Download Inside This Issue Study Investigates Novel Approach to Bone Loss in

February 2011
Volume 22, Number 2
EDITOR
Arun K. Garg, DMD; Editor in Chief
EDITORIAL ADVISORS
Editor Emeritus: Morton L. Perel, DDS, MScD
Renzo Casselini, MDT,
Professor of Restorative Dentistry,
Loma Linda University, Loma Linda, CA
Leon Chen, DMD, MS,
Private Practice in Periodontology,
Las Vegas, NV
Scott D. Ganz, DMD,
Private Practice of Prosthodontics, Maxillofacial Prosthetics and Implant Dentistry, Fort Lee, NJ
Zhimon Jacobson, DMD, MSD,
Clinical Professor,
Department of Restorative Sciences/Biomaterials, Boston
University
Jim Kim, DDS, MPH, MS,
Private Practice of Periodontics,
Diamond Bar, CA
Robert E. Marx, DDS,
Professor of Surgery,
Chief, Oral & Maxillofacial Surgery
Peter Moy, DMD,
Private Practice,
West Coast Oral and Maxillofacial Surgery Center and
Center for Osseointegration, Los Angeles, CA
Myron Nevins, DDS,
Associate Professor of Periodontology,
School of Dental Medicine, Harvard University, Boston,
MA
H. Thomas Temple, MD,
Professor of Orthopedic Surgery and Director of University of Miami Tissue Bank, University of Miami School of
Medicine Miami, FL
• The images contained within the first are from
Dr. Smith’s practice and the images from the second article
are from Dr. Garg’s practice; they were designed by Aurelio
Gonzalez, MD
The official publication of the
American Dental Implant Association
Innovations in Bone Growth
This month’s issue focuses on recent advancements in the understanding
of bone and tooth development, specifically, innovations that will enhance
dental implantology in the years to come. The cellular level of function is
described, with a focus on the etiologies and pathophysiologies of common
chronic, systemic disease processes that have a direct effect on the way that
practitioners manage dental-implant patients.
Study Investigates Novel
Approach to Bone Loss in the Jaw
Arun Garg, DMD, and Ghislaine Guez, MD, MBA
A
16 th, 2010 issue of the new eng land Journal of Medicine documents a novel approach to the treatment of alveolar bone loss as a result of periodontitis. Teriparatide — a
drug previously used in the treatment of osteoporosis — used daily for
six weeks was found to increase alveolar bone volume, as well as bone
strength and density. 1 The drug was given to patients with severe periodontal disease in order to determine if this parathyroid hormone-like
compound would improve specific features associated with periodontitis;
both primary and secondary outcomes were established and measured for
up to one year of follow-up. The results were surprising, and may hold
the key to understanding the etiology of osteonecrosis of the jaw, a deleterious side effect of bisphosphonate use, especially in high-dose users
of the drugs, such as individuals with bony metastases. The New England
Journal of Medicine published three components regarding this topic in
that particular issue — a case-report letter, an editorial commentary, and
the original research article described herein. The impact of this original
research on the dental-implant community remains to be seen; clearly,
the medical co-management of refractory cases of periodontitis has an
important role in the future of implant
dentistry. But, of special import, and
one of the themes that Dental Implantology Update often emphasizes, is the
Growing the Next Implant . . 15
convergence of oral pathophysiology
with systemic disease processes and,
new study published in the december
Inside This Issue
NOW AVAILABLE ON-LINE!
Go to www.ahcmedia.com/online.html for access.
10
Figure 1: Disruption of the micro-architecture of bone - changes seen in osteoporosis. First vertebra graphically represents normal bone, second represents
osteopenia and third osteoporosis.
as in this case, the management of
oral disease, with the understanding
of the multiple systemic factors at
work.
Background
Parathyroid Hormone and Bone
Parathyroid hormone is produced
by four parathyroid glands located
on the posterior lateral lobes of the
thyroid gland. The major function
of these glands is the homeostatic
regulation of calcium. Normal serum calcium levels range between
8.5 and 10.2 mg/dL. Hyper- and hypocalcemia can indicate any number of aberrant processes, some of
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Figure 2: Periodontitis. Illustration by
Aurelio Gonzalez.
which are related directly to the
parathyroid glands, others of which
may be indicative of a different
source of calcium leak (bony metastases in the case of hypercalcemia,
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Dental Implantology Update™
kidney disease in hypocalcemia).
Parathyroid hormone acts directly
on the bone and on the kidney, and
indirectly on the gastrointestinal
tract, through Vitamin D. Parathyroid hormone serves to increase the
level of calcium in the blood; it does
so by releasing calcium from bone
(bone and teeth store 99% of the
body’s calcium) and by increasing
calcium resorption by the kidney.
Parathyroid hormone facilitates the
conversion of 25-hydroxyvitamin D
(the inactive precursor) to 1,25-dihydroxyvitamin D, the active form
of Vitamin D (calcitriol). Calcitriol
stimulates the GI tract to absorb
more calcium from that source. Calcitriol also increases bone resorption, which results in further increase in serum calcium levels.
The human skeleton exists in a
dynamic steady state, constantly
being broken down and reformed
by specific cells called osteoblasts
and osteoclasts. 2 The bone matrix is
composed of a complex network of
collagen protein fibers laced with
mineral salts that include calcium
phosphate (85%), calcium carbonate (10%), and small amounts of
calcium fluoride and magnesium
fluoride (5%). 3 Osteoblasts build
bone by depositing bone matrix,
and osteoclasts are responsible for
bone resorption, which leads to calcium levels rising in the blood. Ostrademark Dental Implantology Update™ is used herein
under license. All rights reserved. Reproduction, distribution, or translation of this newsletter in any form or incorporation into any information retrieval system is strictly
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Executive Editor: Russ Underwood, (404)
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Managing Editor: Leslie Hamlin, (404)
262-5416, ([email protected]).
February 2011
11
Table 1: The T Score Implemented by the World Health Organziation
T-Score
Significance
0 to – 1
Healthy young adult
- 1 to – 2.5
Osteopenia
< - 2.5
Osteoporosis
< - 2.5 with evidence of fractures
Severe osteoporosis
•• The score represents the number of standard deviations from the mean bone density values in young adults.
Table 2: Drugs Used in the Treatment of Osteoporosis
Drug
Mechanism of Action
Selective Estrogen-receptor modulator (SERM) Selectively acts on estrogen receptors and
decreases bone resorption
Estrogen replacement therapy
Hormonal therapy that increases systemic
estrogen; associated with increased risk of
breast cancer and thromboembolic events
Bisphosphonates
Stable analogue of inorganic pyrophosphate
that bind to hydroxyapatite crystals; prohibit
bone resorption. Osteoclast activity decreases
with chronic use of this medication. Compound
shown to build up in bones.
Parathyroid hormone
Anabolic agent for bone growth; increases
osteoblast and osteoclast activity
teoclasts are large multinucleated
cells derived from the monocytemacrophage line of precursor cells
that contain lysosomal enzymes. A
specific area of their cell membrane
forms adjacent to the bone surface
that will be resorbed — this area
is called the ruffled border, and it
is the site of bone resorption. Osteoblast and osteoclast activities
are intimately linked, especially
in regard to PTH. The endocrine
system, at a cellular level, is very
tightly controlled and complex, in
that there are numerous activators
and inhibitors involved in most processes, which allows for functioning feedback loops. PTH activates
the osteoblasts, not the osteoclasts
(osteoclasts lack PTH receptors),
which in turn causes the increased
expression of a factor that binds to
osteoclast precursors and stimulates
their differentiation. Ongoing with
the process of resorption is the process of new bone synthesis via matrix deposition and mineralization
(because both cell types are stimulated). This is known as bone turnover, or remodeling. It is the coupling of these functions, mitigated
by parathyroid hormone, that actually strengthens and, in a sense, renews bones. This coupling of osteoclast and osteoblast activity is the
sought-after process that allows for
February 2011
the use a parathyroid analog in the
treatment of osteoporosis and now,
remarkably, periodontitis.
Osteoporosis, Cancer and
Osteonecrosis of the Jaw
Osteoporosis is a condition in
which the micro-architecture of
bone deteriorates (see Figure 1),
leaving it weaker and more susceptible to fracture. 4 Osteoporosis
is diagnosed by the dual-energy
X-ray absorptimontry (DXA) scan
and measured by T-score (see table
1). It is a chronic condition more
commonly seen in postmenopausal
women, though it can occur in both
sexes and in individuals of younger
Dental Implantology Update™
12
Table 3: Significant Adverse Reactions to Teriparatide
Significant Side Effects
Endocrine
Hypercalcemia, transient
Cardiovascular
Orthostatic hypotension
Chest pain
Syncope
Dermatologic
Rash
Endocrine and Metabolic
Hyperuricemia
Gastrointestinal
Nausea
Gastritis
Dyspepsia
Vomiting
Tooth disorder, unspecified
Neuromuscular and skeletal
Arthralgia
Weakness
Leg cramps
Respiratory
Rhinitis
Pharyngitis
Dyspnea
Pneumonia
Miscellaneous
Hypersensitivity
Herpes zoster
• Other adverse reactions include acute dyspnea, allergic reaction, facial or oral edema, reaction
at the injection site, muscle spasm, urticaria.13 One case of osteosarcoma caused the FDA to give
the drug a black-box warning.
age with certain predisposing factors. A low estrogen state in females is a predisposing risk factor
toward the development of osteoporosis, and the reason it is routinely
screened for in this population.
Dental Implantology Update™
Both osteoclasts and osteoblasts
express estrogen receptors, and it is
understood that increased bone resorption in the setting of decreased
bone deposition leads to demineralization of bone over time. Low
calcium absorption plays a role in
many of these cases, as does vitamin D deficiency. Treatment of osteoporosis includes administration
of vitamin D analogs, exercise, estrogen-replacement therapy, and the
administration of bisphosphonates
and parathyroid hormone. A summary of these treatments and their
mechanism of action are listed in
Table 2. One of the most commonly
used and successful treatments for
osteoporosis is a class of medications called the bisphosphonates.
Bisphosphonates are stable analogues of inorganic pyrophosphate
that bind to the hydroxyapitite in
bone and, therefore, are not broken down by the resorptive process
driven by osteoclasts. They have
been shown to improve bone density over time.
Cancer patients who have metastatic lesions to the bone are given
bisphosphonates to stabilize bone
and decrease pathologic fracture
risk by decreasing osteoclastic resorption of bone. Data shows that
this class of medication significantly limits skeletal events (such as
fractures) in certain cancer populations. 5,6 Bisphosphonates have proven to be a safe and effective class
of medications, and are also used
by a large portion of the population
in the treatment of osteoporosis,
though cancer patients receive much
higher doses, as well as intravenous
therapy. This class of medications is
not without certain side effects, and
the effects of long-term use have
not yet been properly elucidated in
the literature. Perhaps the most debilitating complication of bisphosphonate treatment is osteonecrosis
of the jaw, seen more commonly in
individuals receiving high doses of
these drugs. Osteonecrosis of the
February 2011
13
Table 4: Bashutski, et al Study-design Details
Number of
Patients
40
Patients
35 -70 year
old men and
women with
advanced
periodontal
disease
Intervention
Trial
Follow-up Primary
Length Time
Outcome
6 weeks 1 year
Linear
Daily 20 µg
measurement
injection of
of alveolar
teriparatide
bone
versus placebo
(radiograph)
Secondary
Outcomes
Clinical
outcomes, bone
turnover markers,
systemic bone
density, quality of
life
Table 5: Inclusion Criteria Required for Study Participation
Dental Inclusion Criteria
Medical Inclusion Criteria
Vertical osseous defect adjacent to a tooth AND
Normal serum calcium level AND
Periodontal probing depth > 6mm AND
25-hydroxy-vitamin D at least 16 ng/mL
Loss of a clinical attachment of > 6mm
• Exlusion criteria included metabolic bone disease, cancer, growth hormone deficiency, renal disease, smoking, pregnancy, and history of
radiation therapy.
jaw is a chronic inflammatory condition in which maxillofacial bone
becomes necrotic and exposed.
The exact etiology of osteonecrosis of the jaw in bisphosphonate
users remains poorly understood;
it can occur spontaneously or following oral surgery. The mainstay
of treatment has been conservative
surgical treatment, symptom palliation, and antibiotics for the treatment of dental and periodontal infections, though treatment remains
a challenge for most practitioners
and patients. The painful condition
is associated with poorer quality
of life, 7 largely because it can be
disfiguring, and so refractory to
treatment. Still, bisphosphonateassociated osteonecrosis of the jaw
remains a very rare complication
for patients taking oral bisphosphonates. Implant-outcomes data
show no difference in safety for
patients taking oral bisphosphonates compared to those not on
this class of medication, and no
change in implant survival rates
for patients on the medication for
three to five years. 8,9
A case study was presented
in The New England Journal of
Medicine describing the treatment of osteonecrosis of the jaw
with teriparatide. The patient
was an 88-year-old female who
had known severe osteoporosis,
chronic prednisone use, and a 10year history of oral alendronate
use. Despite site debridement and
antibiotic therapy, her left-mandible osteonecrosis, which came
about after a tooth extraction,
did not heal until an 8-week trial
of the PTH analog was administered, at which point it resolved.
The letter’s authors, Ada Cheung
and Ego Seeman, suggest three
mechanisms that contribute to the
development of osteonecrosis of
the jaw in bisphosphonate users.
First, that decreased bone remodeling in bisphosphonate users may
lead to failed bone healing after
dental intervention. Second, that
February 2011
bisphosphonates stimulate specific cells that can cause cytokinemediated inflammation. Finally,
she suggests that bisphosphonates
may reduce specific growth factors
and cause local mucosal toxicity.
None of these theoretical models
of disease progression have been
proven to be the underlying cause
of osteonecrosis of the jaw; still,
the fact that teriparatide reversed
the process does provide some
clues. Stimulation of osteoblasts
and (indirectly) osteoclasts with
teriparatide improved bone healing. Whereas bisphosphonates decrease the number of osteoclasts
on bony surfaces over time (due to
apoptosis), the increased number
of these cells is associated with
more bone turnover and improved
bone density. Other case studies
and reviews have shown similar
promising results using a course
of teriparatide in the treatment of
bisphosphonate-associated osteonecrosis of the jaw. 10,11
Dental Implantology Update™
14
There is one caveat: no extensive clinical trials have been set
forth due to the limited number of
patients with oral bisphosphonateassociated osteonecrosis of the jaw.
The majority of the patients who
develop this debilitating complication are bisphosphonate users with
underlying malignancies, who have
a propensity to metastasize to bone
(like multiple myeloma, breast cancer, and prostate cancer). The challenge to researchers is that in this
group of patients, teriparatide use
is contraindicated (see Table 3 for
a list of side effects associated with
the drug). Osteosarcoma resulted
in one user of teriparatide, and this
single adverse event garnered the
drug a black-box warning by the
FDA, and makes it contraindicated
in individuals with metabolic bone
disease and malignancy. 12 Unfortunately, finding patients with osteonecrosis of the jaw related to
bisphosphonate usage is exceedingly rare in the non-cancer population
due to lower the lower dosing.
Periodontitis
There was little relationship between the PTH analog teriparatide
and periodontitis until the recent
study, detailed below. Periodontitis
is marked by soft-tissue and bone
destruction as a result of chronic
inflammatory processes of the oral
cavity caused by infection starting
at the gingival line and descending into plaque- and bacteria-filled
pockets around teeth (see Figure 2).
Bone loss was considered a permanent change (without bone grafting
techniques after surgical debridement). In fact, implant-failure rates
are known to be slightly higher in
individuals with severe periodontitis. That a medication regimen can
improve bone density and indeed
lead to bone remodeling at the effected site is a promising development for individuals with severe
periodontitis.
Teriparatide
Teriparatide is recombinant human parathyroid hormone that contains a 34-amino-acid sequence
identical to the N-terminal portion
of the hormone, which is the metabolically active portion of PTH. 13
Its mechanism of action, therefore,
is to pharmacologically perform the
same functions as the hormone, as
detailed above; namely, to stimulate osteoblasts that will, in turn,
elicit an osteoclastic differentiation that leads to bone turnover —
bone remodeling. The end result
is increased bone-mineral density
and increased bone mass. It has
been shown to decrease fractures
in postmenopausal women with osteoporosis. It should be mentioned
that the FDA did impose a blackbox warning on the drug because of
the increased risk of osteosarcoma
seen after two years of use (there is
one case of this complication). For
this very reason, it is also not recommended for patients with bony
metastasis or metabolic bone disorders like Paget’s disease. More
common side effects of the drug
include dizziness, orthostatic hypotension, transient hypercalcemia,
arthralgias, rhinitis, weakness, and
nausea; see Table 3 for significant
adverse reactions
Summary of the McCauley study
The study out of Laurie McCauley’s research group at the University of Michigan was a randomized, double-blind clinical trial
that included 40 patients split into
two groups, a placebo group and
an experimental group given daily
teriparatide. Both groups underwent
periodontal surgery and received
1,000 mg of calcium and 800 IU of
vitamin D for a total of six weeks.
Placebo and teriparatide were given
three days prior to periodontal surgery and continued for six weeks.
Study details and inclusion criteria
are summarized in Tables 4 and 5.
Dental Implantology Update™
Periodontal surgery, performed
by practitioners in this study, was
open-flab debridement under local
anesthesia with careful attention to
root surfaces, with irrigation, and
simple suture closure. Chlorhexidine rinse, a nonsteroidal anti-inflammatory, and low-dose opiate
were prescribed. Close, three-month
follow-up maintenance visits were
given to all patients, as was education in oral hygiene.
Results from the study demonstrated the following: patients in the
teriparatide group gained 1.86 mm
of bone (linear bone gain) compared
to 0.16 mm in the placebo group.
Probing depth in the teriparatide
group was reduced almost twice
that of the placebo group (2.42 mm
vs. 1.32 mm). And clinical attachment gains more than three times
higher in the experimental group
(1.58 mm in teriparatide patients vs.
0.42mm in placebo patients). All of
these findings were considered statistically significant.
Two reviewers independently
analyzed the radiographic data in
this study: a radiologist and a periodontist. Bone gain was assessed by
measuring the deepest segment of
the defect to the first point that bone
fill was detected.
The authors note in their discussion that bone growth continued over
the length of the follow-up — a period of one year, well beyond the
six-week treatment course. In the
placebo group, bone growth peaked
at three months. There is also discussion of the use of systemic biologic
modifiers that improve outcomes in
periodontal surgery — growth factors, antibiotics, and enamel matrix
derivatives. The authors’ study has, in
some, put the recombinant parathyroid hormone treatment on this list,
though they caution that sample size
is small, adverse events may not have
been evident with the limited population of the study, and that more studies are needed before widespread application of this therapy.
February 2011
15
The Significance for
Implant Dentistry
Though studies have not yet
investigated its potential to serve
this purpose, the question that arises from this new research is readily apparent: if teriparatide can
be used to increase alveolar bone
loss in patients with periodontitis,
can it enhance, or even hasten, osseointegration in dental-implant
patients? Is the drug suited for
individuals thought to be at high
risk for implant failure? Researchers involved in the aforementioned
study have already begun to investigate the role of teriparatide
in patients undergoing placement
of dental implants. The authors
are also working on local delivery
systems that would serve the oral
cavity, as opposed to the whole
body, possibly decreasing the risk
of systemic side effects. 14 The role
of this drug in bone healing is only
beginning to come to light, and it
appears that it holds a promising
place in all facets of implant dentistry. n
6.
7. 8.
9.
References
1. Bashutski JD, Eber RM, Kinney
JS, Benavides E, Maitra S, Braun
TM, Giannobile WV, McCauley
LK. Teriparatide and osseous regeneration in the oral cavity. New
England Journal of Medicine.
2010;363(25):
2396-2404.
2. Garg AK. Bone: Biology, Harvesting, and Grafting for Dental Implants. Quintessence Publishing.
Hanover Park, IL. 2004.
3. Dalen N. Olsson KE. Bone mineral content and physical activity.
Acta Orthop Scand. 1974;45:170176.
4. Jacobs-Kosmin D, Hobar C, Shanmugam S. Osteoporosis. Accessed
online at eMedicine.com.
5. Pavlakis N, Schmidt RL, Stockler
MR. Bisphosphonates for breast
cancer. uCochrane Database of
10.
11.
12.
13.
Systematic Reviews 2005, Issue 3. Art. No.: CD003474. DOI:
10.1002/14651858.CD003474.
pub2
Mhaskar R, Redzepovic J, Wheatley K, Clark OA, Miladinovic B,
Glasmacher A, Kumar A, Djulbegovic B. Bisphosphonates in
multiple myeloma. Cochrane
Database Systematic Reviews.
2010;17(3):CD003188.
Miksad RA, Lai KC, Dodson TB,
Woo SB, Treister NS, Akinyemi
O, Bihrle M, Maytal G, August M,
Gazelle GS, Swan JS. Quality of
life implications of bisphosphonate-associated osteonecrosis of
the jaw. Oncologist. 2011. Epublicatoin ahead of print.
Madrid C, Sanz M. What impact
do systematically administrated
bisphosphonates have on oral
implant therapy? A systematic
review. Clinical Oral Implants
Research. 2009;20(Suppl 4):87-95.
Grant BT, Amenedo C, Freeman
K, Kraut RA. Outcomes of placing dental implants in patients
taking oral bisphosphonates: a
review of 115 cases. Journal of
Oral and Maxillofacial Surgery.
2008;66(2):223-230.
Narongroeknawin P, Danila MI,
Humphreys LG, Barasch A, Curtis
JR. Bisphosphonate-associated
osteonecrosis of the jaw, with
healing after teriparatide: a
review of the literature and a case
report. Special Care Dentistry.
2010;30(2):77-82.
Lau AN, Adachi JD. Resolution
of osteonecrosis of the jaw after
teriparatide [recombinant human
PTH-(1-34)] therapy. Journal of
Rheumatology. 2009;35(8):18351837.
Solomon DH, Rekedal L,
Cadarette SM. Osteoporosis treatments and adverse events. Current Opinion in Rheumatology.
2009;21(4):363-8.
Teriparatide (recombinant human
parathyroid hormone (1-34)):
February 2011
Drug information. In: UpToDate,
Basow, (Ed), UpToDate, Waltham,
MA, 2011.
14. Heath V. Teriparatide improves
outcomes of periodontal surgery.
Nature Reviews Endocrinology.
2011;7:4.
Growing the Next
Dental Implant
By Arun Garg, DMD, and
Ghislaine Guez, MD, MBA
I
mplant dentistry has emerged as
the gold-standard approach for
the restoration of function and aesthetic to the edentulous patient.
And the history of the development
of dental implants has, as common
themes, progress and innovation
at its core. So what is in store for
dental-implant professionals and
patients as the next wave of therapeutic advancement?
A researcher out of Columbia
University published work on his
approach to tooth regeneration,
performed by cell homing. And
while this technology is a long
way from human application, the
concept is by no means trivial.
And the process, which involves
implantation of an anatomically
correct, porous scaffold, would
not obviate the need for dentalimplant experts entirely.
Jeremy Mao and his colleagues
K. Kim, C. Lee, and B. Kim extracted the mandibular incisors of
22 rats and implanted an anatomically correct tooth scaffold at the
site. 1 Additionally, a human molar
scaffold was implanted into the
dorsum of the rats. Two growth
factors, stromal-derived factor 1
(SDF1) and bone morphogenetic
protein-7 (BMP7), were administered in the micro-channels of
the scaffolds. After nine weeks,
early evidence of tooth regeneration was present in the ectopically
placed human molar — angiogenesis within the micro-channels was
Dental Implantology Update™
present, as was mineralized tissue.
In the rat incisor scaffold, these
signs of periodontal regeneration
were also present, as was a periodontal ligament and de novo alveolar bone, implying that direct implantation improved generation of
tooth precursors. The authors also
implanted scaffolds that were not
suffused with specific growth factors — these showed less evidence
of neovascularization and mineralization.
This research strengthens the role
of specific growth factors, like the
bone morphogenetic proteins, in
the bone growth and mineralization processes, and underscores the
usefulness of these additives in current periodontal grafting techniques
and sinus-lift techniques. 2 Bone
morphogenic protein 2 functions
to differentiate mesenchymal precursor cells into mature osteoblats,
and is thought to be chemotactic for
osteoblastic-type cells. It plays an
important role in the early stage of
osteoinduction (the chemical process by which bone morphogenic
proteins convert precursor cells into
osteoblasts).
The process described in the article
is called cell homing, and it begs the
question — if the model is suitable
for viable implantation and the precursor growth proteins are known and
available for use, can different tissues
be grown in vivo? Indeed, this type
of work has been ongoing in various
forms, and other scaffold and stemcell growth models include a functioning jaw bone, also from research
out of Columbia University.3 What
makes this study particularly interesting, is that it is an in vivo study with
practical application. Still, not all
components of the tooth have proven
to develop from this early study. But,
it does hold promise. The day may
come when dental-implant specialists
are placing biosynthetic scaffolding,
16
rather than titanium alloy, in anticipation of gradual tooth regeneration. n
References
1. Kim K, Lee CH, Kim BK, Mao JJ.
Anatomically shaped tooth and
periodontal regeneration by cell
homing. Journal of Dental Research. 2010;89(8):842-847.
2. Garg A. Bone morphogenetic protein for sinus lift. Dental Implantology Update. 2010;21(4):25-29.
3. Grayson WL, Frohlich M, Yeager
K, Bhumiratana S, Chan ME,
Cannizzaro C, Wan LQ, Liu XS,
Guo XE,Vunjak-Novakovic G.
Regenerative medicine special
feature: Engineering anatomically shaped human bone grafts.
Proceedings of the National
Academy of Sciences USA. 2010;
107(8):3299-3304.
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Dental Implantology Update™
February 2011