 4. Photomicrographs revealing typical pathology of a multicystic ameloblastoma. Note the
basal cell layer containing columnar cells resembling ameloblasts
with hyperchromatic nuclei (black
arrows)
Volume 10 : 2005-2006
Fig. 5. Photograph shows the resected portion of the

mandible. Note the ameloblastoma plus adjacent bone
was removed
unicystic ameloblastomas. One option for conservative

treatment involves curettage or the surgical scraping
of the wall of the cavity within the soft tissues or bone
for removal of its content19. The rate of recurrence
after curettage is often high. However, both Feinberg
et al.27 and Emmings et al.28 report a decreased recurrence rate when curettage is combined with liquid
nitrogen spray cryosurgery. When the lesion is larger
or multilocular, wide resection is required. Wide resection is based on the principle that the exact margins of
the ameloblastoma are not radiographically apparent.
Most investigators agree that it is necessary to resect
at least 1-1.5 cm of normal bone beyond the apparent tumor margin19,29. Resection can be marginal and
segmental, or hemisections creating continuity defects
of the mandible or maxilla may need to be performed
Fig. 6. Photograph of the mandible after being rebuilt

with a reconstruction plate
Volume 10 : 2005-2006
depending on the extent of the lesion19. Adjacent soft

tissue structures may also need to be removed.
At the present time, radiotherapy has not been accepted as a form of primary treatment for ameloblastoma.
It is believed that it should only be utilized in inoperable
cases25,30. Some investigators have reported some success with the management of patients with radiotherapy utilized in conjunction with surgery25,30-31. However,
this form of combination therapy is only recommended
for management of the recurrent ameloblastoma.
There are various reconstruction options for patients
who need to have large sections of bone removed. The
most commonly used alloplastic implants for mandibular reconstruction are bone plates and screws. The
use of mandibular reconstruction plates is typically indicated in patients with poor performance status or in
cases where the soft-tissue defect of the oral cavity is
more extensive than the bony mandibular defect32. Historically, free bone grafts were also frequently used for
mandibular reconstruction. Grafts from the calvarium,
rib, ilium, tibia, bula, scapula and radius have been
used33. However due to their higher long term success
rates, vascularized bone grafts are now replacing free
bone grafts as treatment of choice32.
CONCLUSION
Ameloblastomas can resemble several lesions clinically,
including dentigerous and residual cysts. Radiographic
imaging and specimen biopsy are essential for accurate diagnosis and appropriate treatment planning.
Furthermore, to prevent recurrence, it is often necessary to employ a radical surgical resection as described
in this case report.
REFERENCES
1. Gorlin RJ, Chaudhry AP, Pindborg JJ (1961) Odontogenic
tumors: classication, histopathology and clinical behavior in man and domesticated animals. Cancer 14:73-101
2. Small IA, Waldron CA (1955) Ameloblastomas of the jaw.
J Oral Surg 8:281-297
3. Jackson IT, Callan PP, Forte RA (1996) An anatomical classication of maxillary ameloblastoma as an aid to surgical treatment. J Craniomaxillofac Surg 24:230-6
4. Reichart PA, Philipsen HP, Sonner S (1995) Ameloblastoma: biological prole of 3677 cases. Eur J Cancer B Oral
Oncol 31B:86-99
5. Nakamura N, Mitsuyasu T, Higuchi Y (2001) Growth Characteristics of ameloblastoma involving the inferior alveolar nerve: A clinical and histopathological study. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 91:557-62
6. Appel BN, Verbin RS (1985) Odontogenic tumors. In: Surgical Pathology of the Head and Neck. (EI Barnes, ed.)
New York, Marcel Decker. pp. 1331-1409
7. Waldron CA (2002) Odontogenic tumors. In: Oral and Maxillofacial Pathology. (BW Neville, DD Damm, CM Allen,
JE Bouquet, eds.) Philadelphia, W.B Saunders Company.

pp. 611
8. Ashman SG, Corio RL, Eisele DW, Murphy MT (1993) Desmoplastic ameloblastoma. A case report and literature
review. Oral Surg Oral Med Oral Pathol 75(4):479-82
9. Rapidis AD, Angelopolous AP, Skouteris CA (1982) Mural
(intracystic) ameloblastoma. Int J Oral Surg 11:166-74
10. Gardner DG, Corio RL (1984) Plexiform unicystic ameloblastoma: a variant of ameloblastoma with a low recurrence rate after enucleation. Cancer 53:1730-5
11. Campbell D, Jeffrey RR, Wallis F (2003) Metastatic pulmonary ameloblastoma. An unusual case. Br J Oral Maxillofac Surg 41:194-96
12. Olasoji HO, Enwere ON (2003) Treatment of Ameloblastoma A review. Nigerian J Med 12(1):7-11
13. Shear M, Singh S (1978) Age-Standardized incidence
rates of ameloblastoma and dentigerous cyst on the Witwaterstrands, South Africa. Community Dent Oral Epidemio 6:195-199
14. Sawyer DR, Mosadomi A, Page DG (1985) Racial predilection of ameloblastoma: a probable answer from Lagos (Nigeria) and Richmond, Virginia (USA). J Oral Surg
40:27-31
15. Gardner DG (1981) Plexiform unicystic ameloblastoma: a
diagnostic problem in dentigerous cysts. Cancer 47:135862
16. Ackerman GL, Altini M, Shear M (1988) The unicystic ameloblastoma: a clinicopathologic study of 57 cases. J Oral
Pathol 17:541
17. Gold L (1991) Biological behavior of ameloblastoma. Clin
Oral Maxillofac Surg 3:21
18. Robinson L, Martinez MG (1977) Unicystic ameloblastoma.
A prognostically distinct entity. Cancer 40:2278-2285
19. Gardner DG, Pecak MJA (1980) The treatment of ameloblastoma based on pathological and anatomical principles. Cancer 46:2514-2519
20. Leider AS, Eversole LR, Barkin ME (1985) Cystic ameloblastoma. A clinicopathologic analysis. Oral Surg 60:624630
21. Williams TP (1993) Management of ameloblastoma a
changing perspective. J Oral Maxillofac Surg 51:10641070
22. Avon SL, McComb J, Clokie C (2003) Ameloblastic Carcinoma: Case report and literature review. J Can Dent
Assoc 69(9):573-6
23. Elzay RP (1982) Primary intraosseous carcinoma of the
jaws: review and update of odontogenic carcinomas.
Oral Surg 54:299-303
24. Chapelle KA, Stoelinga PJW, deWilde PCM, Brouns JJA,
Voorsmit RA (2004) Rational approach to diagnosis and
treatment of ameloblastomas and odontogenic keratocysts. Br J Oral Maxillofac Surg 42:381-90
25. Miyamota CT, Brady LW, Markoe A, Salinger D (1991) Ameloblastoma of the jaw: treatment with radiation therapy
and case report. Am J Clin Oncol 14:225-30
26. Minami M, Kaneda T (1992) Ameloblastoma in the maxillomandibular region: MR imaging. Radiology 184:389-93
27. Feinberg SW, Steinberg B (1997) Surgical management
of ameloblastoma of the jaws with liquid nitrogen spray
cryosurgery. Oral Surg Oral Med Oral Pathol 84:339-44
28. Emmings FG, Gage AA, Koepp SW (1991) Combined curettage and cryotherapy for recurrent ameloblastoma of
the mandible. Report of a case. J Oral Surg 29:41-44
29. Muller H, Slootweg PJ (1985) The ameloblastoma: the

controversial approach to therapy. J Maxillofac Surg
13:994-96
30. Anastossov GE, Rodrguez ED, Adamo AK, Friedman JM
(1998) Aggressive ameloblastoma treated with radiotherapy, surgical ablation and reconstruction. J Am Dent
Assoc 129:84-87
31. Pinsolle J, Michelet V (1995) Treatment of ameloblastoma
of the jaws. Arch Otolarynol Head Neck Surg 121:99496
32. Mehta RP, Deschler DG (2004) Mandibular reconstruction
in 2004: an analysis of different techniques. Curr Opin
Otolaryngol Head Neck Surg 12(4):288-93
33. Urken ML, Buchbinder D (1998) Oromandibular Reconstruction. In: OtolaryngologyHead and Neck Surgery,
3rd edition. (CC Cummings, ed.) St Louis, Mosby Year
Book, Inc. pp. 16541668
Volume 10 : 2005-2006
Spontaneous mandibular bone regeneration is a well known but rare phenomenon

that occurs more frequently in children but is rare in the adult population. The regeneration may take place after the occurrence of critical-size segmental defects in the
mandible secondary to trauma and tumor resection. Several mechanisms have been
suggested for such idiopathic bone deposition. This article will serve to review basic
mechanisms of bone biology and current literature regarding spontaneous mandibular bone formation. A case report of spontaneous mandibular bone regeneration in
a 39 year old male has been included followed by a discussion of several postulated
mechanisms for such regeneration.
Class of 2006, College of Dental Medicine, Columbia University, New York, NY

3
Chief Resident, Division of Oral Maxillofacial Surgery, New
York Presbyterian Hospital, Columbia University, New York, NY
4
Associate Program Director, Division of Oral Maxillofacial
Surgery, New York Presbyterian Hospital, Columbia University,
New York, NY
1
CDR
MECHANISMS OF BONE BIOLOGY

Bone serves multiple functions, including the provision
of structural stability and calcium hemostasis. Its morphology is partially governed by genetic control and
partially modied by remodeling. This remodeling, according to Wolfs law, is a result of the stresses and
strains throughout life. Wolfs law explains bone remodeling by simply stating that any bone under stress,
given time, incorporates calcium salts as a protective
measure to resolve any intrinsic weakness.
The healing of a bony fracture can occur under two
sets of circumstances. Primary bone healing occurs
when two fractured segments are placed in intimate
contact with each other. Direct bone contact achieved
across the fracture site eliminates the need for callus
formation. This method of healing usually requires stabilization of the fragments decreasing the mechanical
stress placed along the fracture line. Secondary bone
healing begins with the formation of a hematoma rich
in mesenchymal stem cells, derived from both bone
marrow and endosteal surfaces. A primary callus appears as an initial reaction of bone to injury. Cellular
activity forms a bridging external callus whose primary
purpose is to maintain the stability of the fragments.
The temporary fracture callus is reorganized by both
osteoclastic activity and vascularization with Haversian
canal systems- constituting mature bone.
Fig. 1. Growth factor involvement in osteoblast production

Volume 10 : 2005-2006
David Webb1
Stephen Petty2
Rick Tsay, DMD, MD3
Vincent Carrao, DDS, MD4
Both primary and secondary bone healing are dependent on the formation of bone from osteoblasts. Several growth factors involved in the process necessary
to produce the osteoblastic phenotype are outlined in
Fig 1.
LITERATURE REVIEW
There are 19 cases of reported spontaneous bone
regeneration in critical-size segmental defects of the
mandible in the English literature for the last 53 years.1
Signicant to this case report is that of these 19 cases,
only 3 occur in adult patients.
CASE REPORT
Mr. C.J. is a 39-year-old otherwise healthy male who
presented to an oral surgeon with a complaint of right
facial swelling and pain. A panoramic radiograph revealed a 4.0 cm round radiolucency associated with
erupted teeth #31 and 32 (Fig. 2). The initial treat-
Fig. 2. Panoramic radiograph revealing a 4.0 cm

round radiolucency associated with erupted teeth
#31 and 32 (blue arrows)
ment plan called for surgical extraction along with si- DISCUSSION
multaneous biopsy of the radiolucent lesion.
An unfortunate complication of the procedure was the Chalmers et al2 suggested in 1975 that three requirepatients mandible was fractured as teeth #31 and 32 ments must be met if bone formation is to occur.
were extracted. As a result of the fracture the patient These requirements are 1) an inducing agent must be
was placed in maxillomandibular xation (MMF) and present, 2) there must be osteogenic precursor cells
superior border wire was placed.
present, and 3) the environment must be hospitable to
After histopathology conrmed the radiolucent cystic osteogenesis. A few noteworthy proposals explaining
lesion to be an ameloblastoma a denitive treatment spontaneous mandibular osteogenesis which satisfy
plan was established, consisting of En Bloc resection varying aspects of these three landmark requirements
with 1 cm peripheral margins. Interim stabilization include the development of bone from intact and fragwould be attained with a reconstruction plate followed mented periosteum, infection, and articial stabilizaby insertion of a posterior iliac crest bone graft eight to tion.
nine months post resection. Endosteal implants were Explaining the molecular biology of fracture healing,
planned six months after interim stabilization.
Einhorn3 reports that, the presence of committed and
On the day of the surgical resection, the patients oc- uncommitted undifferentiated mesenchymal cells in
clusion and the stability of the bony segments were the periosteum contributes to the process of fracture
assessed and deemed satisfactory prior to removing healing by recapitulation of the embryonic intramemthe MMF. The patient received two grams of Ampicillin branous and endochondral bone formation. Kisner4
and 125mg of Solu-medrol. Full thickness mucoperi- further adds that a fragmented periosteum and the
osteal aps were elevated both buccally and lingually. remaining mandible may both serve as the source of
A Lorenz 2.7 reconstruction plate was pre-bent and regenerated bone.
screw holes were pre-drilled prior to
resection. En Bloc segmental resection from the distal surface of tooth
#27 to the angle was performed
using both reciprocating and oscillating saws. The mandibular pathologic specimen measured 6.0 x 3.0
x 1.7 cm with no tumor on resection
margins. MMF was then reapplied
and the reconstruction plate was
secured to the distal and proximal
segments. At this time MMF was
released and proper occlusion was
conrmed. The operation concluded with primary closure of periosteal and mucosal layers (Fig. 3).
Fig. 3. Post-operative radiograph
The post-operative course was
uneventful- the patient was discharged on post-op day two and PO
antibiotics were administered for
one week. The occlusion was stabilized with light elastic bands for the
entire post op period.
An eight month post-resection panoramic radiograph taken in preparation for the autogenous bone graft
revealed a regenerated mandible
(Fig. 4). This radiographic appearance of a spontaneously regenerated mandible was conrmed clinically during the extraoral mandibular reconstruction (Fig. 5).
Fig. 4. Eight month post-resection radiograph revealing a regenerated mandible (blue arrows)
Volume 10 : 2005-2006
Fig. 5. Clinical picture of

spontaneously regenerated
mandible
Fig. 6. Clinical picture depicting over-countered reconstruction plate (double-headed

blue arrow)
Although infection is suspected to have inhibitory effects on osteoblasts5, it is known that condensing osteitis, critically associated with an area of inammation, results in increased deposition of bone6. Elbeshir7
noted that periosteum will lay down new bone when
provoked by chronic infection. Although not a factor
in this case report, it is of statistical signicance that
almost one-third of all reported cases of spontaneous
mandibular regeneration involve infection.1
Articial stabilization promotes bone regeneration in
two ways. First, it precludes the collapse of soft tissue into the mandibular defect. Lemperle et al8 demonstrated that merely restricting soft tissue interposition served as sufcient impetus to allow for adequate
healing when an osteogenic periosteum was present.
Second, the articial stabilizer may act as scaffolding,
along or within which new bone may be formed- analogous to the developmental ossifying centers forming at a fork of a branching nerve. This scaffolding
phenomenon has been demonstrated in the ndings
of Boyne9, Whitmyer et al10, and Kisner4. Both of the
aforementioned attributes of articial stabilization may
be ascribed to the mandibular regeneration in this case
report secondary to an over-contoured reconstruction
plate (Fig. 6 and Fig. 7).
In conclusion, although spontaneous mandibular regeneration is a rare phenomenon, potential stimuli,
such as intact and fragmented periosteum, infection,
and articial stabilization, may initiate mechanisms to
bring about the event.
Fig. 7. Radiograph depicting

over-countered reconstruction plate (double-headed
blue arrow)
57(1):36-45
3. Einhorn TA (1998) The cell and molecular biology of fracture healing. Clin Ortho (355S):S7-S21
4. Kisner WH (1980) Spontaneous posttraumatic mandibular
regeneration. Plast Reconstr Surg 66(3):442-7
5. Azuma H, Kido J, Ikedo D, Kataoka M, Nagata T (2004)
Substance P enhances the inhibition of osteoblastic cell
differentiation induced by lipopolysaccharide from Porphyromonas gingivalis. J Periodontol 75(7):974-81
6. Neville BW, Damm DD, Allen CM, Bouquot JE (2001) Oral
and Maxillofacial Pathology, 2nd ed. Philadelphia, W.B.
Saunders Co.
7. Elbershir EI (1990) Spontaneous regeneration of the mandibular bone following hemimandibulectomy. Br J Oral
Maxillofac Surg 28(2):128-30. Review
8. Lemperle SM, Calhoun CJ, Curran RW, Holmes RE (1998)
Bony healing of large cranial and mandibular defects
protected from soft-tissue interposition: A comparative
study of spontaneous bone regeneration, osteoconduction, and cancellous autografting in dogs. Plast Reconstr
Surg 101(3):660-72
9. Boyne PJ (1983) The restoration of resected mandibles in
children without the use of bone grafts. Head Neck Surg
6(2):626-631
10. Whitmyer CC, Esposito SJ, Smith JD, Zins JE (1996) Spontaneous regeneration of a resected mandible in a preadolescent: a clinical report. J Prosthet Dent 75(4):356-9
REFERENCES
1. de Villa GH, Chen CT, Chen YR (2003) Spontaneous bone
regeneration of the mandible in an elderly patient: a case
report and review of the literature. Chang Gung Med J
26(5):363-9. Review
2. Chalmers J, Gray DH, Rush J (1975) Observations on the
induction of bone in soft tissues. J Bone Joint Sur Br
Volume 10 : 2005-2006
Reconstruction of the Temporomandibular Joint

with Distraction Osteogenesis in the Minipig Animal Model
Restoration of mandibular function in patients with diseased temporomandibular joints
has been a challenge for the oral and maxillofacial surgeon. It is estimated that 5%
of the U.S. population has temporomandibular joint disease that is severe enough to
require treatment.1 Although conservative therapies are often successful in reducing
symptoms, there is a population of patients who do not improve and become candidates for surgical intervention. Treatment of patients with severe temporomandibular
joint brosis, osteoarthritis and/or ankylosis remains controversial, as evidenced by
the numerous surgical options that have been proposed. Total joint replacement
systems have emerged, but long-term success rates have not been established and
this is particularly important as the patient population for temporomandibular joint
disease is usually in the mid-thirties. Although recent orthopaedic studies of total
joint replacement of knees and hips describe longer survival rates than in the past,
the average age of this patient population is usually in the mid-sixties.2 This report
describes an animal model for TMJ reconstruction.
David Koslovsky1
Howard Israel, DDS2
Stephanie Drew, DMD3
Tara Plansky, DMD2
C.J. Langevin, DMD, MD2
Laike Stewart, DVM2
David Behrman, DMD2
Department of Oral and Maxillofacial Surgery, Weill
Cornell Medical College, Cornell University, New
York, NY
3
Department of Oral and Maxillofacial Surgery, Long
Island Jewish Medical Center, New Hyde Park, NY
1
CDR
CURRENT TECHNIQUES FOR TMJ RECONSTRUCTION
Techniques for reconstruction of the temporomandibular joint in human patients with severe degenerative joint disease have been unsuccessful. In the
1980s, many of these patients had implant placement
with proplast-teon and silastic. Trumpy and Lyberg
have shown that most of these patients developed
temporomandibular joints with osteoarthritis, brosis
and further limitation of mandibular function.3 Furthermore, there are many other indications for total
temporomandibular joint reconstruction, particularly in
patients with neoplasia, infection and trauma.4 Surgical techniques for autogenous temporomandibular
joint reconstruction include costochondral grafts, iliac
grafts, microvascular free aps (clavicle, bula), and
cadaveric mandible cribs with autogenous cortico-cancellous bone. These techniques have been used with
variable success with the major disadvantage of requiring a second surgical site. Sliding posterior mandibular
ramus osteotomies have been used, but still require
additional bone grafting.5,6 Although there are anecdotal reports of the use of distraction osteogenesis for
human temporomandibular reconstruction; there is a
paucity of literature on this subject.
BENEFITS OF DISTRACTION OSTEOGENESIS
Tissue engineering techniques are being developed for
the reconstruction and replacement of diseased human
tissues. A recent investigation has demonstrated production of a minipig mandibular condyle using in vitro
tissue engineering techniques.7 Distraction osteogenesis has potential to provide autogenous reconstruction of the temporomandibular joint, using an in vivo
Volume 10 : 2005-2006
tissue engineering technique. A major advantage of

this technique is that the mandibular transport segment has a blood supply from the medial pterygoid
muscle.
Distraction osteogenesis is a relatively new method of
treatment for selected deformities and defects of the
oral and facial skeleton. It was rst used in 1903 by
Codivilla.8 In the 1950s Ilizarov, a Russian orthopedic
surgeon, described the surgical and postoperative management of distraction osteogenesis treatment to correct deformities and repair defects of the long bones.9
Simply stated, distraction osteogenesis means the slow
movement apart (distraction) of two bony segments in
a manner such that new bone is allowed to ll in the
gap created by the separating bony segments.
In 1977, Michieli and Miotti lengthened the mandibular body of dogs via distraction osteogenesis.10 This
procedure was rst used to treat defects of the oral
and facial region of humans in 1990.11 Since then, the
surgical and technological advances made in the eld
of distraction osteogenesis have provided the oral and
maxillofacial surgeon with a safe and predictable method to treat selected deformities of the oral and facial
skeleton.
Distraction osteogenesis surgical procedures typically
produce less pain and swelling than the traditional surgical procedure for a similar condition. This technique
eliminates the need for bone grafts, and therefore, another surgical site. Lastly, distraction osteogenesis is
associated with greater stability when used in major
cases where signicant movement of bony segments
is involved.
Reconstruction of the Temporomandibular Joint with Distraction Osteogenesis in the Minipig Animal Model
Fig. 1A
Fig. 2
Fig. 1B
Fig. 1. Injection of Sclerosing Solution. Fig. 1A. The joint space is palpated. Fig. 1B. 5 cc of 3% Sotradecol (Sodium
Tetradecyl Sulfate 3%) or 23.4% Sodium Chloride is injected into the superior joint space of the left temporomandibular joints to induce osteoarthritic changes
Fig. 2. Accessing the TMJ. A preauricular incision is used and dissection to the temporomandibular joint proceeds
through the following layers: skin, subcutaneous tissue, parotidomasseteric fascia, supercial temporal fascia and
joint capsule
SELECTION OF ANIMAL MODEL
OBJECTIVE
Previous animal research on temporomandibular joint

reconstruction and distraction osteogenesis, although
scarce, has involved a variety of animal model systems.12 Rabbits, rats and mice have been used predominantly due to the availability of these species as
well as the relatively low cost. In fact, investigators
have demonstrated that temporomandibular joint reconstruction using distraction osteogenesis in a rabbit model is feasible.13 However, the chewing patterns
and forces generated on the temporomandibular joint
in rodents is very different from humans, and thus, the
results of such investigations will have reduced validity and applicability.14 Several studies have involved
the use of sheep, dogs and monkeys. As mammalian
species, these studies are more valid than those in rodents, but have problems as well. The size and cost
of care of sheep in most hospital or academic research
facilities are problematic.
At an NIH Technology Assessment meeting on Temporomandibular Disorders in 1995, several investigators indicated that the swine would be an excellent animal model for studies involving the temporomandibular joint.15 Numerous investigators have advocated the
use of the pig model for temporomandibular joint studies due to its functional and anatomic similarity to the
human temporomandibular joint.16,17,18,19 The female
Yucatan pig has functional anatomy and mandibular
size that closely resemble the human temporomandibular joint.16,20
The Animal Use Committee of the Weill Cornell Medical College at Cornell University approved the use of
three female Yucatan minipigs for this investigation.
The mean age of the animals at the start of the investigation was 6 months, and the mean weight was 27.5
kg. All procedures and surgeries were performed at
the Research Animal Resource Center at Cornell-New
York Presbyterian Hospital.
The purpose of this investigation was to determine the

feasibility of reconstruction of the temporomandibular joint with distraction osteogenesis using a minipig
model.
10
METHODS
The minipigs were anesthetized and monitored according to standard procedures.19,21 Following satisfactory
induction of orotracheal general anesthesia, the left
temporomandibular joint was prepped with betadine.
5 cc of the sclerosing agent 3% Sotradecol (Sodium
Tetradecyl Sulfate 3%) or 23.4% Sodium Chloride was
injected into the superior joint space of the left temporomandibular joints to induce osteoarthritic changes
(Fig. 1A,B).22
Six weeks following the sclerosing procedure, the animals were anesthetized for the surgical placement of
the distraction devices. During the dissection through
a retromandibular incision, a nerve stimulator was used
to identify the mandibular branch of the facial nerve.
All blood vessels were appropriately tied with 3-0 Vicryl
sutures or cauterized, to achieve hemostasis. A periosteal elevator was used to provide access to the ramus
of the mandible to the level of the mandibular condyle.
Following this, an incision was created through the supercial temporal fascia, 45 degrees to the zygomatic
arch, and the capsule of the joint was removed permitting access to the entire joint (Fig. 2). An osteotomy
was created through the neck of the condyle and the
condylectomy was performed (Fig. 3A-D). The disc
and all brotic tissues of the temporomandibular joint
were removed creating a gap between the glenoid
fossa and remaining mandible of 15 20 mm. The
condyle and disk tissues, which were removed, were
submitted for histologic examination (hematoxylin &
eosin staining).
Volume 10 : 2005-2006
Fig. 3A
Fig. 3B
Fig. 3C
Fig. 3D
Fig. 3. Contents of TMJ. Fig. 3A. Condyle, in 2 segments. Fig. 3B. Articular cartilage. Fig. 3C. Cartilagenous Disc.
Fig. 3D. Condyle, articular cartilage, cartilaginous disc in proper orientation
The mandibular distraction osteogenesis device used in through a small window created in the skin above the
this experiment is produced by KLS Martin, L.P. and has retromandibular incision (Fig. 7A,B). This permitted
the following description: (Stock #02-515-40) Zurich access to activating the device while posing the least
Distractor, 2 Four-Hole Cloverleaf Plates, 20 MM, Left, amount of interference to the animals regular moveEnd Driven, Extended Arm (Fig. 4). Prior to insertion, ments.
the device was sterilized in a steam autoclave. Through Postoperatively, the animals were monitored appropria retromandibular incision, an L-shaped osteotomy was ately and left only once they could maintain sternal
recumbency and were oxygenating
created from the sigmoid notch vertically and inferiorly, and then horiwell.21 During the rst 24 hours,
zontally and posteriorly, to create a
vitals were measured every hour,
mandibular bone transport segment
while vitals were measured every 4
(Fig. 5). The distractor transports
hours during the second 24 hours.
the segment of bone from the manThereafter, the wound was inspectdibular ramus to eventually dock in
ed and the vital signs measured four
the glenoid fossa to form a new contimes daily.
dyle for the reconstructed temporo- Fig. 4. Distraction Device. The The distraction device was not acmandibular joint. The distraction distractor used in this procedure tivated for a six day latency period
features: 2 Four-Hole Cloverleaf
device was secured with 2.0 mm tifollowing its placement. The dePlates, 20 MM, Left, End Driven, Extanium screws inferior and superior tended Arm. Supplied by KLS Mar- vice was activated 1 mm/day, from
to the osteotomy site, stabilizing the tin, LP - Stock #02-515-40
postoperative days 7 to 27, until
transport segment to the remaining
the transport segment had docked
native mandible (Fig. 6A,B). All wounds were irrigated into the glenoid fossa (Fig. 8). The device was left
and then closed in layers, using 3-0 and 4-0 Vicryl su- in place for an additional 40 days allowing the bone
tures. Intradermal sutures were used to permit skin to heal at the previous osteotomy sites of the ramus
closure. The turning screw of the distraction device of the mandible. The distraction device was removed
was either secured within the original incision or placed 67 days postoperatively while the pig continued a nor-
Fig. 5
Fig. 6A
Fig. 6B
Fig. 5. L-Shaped Osteotomy. Through a retromandibular incision, an L-shaped osteotomy is created below the neck
of the condyle in the posterior mandibular ramus to create a bone transport segment
Fig. 6. Securing the Distraction Device. Fig. 6A. Secured distraction device in closed orientation. Fig. 6B. Secured
distraction device in open orientation
Volume 10 : 2005-2006
11
Fig. 7A
Fig. 7B
Fig. 8
Fig. 7. Extended Arm of Distraction Device. Fig. 7A. The turning screw of the distraction device is either secured
within the original incision or Fig. 7B. placed through a small window created in the skin above the retromandibular
incision
Fig. 8. Activation of the Distraction Device
mal diet. The animals were monitored for food intake

and weight while eating a normal diet for an additional
three months.
Fig. 9A
Fig. 9B
Fig. 9C
RESULTS
Fig. 9D
Fig. 9. En bloc resections of the control and

experimental temporomandibular joints. Fig.
9A. Lateral views of the control and Fig 9B. experimental joints. Fig. 9C. Posterior views of the
control and Fig 9D. experimental joints. Note the
difference in the overall mass of the two joints.
12
When using an animal model in such an experiment

one must plan for adverse affects (distress, pain, infection, discomfort, morbidity, etc.) that may arise.23
Minipig #2 developed recurrent infection due to fecal
contamination requiring incision and drainage and IV
antibiotics.
The animals were euthanized 5 months following the
docking of the transport segment into the glenoid fossa. At this time, en bloc resections of both the experimental left and contralateral right temporomandibular
joints were obtained (Fig. 9A-D).
The specimens underwent histomorphologic analysis

and biomechanical testing by the Division of Oral Pathology at Cornell-New York Presbyterian Hospital, NY.
All specimens were sectioned, embedded and graded
appropriately. The initial condylar and disc specimens
that were removed 6 weeks following injection of sclerosing solution demonstrated articular cartilage with
brillation, splitting and necrosis, consistent with degenerative joint disease.24
Comparison was then made between the experimental and contralateral temporomandibular joints (Fig.
10A-C, 11A-D). The new bone in the experimental
left joint appears more bony and of more mass than
the contralateral joint. In addition, the gross shape
and size of the neo-condyle is very similar to that of
the contralateral right condyle. The right (control)
joint displays bony trabeculae of uniform thickness
and cellularity. Osteoblasts lining the bone surface
do not appear as plump as in the left experimental
joint. The left (experimental) joint displays trabeculae that are of variable thickness and very mature
(Fig. 12). The central portions of many trabeculae
are of increased cellularity and the osteocyte lacunae
are very prominent. Rows of plump osteoblasts line
many bone surfaces. There is adipose tissue in the
Volume 10 : 2005-2006
Fig. 10A
Fig. 11A
Fig. 10B
Fig. 10C
Fig. 11B
Fig. 11C
intervening spaces between trabeculae but there is no

evidence of hematopoietic tissue. The surface of trabecular bone immediately adjacent to the joint space is
covered along one side of the specimen by highly vascular brous connective tissue and synovium with multifocal, small aggregates of lymphocytes and plasma
cells. There is no evidence of inammation or brosis.
A dense band of brous tissue resembling discal tissue
appears to articulate over the new condyle. Minipig #2
shows similar results although its synovial membrane
is inamed (Fig. 13A-D). All animals gained weight
throughout the 7 months of the experiment, with the
mean initial weight being 27.5 kg and the mean nal
weight being 41.3 kg (Table 1).
Fig. 11D
CONCLUSION
A functional temporomandibular joint was formed in
the minipig model, with the creation of a joint space,
brous tissue surfaces and synovial tissues.
Day 0
30 Weeks
Minipig #1 Weight (kg)
28.5
40.4
28.0
33.6
26.0
50.0
Table 1. Weight (kg) changes of all three minipigs following the experiment
Fig. 12. Histomorphology Image (H&E stain) of Transport Gap of Left (Experimental) TMJ Minipig #1.
Fig. 13. Sagittal Section and Histomorphology Images (H&E stain) of Left (Experimental) TMJ Minipig #2. Fig. 13A. Gross section of experimental joint
along with Fig. 13B. low power and Fig. 13C. high power views (1. Fibrous connective tissue, 2. Joint space, 3. Fibrocartilage, 4. Condylar subchondral bone)
and Fig. 13D. Inamed synovial membrane can also be seen
Fig. 12
Fig. 13A
Fig. 10. Sagittal Section and Histomorphology Images (H&E stain) of Right (Control) TMJ Minipig #1.
Fig. 10A. Gross section of control joint along with
Fig 10B. low power and Fig. 10C. high power views
(1. Fibrocartilage (disc), 2. Joint space, 3. Fibrocartilage, 4. Condylar subchondral bone)
Fig. 11. Sagittal Section and Histomorphology Images (H&E stain) of Left (Experimental) TMJMinipig #1. Fig. 11A. Gross section of experimental joint.
Fig. 11B. Low power view along with Fig. 11C. high
power view of anterior (1. Fibrous connective tissue, 2. Joint space, 3. Synovium, 4. Fibrocartilage,
5. Condylar subchondral bone) and Fig. 11D. middle
joint segments
Fig. 13B
Volume 10 : 2005-2006
Fig. 13C
Fig. 13D
13
DISCUSSION
The controlled movement of the distraction osteogenesis technique allowed for a large mass of bone to be
formed in the experimental joint. The shape and size
of the neo-condyle had taken on its usual spherical
shape because the animals were allowed to function
normally. The brous tissue layer over the condyle
and temporal bone is believed to be brocartilage. The
dense band of brous tissue amid the reformed joint
space resembles a disc; however no claim can be made
at this time that a reformation of the disc actually occurred. Furthermore, it is difcult in interpreting the
presence of synovial membrane - Did the tissue form
during the recreation of the joint or was there simply
incomplete tissue resection during the original surgery?
An important nding is that minipig #2 formed functional joint tissues despite recurrent infection. In fact,
normal masticatory function was achieved in all of the
animals permitting weight gain and normal growth.
Good animal studies that are transferable to the human temporomandibular joint are lacking, and this is
a major factor that has resulted in multiple failures in
the reconstruction of the human temporomandibular
joint. Although there are several animal studies involving the effects of distraction osteogenesis on the tissues of the temporomandibular joint, none of these
studies actually involved the use of this technique for
reconstruction of a diseased temporomandibular joint.
Therefore, it is necessary to perform appropriate animal studies which have demonstrated successful temporomandibular joint reconstruction, before applying
any of these techniques to human patients with severe
temporomandibular joint disease.
This pilot study demonstrates that reconstruction of
the temporomandibular joint using a distraction osteogenesis technique is feasible. It is anticipated that
further studies using the minipig model are likely to
result in a new and improved technique of autogenous
reconstruction of the temporomandibular joint using
distraction osteogenesis. Additional human clinical trials using distraction osteogenesis for temporomandibular joint reconstruction are required and will offer the
potential for restoring mandibular function in patients
with severe temporomandibular joint disease.
REFERENCES
1. Lipton JA, Ship JA, Larach-Robinson D (1993) Estimated Prevalance and Distribution of Reported Orofacial Pain in the
United States. J Am Dent Assoc 124(10):115-21
2. March LM, Cross, MJ, Lapsley H, Branbic AJM, Tribe KL, Bachmeier CJM, Courtenay BJ, and Brooks PM (1999) Outcomes
after hip or knee replacement surgery for osteoarthritis.
The Medical Journal of Australia 171: 231-8
3. Trumpy IG, Roald B, Lyberg T (1996) Morphologic and immunohistochemical observation of explanted Proplast-Tef-
14
lon temporomandibular joint interpositional implants. J Oral

Maxillofac Surg 54(1):63-8; discussion 68-70
4. Temporomandibular Disorders and Treatments. Available at:
www.hughston.com/hha/a_14_2_4.htm. Accessed on
February 2, 2006
5. Anatomy of Temporomandibular Joint. Available at: www.
xray2000.f9.co.uk/ibase3/osteology/ALBUM24.HTML. Accessed on February 3, 2006
6. Human Temporomandibular Joint. Available at: www.asahinet.or.jp/~df7t-ymd/tmj/tmj-2.html. Accessed on February
2, 2006
7. Abukawa H (2003) Formation of a mandibular condyle in
vitro by tissue engineering. Journal of Oral and Maxillofacial
Surgery 61: 94-100
8. Codivilla A (1905) On the means of lengthening in the lower limbs, the muscles, and tissues which are shortened
through deformity. American Journal of Orthopaedic Surgery 2: 353-369
9. Distraction Osteogenesis of the Mandible. Available at:
www.emedicine.com/ent/topic765.htm. Accessed on December 12, 2006.
10. Michieli S, Miotti B (1977) Lengthening of mandibular body
by gradual surgical-orthodontic distraction. Journal of Oral
Surgery 35(3): 187-192
11. McCarthy JG, Schreiber J, Karp N, Thorne CH, Grayson BH
(1992) Lengthening the human mandible by gradual distraction. Journal of Plastic and Reconstructive Surgery 89:
110
12. Cramer, Donald V, Podesta LG, Makowka L, eds. (1994)
Handbook of animal models in transplantation research.
Boca Raton, Fla.: CRC Press
13. Hikiji H (2000) Expermental study of reconstruction of the
temporomandibular joint using a bone transport technique.
Journal of Oral and Maxillofacial Surgery. 58(11): 1270-6
14. Tominaga K, Yamada Y, Fukuda J (2000) Changes in chewing pattern after surgically induced disc displacement in the
rabbit temporomandibular joint. Journal of Oral and Maxillofacial Surgery 58(4): 400-5
15. NIH Technology Assessment Meeting on Temporomandibular Disorders. (1995) Bethesda, MD
16. Pond, Wilson G, Mermsmann HJ, eds. (2001) Biology of the
domestic pig. Ithaca, N.Y.: Comstock Publishing Associates,
Cornell University Press
17. Beatty M, Nickel J, Iwasaki L, Lieker M (2003) Mechanical
response of the porcine temporomandibular joint disc to
an impact event and repeated tensile loading. Journal of
Orofacial Pain 17: 160
18. Kuboki T, Shinoda M, Orsini MG, Yamashita A (1997) Viscoelastic properties of the pig temporomandibular joint articular soft tissues of the condyle and disc. Journal of Dental
Research 76: 1760
19. Swindle M (1998) Surgery, Anesthesia, and Experimental
Techniques in Swine. Iowa: Iowa State University Press
20. Characteristics of Swine. Available at: netvet.wustl.edu
and www.medaille.edu/vmacer. Accessed on February 4,
2006
21. Lumb, Jones (1996) Veterinary Anesthesia, 3rd ed. Maryland: Williams and Wilkins
22. Popesko P (1992) Colour atlas of the anatomy of small
laboratory animals. London: Wolfe Publishing
23. Leman AD (1982) Diseases of Swine. Iowa: Iowa State University Press
24. Tait DC (1993) Impulsive and static loading of the porcine
temporomandibular joint disc. [thesis] Winnipeg: University
of Manitoba
Volume 10 : 2005-2006
Vascular anomalies are some of the most common congenital abnormalities, but
they are nonetheless challenging to accurately diagnose and manage. Early diagnostic methods were often based on a description and correlation to items that were
encountered in everyday life. In the mid-nineteenth century, Virchow proposed a
histopathologic classication based on the size and appearance of the constituent
vessels.1 This system categorized vascular lesions as angioma complex, angioma
cavernosum, or angioma racemosum and was later extended to lymphatic lesions
by Wegner.2 Classications that followed attempted to correlate clinical observations
with pathologic and embryologic ndings. A well accepted biologic classication by
Mulliken and Glowacki divided vascular anomalies into two major types, tumors (hemangiomas) and malformations, based on clinical and histologic ndings.3
Paul Li1
Tracey Rosenberg, DDS, MD2

2
Associate Professor, Division of Oral and
Maxillofacial Surgery, College of Dental
Medicine, Columbia University, New York, NY
1
CDR
INTRODUCTION
Hemangiomas are tumors composed of capillaries with
active proliferation potential. The proliferative phase is
characterized histologically by plump endothelial cells
with abundant mitotic activity, leading to an increase in
the number of mast cells and multilaminated basement
membranes. These tumors are usually seen soon after
birth, grow rapidly, and involute over the years. Involution is characterized by a decrease in cellularity and
tumor size, formation of larger vascular vessels, brofatty replacement, and development of a lobular architecture with septae. Initial physical ndings of involution include a decrease in turgidity and fading of color
to a dullish or gray shade. Hemangiomas are common
in Caucasians, being evident in up to 12% of all children
and occurring three times more frequently in females.4
According to Mulliken, hemangiomas can be classied
into capillary, cavernous, and capillary-cavernous
types.2,4 Capillary hemangiomas (strawberry hemangiomas) are considered to be supercial and derived
from papillary dermal layer. Cavernous hemangiomas
are located within reticular dermis or subcutaneous tissue and may appear bluish or colorless based on its
location.
HEAD & NECK HEMANGIOMAS
Intraosseous vascular malformations account for less
than one percent of all bony tumor cases. The most
probable sites of malformation include the vertebral
column and the skull. Within the calvarium, the parietal bone is the most commonly involved followed by
the frontal bone. Within the facial skeleton, vascular
anomalies occur in the mandible, maxilla, and nasal
bones but are extremely rare in the zygoma.5 The
location of the bony lesion will dictate the signs and
symptoms presented by the patient. Patients will usu-
Volume 10 : 2005-2006
ally present with a history of gradually enlarging circumscribed swelling which may be tender but is rarely
painful.6
Orbital hemangiomas may obstruct the visual axis or
distort the cornea. The optic cortex is extremely sensitive to stimulus deprivation as demonstrated in both
kittens and baboons.7 If obstruction occurs during the
rst year of life, amblyopia may result in as little as one
week. The mass effect of a periorbital hemangioma,
particularly of the upper eyelid, may deform the developing cornea.1
Parotid gland hemangiomas may lead to obstruction
of the external auditory canal resulting in conductive
hearing loss and possibly affecting speech development in young children. Bilateral lesions which persist
beyond one year of age should be treated to prevent
this occurrence.2, 8, 10
Kasabach-Merritt syndrome (KMS) is a hemangioma
characterized by a rapidly growing vascular anomaly,
consumptive coagulopathy with thrombocytopenia,
prolonged PT, hypobrinoginemia, presence of D-dimers, and hemolytic anemia. However, KMS is not
caused by hemangiomas but by kaposiform hemangioendothelioma or tufted angioma.3
CASE REPORT
A 31-year-old Caucasian female was referred to the
Oral & Maxillofacial Surgery clinic for extraction of a
carious, non-mobile number 16 associated with a left
facial-palatal vascular lesion. Past medical and dental
history included extraction of teeth numbers 1, 17, and
32, asthma, three C-sections, and a ruptured spleen
due to motor vehicle accident in 1992. The patient
was currently taking Advair (daily), Albuterol (prn),
and Micronor with no known drug allergies. On visual
15
inspection, her face was mildly asymmetric, and the

left globe was slightly recessed by comparison with the
right. Upon physical examination, a bluish epithelial
pigmentation was observed by her left temporal and
left auricular region where a denitive pulsating vascular vessel was noted. Intra-orally a similar bluish tinted
lesion was evident on her left side which involved the
hard palate, soft palate, and uvula. Palpation of the
palate yielded a soft tactile response without any underlying bone structure. It was suspected the palate
was the region of vascular malformation. MRI showed
an inltrating hyper-intense lesion involving the palate,
trigone, and parapharyngeal space. The imaging characteristics were compatible with hemangioma, and the
patient was referred to Radiology & Neurological Surgery for further evaluation. Arteriography, facial embolization, and percutaneous sclerotherapy were proposed to reduce the risk of arterial hemorrhage during
the time of extraction. Indications, alternatives, risks,
and benets were discussed with the patient. The patient consented and agreed to proceed.
DIFFERENTIAL DIAGNOSIS
In majority of the cases, hemangiomas can be diagnosed based on clinical presentation. In certain ambiguous cases, imaging studies and biopsy may be
warranted to obtain a denitive diagnosis. Nonetheless, hemangiomas must be differentiated from macular stains, vascular malformations, and other vascular
anomalies.
The most common type of vascular birthmark is the
macular stain. These are at lesions ranging from pink
to red, and are seen in as many as 40 percent of newborns.11, 12 They are likely to be seen on the neck,
glabella region, eyelids, and forehead. Vascular malformations are most commonly found in the oral cavity
and several muscle groups (H&N, masseter, buccinator, orbicularis oris, and tongue). Unlike hemangiomas, vascular malformations do not undergo a rapid
proliferative phase nor do they undergo spontaneous
involution. In addition, the endothelium of vascular
malformations is not considered to be hyperplastic but
is composed of normal endothelial elements. Physical
appearance is dependent on the type of vessel involvement. Venous malformations tend to be bluish masses
and are easily confused with subcutaneous hemangiomas, but they are distinguished by the ability to be
emptied of blood upon compression. Malformations
also do not exhibit the parenchymal staining seen with
hemangiomas on computerized tomography and magnetic resonance imaging studies.
Finally, other nonvascular neoplasms, such as brosarchoma, rhabdomyosarcoma, neurobroma, teratoma,
nasal glioma, dermoid cyst, and myobromatosis, must
be considered during diagnosis because they may
16
masquerade as hemangiomas, especially when found

subcutaneously.2, 14, 15
DIAGNOSTIC IMAGING
In certain cases where more diagnostic tools are warranted, angiography, scintigraphy, and other imaging
techniques will help to establish an accurate diagnosis.
Angiographically, hemangiomas are well-circumscribed
lesions with intense tissue staining and lobular organization.20 Scintigraphy will demonstrate an intense focal
uptake through out the lesion.20
The most informative and non-invasive technique includes MRI or MRA. On a T1 weighted sequence, it
demonstrates an intermediate heterogenous signal.
The signal is simply enhanced on T2.
CT scan is not as useful as MRI although it does elucite
tissue involvement and denes spatial relationship of
anomalies and alterations in skeletal structures.
The use of Doppler, ultrasonography, and MRI concurrently or as single entities enables differentiation of
high-ow versus low-ow lesions and other infant lesions, such as demoid cyst, lipoma, or meningocele.
MANAGEMENT
First and foremost, an accurate diagnosis needs to be
established. Treatment is needed for approximately
10-20% of hemangioma cases involving spontaneous involution.21 These cases are usually of alarming
growth which may lead to serious esthetic and functional concerns.
Typically, oral corticosteroids would be the rst line
of therapy. According to a recent in vitro study, triamcinolone and dexamethasone best inhibited capillary growth, betamethasone produced variable effects,
and hydrocortisone had a negligible effect on capillary
growth.3 Finally, the benet of steroid treatment must
outweigh the systemic side effects including growth retardation and adrenal suppression.
Alpha-interferons are used as antiviral and antiproliferative agents. Alpha-interferons have demonstrated
inhibition of endothelial, broblast, and smooth muscle
proliferation. In addition, a decrease in growth factor
release and collagen synthesis has been documented.22-29 Treatment using interferons is reserved for
cases when steroids are contra-indicated, have failed,
or have had signicant complications.
Generally, surgery is indicated when functional obstructing, ulcerating, or large lesions are unresponsive
to pharmacologic therapy. During the post-proliferative stage, surgery will play an important role to correct any disgurement as the hemangioma enters the
involutional phase. Embolization is an important adjunctive procedure to help decrease blood loss during
Volume 10 : 2005-2006
surgery. In general, a transfemoral approach would be

used for most head and neck vascular malformations.
The choice to embolize particle would be based on the
intended outcome. In cases dealing with preoperative
embolization, Gelfoam powder can be used to temporarily occlude the feeding vessels. For permanent
occlusion, plyvinyl alcohol can be used to embolize
arterial or AV stulas. It is important to realize that
backow of embolic agents and necroses of normal tissue are possible complications of therapy. The aim of
embolization is not to occlude the blood vessels proximal to the lesion. By depositing an inert substance
deep within the capillary network of the hemangioma,
embolization will prevent stimulus for collateralization.
Types of laser treatment include carbon dioxide, ashlamp-pumped pulsed dye, neodymium:yttrium-aluminum garnet, potassium-titanyl phosphate, and argon
lasers.1 Laser treatment is based on the principle of
selective photothermolysis, which states that absorption of laser energy is based on the wavelength of the
emitted light and the physical characteristics of the
tissue that it strikes.1 Commonly used yellow-green
lasers emit light of 532-585 nm which corresponds to
the absorption peaks of oxyhemoglobin. Thus, vascularized tissues are potentially susceptible to this type
of treatment.
Anti-neoplastic agents, cyclophosphamide, and vincristine have been used successfully in treating hemangiomas due to the proliferative nature of these lesions.
Radiotherapy is also an effective treatment modality
because of the increased cellular turnover found in
hemangiomas.
CONCLUSION
The patient pre-operatively underwent arteriography,
sclerotherapy, and embolization in anticipation of extraction of tooth number 16. Vicodin was prescribed
post-operatively for pain management. The patient
was also advised to follow a soft-food diet, gradually
resume her daily activities, and return for follow-up.
Tooth number 16 was extracted under general anesthesia. Greater than normal bleeding was anticipated
and well-controlled. Extraction of number 16 was carried out routinely without additional complications.
The patient was discharged the following day with appropriate post-operative instructions.
Upon one week follow-up, silk sutures were removed
from the extraction site. The extraction site was examined and was healing well. The patient had no complaints of numbness, weakness, or visual problems associated with the left facial-palatal hemangioma. The
patient did however complain of tenderness in the left
post-cervical lymph node region. The patient was prescribed Penicillin VK and was advised to resume daily
activities at a steady pace. In addition, she was inVolume 10 : 2005-2006
structed to chew on the contralateral side and continue

with the soft-food diet.
REFERENCES
1. Gamper TJ, Morgan RF (2001) Vascular Anomalies: Hemangiomas. Plast & Reconstr Surg 110:572-585.
2. Mulliken JB, Young AB (1988) Vascular Birthmarks: Hemangiomas & Malformations. Philadelphia: Saunders, 24103
3. Buckmiller LM (2004) Update on hemagiomas and vascular
malformations. Curr Opin Otolaryngol Head Neck Surg
12:476-487
4. Werner JA, Dunne AA, Folz BJ, Rochels R, Bien S, Ramaswamy A, Lippert BM (2001) Current concepts in the classication, diagnosis and treatment of hemangiomas and
vascular malformations of the head and neck. Eur Arch
Otorhinolaryngol 258:141-148
5. Warman S, Myssiorek D (1989) Imaging case study of the
month: haemangioma of the zygomatic bone. Ann Otol
Rhinol Laryngol 98:655-658
6. Konior RJ, Kelley TF, Hemmer D (1999) Intraosseous
zygomatic hemangioma. Otolaryngol Head Neck Surg
121:122-125
7. Thomson HG., Ward CM., Crawford JS., Stigmar G (1979)
Hemangiomas of the eyelid: Visual complications and
prophylactic concepts. Plast Recontr Surg 63: 641
8. Drolet BA., Esterly NB., Frieden IJ (1999) Hemangiomas in
children. N Engl J Med 341: 173
9. Kushner JB (1982) Intralesional corticosteroids injection
for infantile adnexal hemangioma. Am J Ophthalmol
93:496
10. Fishman SJ, Mulliken JB (1993) Hemangiomas and vascular malformations of infancy. Ped Clin North Am 40:
1177
11. Jacobs AH (1957) Strawberry hemangioma: The natural
history of the untreated lesion. Calif Med 86:8
12. Pratt AG (1953) Birthmarks in infants. Arch Dermatol 67:
302
13. Enjolras O, Mulliken JB (1993) The Current management
of Vascular birthmarks. Ped Dermatol 10: 311
14. Burrows PE, Laor T, Paltiel H, Robertson RL (1998) Diagnostic imaging in the evaluation of vascular birthmarks.
Dermatol Clin 16: 455
15. Mueller BU, Mulliken JB (1999) The infant with a vascular
tumor. Semin Perinatol 23: 332
16. Goldberg DJ., Sciales CW (1991) Pyogenic granuloma in
children. J Dermatol Surg Oncol 17: 960
17. Patrice SJ, Wiss K, Mulliken JB (1991) Pyogenic granuloma (lobular capillary hemangioma): A clinicopathologic
study of 178 cases. Pediatr Dermatol 8:267
18. Glass AT, Milgraum S (1992) Flashlamp-pumped pulsed
dye laser treatment for pyogenic granuloma. Cutis 49:
351
19. Gonzalez S, Vibhagool C, Falo LD, Momtaz KT, Grevelink
J, Gonzalez E (1996) Treatment of pyogenic granulomas
with the 585 nm pulsed dye laser. J Am Acad Dermatol
35: 428
20. Watzinger F, Gossweiner S, Wagner A, Richling B, Millesi-Schobel G, Hollmann K (1997) Extensive facial vascular malformation and haemangiomas: a review of the
literature and case reports. J Cran Maxillofacial Surg 25:
17

335-343
21. Enjolras O (1997) Classication and management of the
various supercial vascular anomalies: hemangiomas
and vascular malformations. J Dermatol 24: 11
22. White CW, Wolf SJ, Korones DN, Sondheimer HM, Tosi
MF, Yu A (1991) Treatment of childhood angiomatous
diseases with recombinant interferon alfa-2a. J Pediatr
118: 59
23. Ezekowitz RA, Mulliken JB, Folkman J (1992) Interferon
alfa-2a therapy for life threatening hemangiomas in infancy. N Engl J Med 326: 1456
24. Bauman NM, Burke DK, Smith RJ (1997) Treatment of
massive or life threatening hemangiomas with recombinant alpha-2a interferon. Otolaryngol Head and Neck
Surg 117: 99
25. Spiller JC, Sharma V, Woods GM, Hall JC, Seidel FG.
(1992) Diffuse neonatal hemangiomatosis treated successfully with interferon alfa-2a. J Am Acad Dermatol
27: 102
26. White CW, Sondheimer HM, Crouch EC, Wilson H, Fan LL
(1989) Treatment of pulmonary hemangiomatosis with
recombinant interferon alfa-2a. N Engl J Med 320: 1197
27. White CW (1990) Treatment of hemangiomastosis with
recombinant interferon alfa. Semin Hematol 27: 15
28. Greinwald JH, Burke DK, Bonthius DJ, Bauman NM, Smith
RJ (1999) An update on the treatment of hemangiomas
in children with interferon alfa-2a. Atch Otolaryngol
Head Neck Surg 125: 21
29. Sgonc R, Fuerhapter C, Boeck G, Swerlick R, Fritsch P,
Sepp N (1998) Induction of apoptosis in human dermal
microvascular endothelial cells and infantile hemangioma
by interferon-alpha. Int Arch Allergy Immunol 117: 209
18
Volume 10 : 2005-2006
Jigs, Guides, Indices, Matrices and Templates in Implant Dentistry:

Prosthodontic Case Control in Implant Dentistry
Case-control in dentistry is a critically fundamental element for clinical success, especially in Implant Prosthodontics. When restoring edentulous or partially edentulous
patients, occlusal vertical dimension, centric relation position, esthetics and phonetics
should be established and maintained throughout the restorative process. This article
addresses these challenges and concerns by describing surgical templates, positioning jigs, verication guides, and vinyl indices. The goal is to ensure accuracy and
increase efciency while reducing errors, chair-time, and labwork.
Candice Zemnick, DMD, MPH1
Postgraduate Clinical Fellow, Division of

Prosthodontics, Columbia University School
of Dental and Oral Surgery, New York, NY
1
CDR
RADIOGRAPHIC TEMPLATES
It all begins with proper placement and orientation of tention on tooth-borne templates, the abutment teeth
implants in order to optimize function and esthetics of can be relined with silicone6. The template should exthe denitive restoration1. Diagnosis of bone quality tend one to two teeth away from the edentulous area
and quantity can be made with the assistance of com- so as to afford stability. Once dislodged from the cast
puterized tomographic (CT) scans and ideal implant and edges smoothed, the pontic teeth on the temsites can be mapped2. Radiographic templates can be plate should be lled with a radiopaque resin (read befabricated for the patient to wear during their CT scan low) so as to be visible on the CT scan and reect their
so as to correlate
intended position
surgical and reover the ridge.
storative treatment
For the completely
planning with raedentulous patient
diographic images3(Fig. 1B):
Pro5
. Tooth-borne and
vided the patient
Fig. 1A
tissue-borne temis wearing acplates are relatively
ceptable complete
easy to fabricate
denture prostheand are based on
ses, or a wax-up
diagnostic wax-ups
has been comFig. 1B
completed during Fig. 1C
pleted, these can
the treatment planbe replicated by
Fig. 1A. Radiographic template supported by anterior dentition. Fig. 1B. using a duplicating
ning stage.
For the partially Duplicate of complete denture serves as a radiographic template. Fig. ask. Alginate is
1C. Radiographic markers of gutta percha placed occlusally and axiedentulous patient
mixed and applied
ally
(Fig. 1A): Once the
to one half of the
complete wax-up is
ask and the dennished and factors such as occlusion, vertical dimen- ture can be placed, teeth-rst, until just the intaglio
sion, and esthetics are addressed, the cast can be now surface is visible. The land area of alginate surrounding
duplicated and converted into a working cast (Type the denture should be smoothed and not exceed the
III gypsum). A rigid thermo-forming sheet of .080 or perimeter of the ask so that it may be closed comabove can then be vacu-formed over the cast and sub- pletely without interference. Once the alginate has set,
sequently removed using a hand-piece with preferred additional alginate may be placed in the other half of
bur or disc. The clinician should cut back to the height the ask, and manually applied to the inner-surface of
of contour in the region of the abutment teeth which the denture (thus avoiding the incorporation of air bubwill support the template so that it will snugly t but bles). The ask is then closed slowly and excess alginot lock on to the patients teeth. However, the entire nate is allowed to escape. Once the second increment
outline of the teeth which are in the edentulous area of alginate has set, the ask can be opened, and the
should be preserved. Distal extension anges should be duplicate denture is removed. A radiopaque mixture of
retained and relined for stability if necessary as long as autopolymerizing acrylic is then applied by syringe to
there is no interference with ap design. For added re- the tooth areas of the mold. Pre-mixed barium sulfate
Volume 10 : 2005-2006
19
Jigs, Guides, Indices, Matrices and Templates in Implant Dentistry
Fig. 2A. Radiographic template relieved and converted to surgical

template. Buccal facade preserved
while ample room exists to accommodate mucoperiosteal reection
Fig. 2B. Mandibular surgical template
intraoral. Fig. 2C. Surgical template is
trimmed to t over supporting teeth
while reecting entire prole of #8 &
9. Fig. 2D. Occlusal view reveals areas of relief to guide surgeon as to the
proper placement of xtures, while allowing some degree of re-angulation
in the presence of bone resorption
Fig. 2A
Fig. 2B
Fig. 2C
Fig. 2D
acrylics are available, however an economical alternative is to purchase barium sulfate from a pharmacy (no
prescription necessary), and mix it with traditional clear
autopolymerizing resin so that it accounts for about
10-15% of the mixture by weight, i.e., 85g resin/15g
BaSO44,7,8. Once the tooth areas are lled, additional
clear autopolymerizing acrylic is now applied on top
so that upon closure there will be excess escaping the
ask. The ask can then be placed in warm water in a
pressure-pot at 20 psi for about 15-20 minutes. Once
polymerized, the duplicated denture can be removed
and the surfaces checked for areas that may irritate
the patient. Occlusion of template should be veried to
ensure stability of the prosthesis during the CT scan.
The patient should be instructed to only take the CT
scan while wearing this template. An inter-occlusal record with a minimum of 4-6mm inter-occlusal space
needs to be worn to avoid scatter if opposing dentition
has metallic restorations.
Other radiographic markers can be used such as gutta
percha (Fig. 1C) or metal wires which can be placed
along the facial/buccal axial surfaces or in channels
placed occlusally within the connes of the intended
prosthetic restoration.
SURGICAL TEMPLATES (FIG. 2A-D)
Once the CT is completed, it can be analyzed by both
the surgical and restorative clinicians and optimal locations for implants can be visualized as facilitated by
the radiographic markers and the topography of bone.
Surgical templates or implant placement guides are
rigid stable devices that facilitate the precise position
and angulations of implants to optimize the design of
the intended nal prosthesis while respecting anatomical limitations6,7,9. Radiographic templates can be easily
converted into surgical templates by drilling holes in
20
locations which direct the surgeon during osteotomy

procedures so as to optimize the prosthetic outcome1013
. Communication and coordination with the surgeon
is absolutely paramount. Surgical techniques should be
addressed when modifying the radiographic template
so as to maximize its utility during surgery. Specic
dimensions of guide holes, angulations, and accommodation for mucoperiosteal ap reection are denite
considerations.
If a radiographic template was not fabricated initially,
a new surgical template can be created by duplicating
a pre-existing acceptable prosthesis either by using a
duplicating ask (as previously described), or a vinyl
polysiloxane putty matrix technique14. Also mentioned
above is the utilization of vacuform templates of adequate thickness and rigidity (0.08+) that can be used
on stone casts of patients who possess teeth that can
be used as abutments to support the template. It is
important to recognize the inherent limitations that exist when fabricating surgical templates on casts. The
stone models represent a rigid representation of soft
tissue, and thus do not account for varying thickness
of mucosa, topography of underlying bone or vital anatomical structures that lie within.
Stereolithographic drilling templates have been utilized
over the past several years and can offer interchangable, incrementally-sized drill guide inserts to rigidly
guide all the osteotomies necessary for implant placement, from the initial pilot osteotomy to the nal placement of the implant through the template15-16. The osteotomies are made in the exact location, angle and
depth as planned on CT surgical simulation software
which can appreciate bone quality and anatomy17-18.
SimPlant by Materialise is a commonly used interactive software for treatment planning and the production of virtual 3D models of mandibles, maxillae and
entire skulls. Various companies can use the program
Volume 10 : 2005-2006
Fig. 3A
Fig. 3C
Fig. 3B
Fig. 3A. Dental oss used as scaffolding for jig. Fig. 3B. Light Activated urethane acrylate gel applied. Fig. 3C. Facial
view of jig
to facilitate the CAD/CAM manufacturing of tooth-supported, mucosa-supported as well as bone-supported

surgical templates.
CAST ACCURACY & VERIFICATION- PICK-UP
COPING JIG (FIG. 3A-3C)
Once Stage I and Stage II implant surgeries are completed, an accurate implant-level impression must be
obtained so that the master casts are, in turn, accurate19-20. Impression copings should be placed and
radiographs should be taken to conrm seating especially with external designs. In cases with multiple implants, impression copings should be connected and
an open-tray or pick-up technique utilized21-23. Closed
tray techniques are sometimes considered undesirable
because of difculty in tray removal in the case of divergent multiple implants, and the subsequent need
to replace individual transfer copings into the impression, thus possibly introducing error. A support trellis
of dental oss is formed by intertwining it between
the copings, and pattern resin or light-cured acrylic gel
can be added to preserve the coping relationship. A
nal impression is then made and a soft-tissue cast
created. The model should be poured in two phases
using Type IV gypsum so as to minimize the effects of
expansion7. This jig, or a new one directly fabricated on
the cast can subsequently be segmented, luted again
intra-orally, and then replaced on the cast. If there is
a passive seating, the accuracy of the cast is veried.
If not, another impression needs to be made. If an imFig. 4A. Initial wax-up of #4-6,
12,13. Fig. 4B. Clear matrix that
reects contours of wax-up. Fig.
4C. Matrix in place on xturelevel cast with visualization of
platforms. Guidepins can be
placed to project xture angulation and determine need for
correction. Fig. 4D. Template in
place with occlusal relief to accommodate guidepin extending
from xture analog in #3 position. Fig. 4E. Guidepin passes
perfectly through middle of occlusal surface. No reangulation
required. Fig. 4F. Buccal view of
single unit #3
Volume 10 : 2005-2006
Fig. 4A
mediate-load prosthesis was used, it can be removed

from the patients mouth and placed on the cast. If
there is a passive t, it is an additional verication of
accuracy.
ABUTMENT SELECTION- CLEAR TEMPLATES AND
VINYL INDICES (FIG. 4A-F)
A number of different approaches are possible when
selecting abutments.
Partially-edentulous patients: A simple thin (0.020 coping) thermo-forming sheet can be vacuformed on the
original stone cast of the wax-up and then placed on
the implant-level cast. These templates represent the
contour of the nal restoration. The occlusal surface
should be relieved to allow room for the placement of
guidepins on the implant analogs. Ridge relationships,
future location of screw access holes, and angulation
issues can be visualized and addressed at this time.
Completely edentulous patients: A similar thermoplastic
template can be created and stabilized by the primary
areas of support. A more accurate method is to reline
the current removable prosthesis intraorally- stabilized
by healing abutments (provided the prosthesis possesses acceptable esthetic and functional landmarks).
These same healing abutments are then transferred
to the implant-level cast and the prosthesis is subsequently attached. Positioning grooves are made on the
lateral aspect of the cast and a vinyl index is then fabricated that reects the occlusal, buccal and if desired,
lingual aspects of the planned restoration (Refer to Fig.
Fig. 4B
Fig. 4C
Fig. 4F
Fig. 4D
Fig. 4E
21
Fig. 5A
Fig. 5C
Fig. 5B
Fig. 5A. Angulated abutments placed on cast in ideal formation. Guidepins are attached which project orientation.
Silicone Putty is pressed up against guides. Fig. 5B. Intra-oral use of vinyl index. Fig. 5C. Lateral view of index
6A & B). If the patient is wearing a xed full-arch interim prosthesis, then the process is quite easy as it
can be removed from the patients mouth and screwed
onto the implant-level cast. A vinyl index as described
before can then be fabricated and guidepins placed.
Straight, angulated or custom abutments can now be
easily be selected so as to optimally support the nal
restoration24.
ABUTMENT TRANSFER JIG: VINYL MATRICES
(FIG. 5A-C)
Multi-unit angulated abutments often possess 12 different positions of orientation. Difculties can arise when
attempting to place several abutments at one time to
accommodate metal framework superstructures. In order to facilitate intraoral placement, an acrylic or vinyl
index can be fabricated and the orientation of each
abutment is easily established. In full-arch cases, a
implant-level immediate load prosthesis precludes the
permanent placement of angulated abutments until nal delivery. Therefore, for every framework and waxup verication procedure, this index provides an effective and time-saving method of accurate multi-unit or
custom abutment transfer from the cast to the mouth.
Once the abutments have been selected, they should
be placed on the cast in the ideal orientation. Guidepins are then placed so that the angulated relationship is projected upward and will be impressed by the
silicone material. Sufcient material should also extend
onto adjacent teeth, or in an edentulous case, into the
lingual vestibule/palatal vault area for stability. Abutments can be placed in the patients mouth and their
position veried by attaching the guidepins and seeing
if they passively t into the index.
Acrylic templates can also be fabricated to preserve the

position of custom or angulated abutments. Although
they are harder to manipulate intraorally on larger cases, they certainly have a place and utility in maintaining
relationships and it is up to the individual practitioner
to decide which material they prefer. Keep in mind that
screw access holes must be blocked-out and that the
patients inter-occlusal distance may be inadequate to
accommodate both an acrylic jig and driver.
METAL FRAMEWORK DESIGN: VINYL MATRICES
(FIG. 6A & B)
The same vinyl index used to select abutments can
also be used to visualize the position of the teeth in
relationship to the framework and the ridge24. This is
especially important in full-arch cases where an acrylic
hybrid is to be fabricated. Sufcient room has to exist for acrylic and prosthetic teeth and the framework
must accommodate both without altering structural
strength, phonetics, or adversely affecting the comfort
of the patient. Communication to the laboratory via a
vinyl index can clarify and dene the parameter within
which the framework can be created.
FINAL PROSTHESIS FABRICATION: VINYL MATRICES (FIG. 7A & B)
Previous vinyl matrices and acrylic templates can all aid
in the nal wax-up and porcelain addition of the prosthesis. Esthetic and phonetic contours are preserved
and the positive attributes of temporary prostheses
can be translated into the nal prostheses. For hybrid
prostheses, the vinyl index can also be used as a waxup template. Prosthetic teeth can be sticky-waxed in
Fig. 6A. Guidepins placed and angulated abutments are selected. Fig. 6B.
Anterior-Posterior Spread, Cantilever
design and Framework planning are
developed based on matrix
Fig. 6A
22
Fig. 6B
Volume 10 : 2005-2006
Fig. 7A. Acrylic teeth luted to vinyl index and framework design
veried. Fig. 7B. Screw Access
holes blocked with guidepins and
hot wax subsequently added
Fig. 7A
Fig. 7B
the appropriate positions, screw access holes are then

blocked, and liquid wax can be added, thus quickly creating a wax-up suitable for try-in. Ultimately the indices
and templates serve as the physical communication to
the laboratory technician of exactly what the nal prosthesis should simulate24.
MAXILLOFACIAL PROSTHETICS
Positioning guides are not only helpful for intraoral applications, but also for extraoral implant-retained prostheses. Surgical templates are used to ensure proper
positioning and angulation of the implants to allow the
attachment of retentive elements within the connes
of an esthetic prosthesis. Preoperative wax patterns of
auricular, orbital, nasal or midfacial prostheses can be
impressed as previously described and duplicated in
clear acrylic. Holes can then be drilled to guide the surgeon and optimize the prosthetic outcome. The original wax pattern is not harmed and can still be used in
the fabrication of the nal prosthesis25.
CONCLUSION
This report has described are various methods and
approaches used to establish and preserve a lineage
of case control in implant dentistry. Too often, complicated cases can overwhelm clinicians and inaccuracies
may be introduced early on and perpetuated throughout the care of the patient. However, the treatment
planning phase offers the opportunity to acknowledge
the patients esthetic and functional needs, and optimize the prosthetic outcome given the limiting factors
of anatomy. An additional restorative goal is to maintain accuracy that will serve to limit mists, uneven
force distribution, and prosthesis complications and
failures. The wise investment of time and effort, and
creation of an initial wax-up, leads to radiographic and
surgical templates, interim prostheses, clear templates,
matrices and vinyl indices. All of these serve as tools
for evaluation that maintain a ow of care that begins
with surgical guidance and ends with prosthetic delivery. Several of these principles and approaches can be
applied toward restoring the natural dentition as well.
Volume 10 : 2005-2006
ACKNOWLEDGEMENTS
The author wishes to acknowledge the contributions of
Drs. White, Alfonso, Lal, and Piro for their clinical and
laboratory instruction.
REFERENCES
1. Engelman MJ, Sorensen JA, Moy P (1988) Optimum
placement of osseointegrated implants. J Prosthet Dent
59(4):467-73
2. Besimo C, Lambrecht JT, Nidecker A (1995) Dental implant
treatment planning with reformatted computed tomography. Dentomaxillofac Radiol 24(4):264-7
3. Basten CH (1995) The use of radiopaque templates
for predictable implant placement. Quintessence Int
26(9):609-12
4. Basten CH, Kois JC (1996) The use of barium sulfate for
implant templates. J Prosthet Dent 76(4):451-4
5. Takeshita F, Suetsugu T (1996) Accurate presurgical determination for implant placement by using computerized
tomography scan. J Prosthet Dent 76(6):590-1
6. Kuzmanovic DV, Waddell JN (2005) Fabrication of a self-retaining surgical template for surgical placement of dental
implants for the partially edentulous patient. J Prosthet
Dent 93(1):95-6
7. Misch CM (1999) Use of a surgical template for autologous
bone grafting of alveolar defects. J Prosthodont 8(1):4752
8. Israelson H, Plemons JM, Watkins P, Sory C (1992) Bariumcoated surgical stents and computer-assisted tomography in the preoperative assessment of dental implant patients. Int J Periodontics Restorative Dent 12(1):52-61
9. Sicilia A, Enrile FJ, Buitrago P, Zubizarreta J (2000) Evaluation of the precision obtained with a xed surgical template in the placement of implants for rehabilitation of
the completely edentulous maxilla: a clinical report. Int J
Oral Maxillofac Implants 15(2):272-7
10. Walker M, Hansen P (1999) Dual-purpose, radiographicsurgical implant template: fabrication technique. Gen
Dent 47(2):206-8
11. Cehreli MC, Sahin S (2000) Fabrication of a dual-purpose surgical template for correct labiopalatal positioning of dental implants. Int J Oral Maxillofac Implants
15(2):278-82
12. Solow RA (2001) Simplied radiographic-surgical template for placement of multiple, parallel implants. J Prosthet Dent 85(1):26-9
13. Sykaras N, Woody RD (2001) Conversion of an implant
radiographic template into a surgical template. J Prostho-
23
dont 10(2):108-12
14. Sukotjo C, Radics A (2004) Use of vinyl polysiloxane for
the fabrication of implant surgical guide. J Prosthet Dent
92(6):596-597
15. Fortin T, Champleboux G, Lormee J, Coudert JL (2000)
Precise dental implant placement in bone using surgical
guides in conjunction with medical imaging techniques. J
Oral Implantol 26(4):300-3
16. Kopp KC, Koslow AH, Abdo OS (2003) Predictable implant
placement with a diagnostic/surgical template and advanced radiographic imaging. J Prosthet Dent 89(6):6115
17. Cehreli MC, Calis AC, Sahin S (2002) A dual-purpose
guide for optimum placement of dental implants. J Prosthet Dent 88(6):640-3
18. van Steenberghe D, Naert I, Andersson M, Brajnovic I,
Van Cleynenbreugel J, Suetens P (2002) A custom template and denitive prosthesis allowing immediate implant loading in the maxilla: a clinical report. Int J Oral
Maxillofac Implants 17(5):663-70
19. McCartney JW, Pearson R (1994) Segmental framework
matrix: master cast verication, corrected cast guide,
and analog transfer template for implant-supported prostheses. J Prosthet Dent 71:197-200
20. Jacobson Z, Peterson T, Kim ED (1996) Positioning jig for
implant abutments:procedures and clinical applications. J
Prosthet Dent 75:435-9
21. Assif D, Marshak B, Schmidt A (1996) Accuracy of implant
impression techniques. Int J Oral Maxillofac Implants
11(2):216-22
22. Assif D, Nissan J, Varsano I, Singer A (1999) Accuracy of
implant impression splinted techniques: effect of splinting material. Int J Oral Maxillofac Implants 14(6):885-8
23. Vigolo P, Fonzi F, Majzoub Z, Cordioli G (2004) An evaluation of impression techniques for multiple internal connection implant prostheses. J Prosthet Dent 92(5):470-6
24. Chaimattayompol N, Stanescu J, Steinberg J, Vergo TJ
Jr. (2001) Use of a cross-mounting buccal index to help
transfer the spatial relationships of an interim prosthesis
to the denitive implant-supported prosthesis. J Prosthet
Dent 85(5):509-15
25. Wang R (1999) Preoperative auricular wax pattern duplication for surgical template fabrication. J Prosthet Dent
81(5):634-7
24
Volume 10 : 2005-2006
Parotid Gland Swelling in Patients Seropositive for

Human Immunodeciency Virus
During the period of October 1980-May 1981, ve young men, all active homosexuals, were treated for biopsy-conrmed Pneumocystis carinii pneumonia at 3 different
hospitals in Los Angeles, California. Two of the patients died. All 5 patients had laboratory-conrmed previous or current cytomegalovirus infection and candidal infection
of the oral mucosa1. With these ve cases began the recognition of what we have now
come to know as acquired immunodeciency syndrome (AIDS). The term AIDS was
coined by the Centre for Disease Control (CDC) after that milestone case report. The
denition highlights the acquired, as opposed to congenital, aspect of this disease.
Human immunodeciency virus (HIV) was subsequently named and identied as the
pathogen after evidence showed that a newly recognized retrovirus was the cause of
AIDS2. Infection with HIV, whether it be acquired or congenital, will most likely lead to
the development of AIDS. Systemic involvement and multiple opportunistic infections
due to an impaired immune response are to be expected.
HIV AND THE PAROTID
Mussaad Razouki1
Louis Mandel, DDS2

2
Director, Salivary Gland Centre; Clinical
Professor, Department of Oral and Maxillofacial Surgery, College of Dental Medicine,
1
CDR
It has been documented that at the time of their initial DIAGNOSIS

visit, 41% of HIV-positive patients have head- and neckrelated symptoms3, the most prominent being those in- The DILS patient usually demonstrates bilateral pavolving the salivary glands. Enlargement of the parotid rotid gland swelling (Fig. 1). However, if the problem
gland has been reported in approximately 5% to 10% is clinically unilateral, imaging studies will conrm the
of the HIV-1 population4-5. These patients represent a subclinical existence of bilateral involvement15. These
subset of HIV, known as diffuse inltrative CD8 lym- swellings commonly involve the supercial lobe of the
phocytosis syndrome (DILS)6-9. In DILS, a diffuse CD8 parotid gland. They are also usually quite large and
lymphoproliferation causes both an intense swelling of cosmetically deforming. The swellings are a manifestation of the presence of
both parotid glands and a
lymphoepithelial
cysts
cervical lymphadenopathy.
and/or the characteristic
It is thought that this inCD8 lymphoproliferation.
creased lymphocytic presThe swellings can be rm
ence in the parotid is reor soft upon palpation.
lated to the phagocytosis
The rmness probably is
of HIV antigens by parotid
due to the massive celgland macrophages10. The
lular lymphoproliferative
lymphoproliferation may
inltration, whereas the
develop from the lymph
softness is probably a renodes normally present
ection of presence of the
within the parotid gland
lymphoepithelial
cysts.
or it may originate exThe swellings are painless
traglandularly11-12. It has
and not associated with
been demonstrated that
meals16.
although CD 8 cells preUpon clinical examination
dominate in DILS, both
CD 4 cells and even B cells Fig. 1. Bilateral parotid gland swelling (right side shown) of a patient with bilateral
swelling of the parotid
are present and constitute
gland, one must also keep in mind the vast array of
20% to 25% of the lymphoproliferation13.
Bilateral benign parotid lymphoepithelial cysts may diseases and syndromes that may lead to such a prealso be a cause of the swelling. Such cysts are thought sentation. This includes a false positive diagnosis. One
to originate from included epithelium trapped within must rule out masseteric hypertrophy and asymptomatic bilateral parotid swelling (sialosis), frequently seen
developing intraparotid lymph nodes14.
in alcoholics, diabetics and malnutritional syndromes,
Volume 10 : 2005-2006
25
Parotid Gland Swelling in Patients Seropositive for Human Immunodeciency Virus
and patients with autoimmune Sjogrens syndrome.

Bilateral parotid gland swelling can also be iatrogenically induced during administration of iodine dyes for
imaging purposes or following the use of radioactive
iodine (131I). Acquired diseased states of both bacterial (acute suppurative parotitis) and viral (mumps and
HIV) etiologies, must also be considered in differential
diagnosis.
IMAGING
Ultrasonography represents a simple, noninvasive and
inexpensive diagnostic modality that has been uniquely
adapted for use with supercially located anatomic soft
tissue structures. No radiation is involved and the results are rapidly reproducible17. Therefore ultrasound
screening for HIV has been suggested18-20, because the
cystic and the lymphoproliferative nature of HIV-related parotid swellings can be visualized as characteristic
sonolucent patterns.
When analyzing the sonograph of an HIV patient with
parotid swellings, large , hypoechoic areas with debris
and septa represent the existence of lymphoepithelial
cysts (Fig. 2), while numerous small hypoechoic nodules suggest lymphocyte inltration21-23.
A CT scan of the parotid glands will show the presence
of multilocular cysts usually bilaterally (Fig. 3) and at
times unilaterally. In addition, cervical lymphadenopathy is extensively present. On occasion am increased
density with signicant parotid gland enlargement is
evident and mirrors massive CD8 lymphocytosis inltration.
Since no denitive diagnosis by the imaging above can
be made, it is obvious that serology and the totality of
the patients clinical symptoms must be factored into
the diagnosis.
Fig. 3. A CT scan of the parotid glands will show the presence of multilocular cysts usually bilateral
TREATMENT
Antiviral drug therapy is the most effective HIV treatment plan. There are currently 20 FDA approved retroviral drugs falling into ve different classes:
1.Nucleoside analog reverse transcriptase inhibitors
(NsRTIs)
2.Nucleotide analog reverse transcriptase inhibitors
(NtRTIs)
3.Non-nucleoside reverse transcriptase inhibitors
(NNRTIs)
4.Protease Inhibitors (PIs)
5.Fusion (entry) inhibitors.
The diversity of the classes reects the fact that every
step in the HIV retroviral lifecycle is a potential target
for therapy. Indeed, it has been accepted that antiviral therapy is the most effective HIV treatment plan.
Treatment with multiple drug classes in a variety of
combinations is known as highly active antiretroviral
therapy (HAART)24-25.
The primary goal of HAART is to stop the impeding viral
replication. Simultaneously, some restoration of immunity is to be expected. HAART is indicated in patients
with HIV viral loads greater than 20,000 copies/mm3 or
CD4 cell counts below 500/ mm3. Therapy lowers the
viral load and elevates the level of CD4 cells26. HAART
has also succeeded in both eradicating parotid gland
swellings27-28 and their recurrences16.
RECENT DEVELOPMENTS
Fig. 2. Large, hypoechoic areas with debris and septa

represent the existence of lymphoepithelial cysts
26
Evidence on HIV co-receptor expression has suggested

that specic subpopulations may be less susceptible to
the progression from HIV to AIDS. These patients have
been labeled as non-progressors and usually present
with a homozygous deletion in the CXCR4 and CCR5
HIV-2 co-receptor genes29.
Volume 10 : 2005-2006
Parotid Gland Swelling in Patients Seropositive for Human Immunodeciency Virus
Recently, a rare and aggressive form of AIDS was used

to publicize dangers of unprotected sex30. The new
strain has shown resistance to 19 out of the 20 FDA
approved retroviral drugs31.Controversy has also arisen
as to whether or not the use of recreational drugs,
methamphetamine in this case, could have somehow
facilitated the rapid progression from HIV to the extremely resistant AIDS32.
REFERENCES
1. Morbidity and Mortality Weekly Report - June 5, 1981 /
30(21);250-2
2. Morbidity and Mortality Weekly Report - January 11, 1985
/ 34(1);1-5
3. Mrsusen D, Sooy C (1998) Otolaryngologic and head and
neck manifestations of acquired immune deciency syndrome (AIDS). Laryngoscope 95:401-5
4. Schiodt M, Greenspan D, Daniels TE (1989) Parotid gland
enlargement with xerostomia associated labial sialadenitis in HIV-infected patients. J Autoimmun 2:415
5. Soberman N, Leonidas JC, Berdon W (1991) Parotid enlargement in children seropositive for human immunodeciency virus. AJR Am J Roentengenol 157:553
6. Itescu S, Dalton J, Zhang H-Z (1993) Tissue inltration in
a CD8 lymphocytosis syndrome associated with human
immunodeciency virus-1 infection has the phenotypic
appearance of an antigenically driven response. J Clin
Invest 91:2216
7. Bachmayer C, Dhote R, Blanche O (1995) Diffuse inltrative
lymphocytosis syndrome with predominant neurological
manifestations in two HIV-infected patients responding
to zidovudine. AIDS 9:1101
8. Mandel L, Kim D, Uy C (1998) Parotid gland swelling in HIV
diffuse inltrative CD8 lymphocytosis sundrome. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod 85:565
9. Patel S, Mandel L (2001) Parotid gland swelling in HIV diffuse inltrative CD8 lymphocytosis syndrome. NY State
Dent J 67(3):22-3
10. Itescu, Brancato LJ, Buxbaum J, Gregersen PK, Rizkt CC,
Corxson S (1990) A diffuse inltrative CD 8 lymphocytosis syndrome in human immunodeciency virus (HIV)
infection: a host immune response associated with HLADR5. Ann Intern Med 112:3-10
11. Kazi, S Cohen PR, Williams F (1996) The diffuse inltrative lymphocytosis syndrome: Clinical and immunological
features in 35 patients. AIDS 10: 385
12. Ryan J, Ioachim H, Marmer J (1985) Acquired Immune
deciency syndrome-realted lymphadenopathies presenting in the salivary gland lymph nodes. Arch Otolaryngol 111: 554
13. Itescu S, Winchester R (1992) Diffuse inltrative lymphocytosis syndrome; a disorder occurring in human immunodeciency virus-1 infection that may present as a sicca
syndrome. Rheum Dis Clin North Am 18:683-97
14. Mandel L, Surattanont F (2002) Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 93:454-9
15. Shugar J, Som P, Jaconbsen A (1998) Study of AIDS-related lymphadenopathy in the intraparotid and perisubmaxillary gland lymph nodes. J Oral Pathol 17: 164
16. Mandel L, Surattanont F (2002) Rregression of HIV pa-
Volume 10 : 2005-2006
rotid swellings after antiviral therapy: case reports with

computated tomographic scan evidence. Oral Surg ral
Med Oral Pathol Oral Radiol Endod 94:454-9
17. Mandel L (2001) Ultransound Findings in HIV positive
patients with parotid gland swellings. J Oral Maxillofac
Surg 59:283-286
18. Gooding GAW, Sooy CD, Haybarger CP (1992) Ultrasonography of cyctic parotid lesions in HIV infection. J Ultrasound Med 11:35
19. Rozanowski F, Walther EK, Rockstroh J (1994) HIV assoziierte Parotiszysten. Laryngorhinootologie 73:215
20. Corr P, Vaihiligum M, Thejpal R (1997) Parotid MALT lymphoma in HIV children. J Ultrasound Med 16:615
21. Soberman N, Leonidas JC, Berdon W (1991) Parotid enlargement in children seropositive for human immunodeciency virus. AJR Am J Roentgenol 157:553
22. Vona S, Colombo E, Damiani G (1994) Salivary gland lesions in HIV-positive patients. Eur Radiol 4:434
23. Pijpe J, Kalk WW, Bootsma H, van der Wal JE, van Imhoff GW, Vissink A (2003) Bilateral swelling of the parotid
glands as part of a systemic disease. Ned Tijdschr Geneeskd 147 (47): 2309-15
24. Reddy P, Ross J (1998) Antiretroviral therapy: an update.
Conn Med 62:25-8
25. Kak V, MacArthur RD, Crane LR (2000) Treatment of HIV
disease in the new millennium. Semin Thorac Cardiovasc
Surg 12:140-4
26. Chaisson RE, Kreuly JC, Moore RD (2000) Association
of initial CD4 cell count and viral load with response
to highly active antiretroviral therapy [research letter].
JAMA 284:3128-9
27. Craven DE, Duncan RA, Stram JR, OHara CJ, Steger KA,
Jhamb K (1998) Response if lymphoepithelial parotid
cysts to antiretroviral treatment of HIV-infected adults.
Ann Intern Med 128:455-9
28. Uccini S, DOfzi G, Angelici A, Prozzo A, Riva E, Antonelli
G (2000) Cystic lymphoepithelial lesions in the parotid
gland in HIV-1 infection. AIDS patient care STDS 14:
14(3): 143-7
29. Blaak H, Boers PH, Gruters RA, Schuitemaker H, van der
Ende ME, Osterhaus AD (2005) CCR5, GPR15, and CXCR6
are major coreceptors of human immunodeciency virus
type 2 variants isolated from individuals with and without
plasma viremia. J Virol 79(3):1686-700
30. Check E (2005) New York draws re over case of drugresistant HIV. Nature 433 (7028): 788
31. Clatts MC, Goldsamt LA, Yi H (2005) Drug and Sexual
Risk in Four Men Who Have Sex with Men Populations:
Evidence for a Sustained HIV Epidemic in New York City.
J Urban Health 82 (1SUPPL 1): i9-17
32. Halkitis PN, Green KA, Mourgues P (2005) Longitudinal
Investigation of Methamphetamine Use Among Gay and
Bisexual Men in New York City. J Urban Health 82 (1SUPPL 1): i18-25
27
A case report of continued tooth development following

traumatic coronal amputation in an 11 month old boy: Phantom tooth?
Traumatic injuries to the primary and young permanent dentition are a fairly common
occurrence in children. A study by Schtzmansky in 1963 showed that 13% of examined school children by the age of 18 years had experienced a traumatic dental injury
in the past1. Injuries to anterior teeth tend to increase in incidence as a child learns
to walk and run due to a developing neuromuscular system. The alveolar bone that
supports primary teeth is not as dense in the rst few years of life and is more elastic
than in adults. Therefore, in young children, intrusion and displacement of the teeth
are more common than fractures and avulsion1, 2.
1
Class of 2004, College of Dental Medicine, Columbia
University, New York, NY
2
Class of 2005, College of Dental Medicine, Columbia
University, New York, NY
3
Assistant Professor, Director of Predoctoral Programs,
Division of Pediatric Dentistry, College of Dental Medicine, Columbia University, New York, NY
CDR
INTRODUCTION
Infants exhibit very little spatial movement, and therefore dental trauma is quite uncommon prior to age one.
At this age, the mineralizing crowns of the primary incisors have just erupted and are merely shells of the
outer enamel. The ameloblasts and odontoblasts occupying the somewhat large pulp chamber inside continue to deposit enamel and dentin matrix. The roots
have not yet developed and are seen radiographically
as an outline of a thin layer of cementum along the
Hertwigs epithelial root sheath (HERS). Traumatic coronal amputation or avulsion are rare in this age group;
an extensive literature search revealed only one case.
Yakushiji et al3 reported the case of a 3 year old child in
Japan in whom the roots of the lower primary incisors
had continued to form after these teeth had been fractured and severed. Despite the coronal amputation,
the intact cells of the pulp and periodontium continued
to produce dentin and cementum.
CASE REPORT
The following case report documents an extremely unusual instance of dental trauma and continued tooth
development in the absence of any remnant dental
hard tissue in an 11 month old boy. The mother and
child presented to the post-doctoral pediatric clinic at
the College of Dental Medicine as an emergency shortly
after the injury. The child had fallen from his bed and
had fractured his right primary maxillary central incisor
(tooth #E). A radiograph revealed a horizontal fracture
along the CEJ (VI Modied Ellis class IV fracture Fried
& Erickson) and a faint outline of the developing primary roots (Fig. 1). Clinically, the tooth exhibited extreme
coronal mobility at the fracture line and was extracted
due to concerns over aspiration while feeding. A second radiograph at this point revealed an edentulous
space at the extraction site with a barely visible outline
of the developing roots (Fig. 2). We decided not to
remove this extremely thin root layer due to the risk
Volume 10 : 2005-2006
Dan Ponce, DDS1

Ji Young Kim, DDS2
Shantanu Lal, DDS3
of inadvertent injury to the underlying and fragile permanent tooth bud. The decision to monitor this case
was appropriate given the pre-cooperative age of the
child and the unusual nature of this case. The mother
received post-operative instructions and was asked to
return in two weeks or earlier if the child exhibited any
discomfort or difculty during feeding. The mother returned 5 months later and a subsequent radiograph revealed a developing tooth at the previously edentulous
extraction site (Fig. 3). It appeared that although the
post extraction radiograph had revealed the absence
of dental hard tissue, the pulp was relatively intact and
healthy and had continued to lay down tooth structure. Unfortunately, the remaining pulp in the extraction socket was exposed to the oral environment during this time and showed signs of inammation. We
extracted the pulp-tooth complex with great care (Fig.
4). The mother returned 2 months later and we took
one last radiograph to rule out any infection (or yet
another tooth). The extraction site was indeed clear
and had healed well.
DISCUSSION
As previously mentioned, dental injuries are infrequent
before the age of one. In this case, an 11 month old
boy suffered a fracture and subsequent coronal amputation of his upper right primary central incisor. The
intact pulpal tissues and continued tooth development
resulted in rudimentary root and some clinical crown
formation. While no formal histological examination
was performed, the probable histological observations
will be discussed. Here we would like to offer some
probable explanations to this phenomenon.
Following fracture to the tooth and subsequent removal of the remaining coronal tooth fragment, the outer
cellular layer of the root was left behind in the socket.
This included HERS and some of the pulp tissue. As
this dental pulp is highly vascular and well innervated, it
29
Continued tooth development following traumatic coronal amputation in an 11 month old boy
Fig. 1
Fig. 5
Fig. 2
Fig. 3
Fig. 1. White arrow indicates a horizontal fracture along the CEJ of tooth # E. Fig. 2.
Immediately following extraction. Note the edentulous socket and the developing permanent tooth bud. Fig. 3. Phantom Tooth. Rudimentary tooth developing 5 months
post-extraction as a result of continued pulpal activity. Fig. 4. Clean edentulous socket
following extraction of the pulp-tooth complex. Fig. 5. Extracted pulp-tooth complex.
The black arrow indicates the brous pulp. The irregular dentine-cemento-enamel
complex lies to the left
is capable of healing by producing reparative dentin in

response to various stimuli4. Many studies have shown
dentinogenesis following pulpal stimulation by injury,
the application of bone morphogenetic protein (BMP),
and the application of pulp capping materials5-7. Reparative dentin is usually formed by a new generation
of odontoblast-like cells, which derive from progenitor cells within the pulp in response to an appropriate
stimulus after the death of the original odontoblasts8.
It can be assumed that after the time of injury, the
pulp was sufciently dentinogenic, having the cellular
capability of differentiating into odontoblast-like cells.
The trauma to the tooth eliminated all existing coronal odontoblasts and this implies that any dentin that
formed following the trauma must have been produced
by new odontoblast-like cells5, 9. Following trauma,
there might have been a partial necrosis on the peripheral layer of the pulp due to exposure to the oral
environment. Presumably, healing of the gingival tissue over the residual pulp tissue could have provided
a protective interface for the formation of new coronal
dentin10. Irritation may also subside once the necrotic
layer covering the exposed pulp tissue is formed.
Tziafas hypothesizes that after pulp exposure a zone
of new collagen is formed subjacent to the wound
surface6. This natural tissue response to a low-grade
irritation creates an area of pulp biomatrix at the exposure site, which is secreted by broblasts or osteodentinoblasts. The cell-biomatrix interactions inuence
movement and orientation of the pulp cells regulating their specic shape and function according to the
genetic program of the dental pulp ectomesenchyme.
Fibronectin may play a mediating role during the cellbiomatrix interactions because of the strong afnity
to the collagenous matrix6. The appearance of these
newly differentiated cells subjacent to the necrotic pulp
layer paves the way for odontoblast-like cells to begin
repair. Another hypothesis, the one that is explored by
Greer et al10, is that cells within the peripheral layer of
30
Fig. 4
the pulp differentiate and form a bridge of new cells

capable of dentinogenesis.
The presence of mesenchymal cells in the pulp tissue may also allow dentinogenesis to occur without
the formation of an odontoblastic cell layer by inducing differentiation of adult pulp cells into odontoblasts.
BMP belongs to the transforming growth factor-beta
(TGF-) superfamily, a large group of signaling proteins with multiple biological activities controlling the
differentiation of a variety of cell types11. BMPs exist
in odontoblasts, ameloblasts, and dentin matrix7. Nakashima11 showed that recombinant BMP-2 and BMP4 may induce differentiation of adult pulpal cells into
odontoblasts and Lianjia et al7 demonstrated that BMPinduced dental pulp cells in dental pulp tissue cultures
may differentiate from mesenchymal to odontoblastlike cells.
Through a histological study of a primary tooth that
suffered a fracture, one would typically nd continued dentin formation along the walls of the unaffected
tooth structure. This dentin will continue its lateral
formation, encompassing the pulp tissue and narrowing the canal space. An abundance of newly deposited
irregular or reparative dentin will likely form coronally
from the trauma site, and osteodentin, which forms
rapidly following trauma, will likely be observed peripheral to the reparative dentin3. A histological study of a
similar case revealed a confusing picture of unbalanced
dentinogenesis, resorption, and repair and suggested
that the initial calcication was something akin to pulp
stone formation10.
CONCLUSION
As reports of this type of traumatic event in the primary dentition are scarce, so is a lack of discussion
in the literature regarding treatment of such an incident. The young dental pulp is full of highly active
cells that have the potential to proliferate and continue
Volume 10 : 2005-2006
Continued tooth development following traumatic coronal amputation in an 11 month old boy
tooth formation. Complete surgical extraction of the

tooth-pulp complex should be carried out with great
care due to risk of injury to the permanent tooth bud.
Such potential damage may include tooth defects such
as minor enamel opacities, enamel hypoplasia, crown
dilacerations, root dilacerations, arrest of root development, and ectopic eruption or even non-eruption of
the permanent tooth12. In this case, protecting the
pulp from the oral environment might have improved
its prognosis. This would require a novel technique
utilizing tissue adhesives to seal the pulp. Until such
treatment modalities are researched, we suggest the
careful observation of such incidences with frequent
follow-up visits and radiographic assessment.
REFERENCES
1. Andreasen JO (1970) Etiology and pathogenesis of traumatic dental injuries. A clinical study of 1,298 cases.
Scand J Dent Res 78(4):329-42
2. Wei SH (1974) Prevention of injuries to anterior teeth. Int
Dent J 24(1):30-49
3. Yakushiji M, Mochizuki K, Machida Y (1996) Clinical and
histological observations of continuously formed bilateral
mandibular deciduous central incisor roots after traumatic coronal destruction. Bull Tokyo Dent Coll 37(2):71-6
4. Igarashi R, Sahara T, Shimizu-Ishiura M, Sasaki T (2003)
Porcine enamel matrix derivative enhances the formation
of reparative dentine and dentine bridges during wound
healing of amputated rat molars. J Electron Microsc (Tokyo) 52(2):227-36
5. Smith AJ, Lesot H (2001) Induction and regulation of crown
dentinogenesis: embryonic events as a template for dental tissue repair? Crit Rev Oral Biol Med 12(5):425-37
6. Tziafas D (1994) Mechanisms controlling secondary initiation of dentinogenesis: a review. Int Endod J 27(2):6174
7. Lianjia Y, Yuhao G, White FH (1993) Bovine bone morphogenetic protein-induced dentinogenesis. Clin Orthop
Relat Res (295):305-12
8. Klinge RF (1999) A microradiographic and electron microscopic study of tertiary dentin in human deciduous teeth.
Acta Odontol Scand 57(2):87-92
9. Murray PE, Smith AJ, Windsor LJ, Mjor IA (2003) Remaining dentine thickness and human pulp responses. Int Endod J 36(1):33-43
10. Greer JM, Moule AJ, Greer PJ (1996) Resumed tooth development following avulsion of a permanent central incisor. Int Endod J 29(4):266-70
11. Nakashima M (1994) Induction of dentin formation on
canine amputated pulp by recombinant human bone
morphogenetic proteins (BMP)-2 and -4. J Dent Res
73(9):1515-22
12. Holan G, Topf J, Fuks AB (1992) Effect of root canal infection and treatment of traumatized primary incisors
on their permanent successors. Endod Dent Traumatol
8(1):12-5
Volume 10 : 2005-2006
31
CDR
Instructions for Authors

The Columbia Dental Review seeks to address topics of
clinical concern. The Editorial Board welcomes articles
from students, faculty, and attendings from afliated
hospitals of the College of Dental Medicine of Columbia
University.
Within the text citations of these references should appear as follows:

(Valverde et al, 2005), (Cowin and Luo, 1997), and
(Drake et al, 2005), or (Valverde et al, Cowin and Luo,
Drake et al 1,2,3)
The case report should be organized in the following

manner:
To cite a journal article:

Valverde P, Kawai T, Taubman MA (2005) Potassium
channel-blockers as therapeutic agents to interfere
with bone resorption of periodontal disease. J Dent Res
84: 488-499
ABSTRACT
The abstract summarizes the principal points of the
case report and specic conclusions that may have
emerged in the discussion. It should be limited to less
than 250 words.
AUTHOR INFORMATION
A description of each authors degrees, titles, department, and afliation should be given.
INTRODUCTION
The introduction should provide a brief description of
the topic, as well as any relevant epidemiology and
current opinion as documented in the literature.
CASE REPORT
A description of the case(s), including pertinent photographs.
DISCUSSION
A thorough review of the literature, including other reported cases that are relevant to the case(s) presented
or reported.
CONCLUSION
Based on the present case(s) and the discussion.
REFERENCES
The authors should be listed in the order in which they
appear in the articles. In the case of multiple authors,
all authors names must be given.
To cite a chapter in a book:

Cowin SC, Luo G (1997) Modeling of ingrowth into implant cavities along the bone-implant surface.
In: Osseointegration in Skeletal Reconstruction and
Joint Replacement (PI Brnemark, BL Rydevik, R Skalak, Eds) Chicago, Quintessence Publishing Co, Inc, pp
57-72
To cite a book:
Drake RL, Vogl W, Mitchell AWM (2005) Grays Anatomy
for Students. Philadelphia, Elsevier.
To cite a website:
American Dental Association. Estrogenic effects of
Bisphenol A lacking in dental sealants. ADA Position
Statement. 2000. Available at: www.ada.org/prac/position/seal-est.html. Accessed April 4, 2005.
FIGURES AND MANUSCRIPTS
Image les and manuscripts will be accepted on CD with
authors name printed on the CD. Image les should
be of high-resolution quality and should be submitted
in TIFF, TIF, TGA, GIF or JPEG format. A brief caption
in the order in which they are mentioned should be
submitted on a separate page. The manuscript should
not exceed 20, letter size, double-spaced pages and
should be written in a text editor, preferably Microsoft
Office Word. Both, the manuscript and gures, should
be submitted in printed format as well as on CD.

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Columbia Dental Review 2005-2006

AIM & SCOPE

2006 Columbia Dental Review

Columbia Dental Review 2005-2006

Ameloblastoma: A Case Report and Literature Review

Spontaneous Mandibular Bone Regeneration

Reconstruction of the Temporomandibular Joint with

Tracey Rosenberg, DDS, MD

Hemangioma: A Case Report and Literature Review

Parotid Gland Swelling in Patients Seropositive for

29 Dan Ponce, DDS

A case report of continued tooth development

Louis Mandel, DDS

Ji Young Kim, DDS

Front Cover: Eleni Michailidis, Class of 2006, College of Dental

2006 Columbia Dental Review

Ameloblastoma: A Case Report and Literature Review

Ameloblastomas are benign, slow-growing odontogenic neoplasms. They are the

Columbia Dental Review

Ameloblastoma: A Case Report and Literature Review

Fig. 3. An Axial CT scan revealed the presence of a soft

solid multicystic variety18.

An ameloblastoma is usually quiescent for some time

Columbia Dental Review

Ameloblastoma: A Case Report and Literature Review

Fig. 5. Photograph shows the resected portion of the

unicystic ameloblastomas. One option for conservative

Fig. 6. Photograph of the mandible after being rebuilt

depending on the extent of the lesion19. Adjacent soft

Columbia Dental Review

Ameloblastoma: A Case Report and Literature Review

29. Muller H, Slootweg PJ (1985) The ameloblastoma: the

Columbia Dental Review

Spontaneous Mandibular Bone Regeneration

Spontaneous mandibular bone regeneration is a well known but rare phenomenon

Class of 2006, College of Dental Medicine, Columbia University, New York, NY

MECHANISMS OF BONE BIOLOGY

Fig. 1. Growth factor involvement in osteoblast production

Fig. 2. Panoramic radiograph revealing a 4.0 cm

Columbia Dental Review

Spontaneous Mandibular Bone Regeneration

Columbia Dental Review

Spontaneous Mandibular Bone Regeneration

Fig. 5. Clinical picture of

Fig. 6. Clinical picture depicting over-countered reconstruction plate (double-headed

Fig. 7. Radiograph depicting

Columbia Dental Review

Reconstruction of the Temporomandibular Joint

tissue engineering technique. A major advantage of

Columbia Dental Review

SELECTION OF ANIMAL MODEL

Previous animal research on temporomandibular joint

The purpose of this investigation was to determine the

Columbia Dental Review

Columbia Dental Review

mal diet. The animals were monitored for food intake

Fig. 9. En bloc resections of the control and

When using an animal model in such an experiment

The specimens underwent histomorphologic analysis

Columbia Dental Review

intervening spaces between trabeculae but there is no

Minipig #1 Weight (kg)