Sei sulla pagina 1di 6

ACADEMICS AND EDUCATION

Osteoporosis and Osseointegration of


Implants
J. Cystal Baxter, DMD, MDS, * and LaDeanne Fattme, DDS,MS*
According to medical literature, osteoporosis and related bone pathologies are increasing in
epidemic proportions. The exact etiology of the disease is unknown, but hormonal, dietary, and
genetic factors all contribute to the related loss of bone density. In the disease process, bone loss
occurs throughout the body. Research indicates that the mandible and maxilla are affected, and
show oral manifestations. There is no scientific data to contraindicate the use of two-step
osseointegrated implants in osteoporotic individuals. The purpose of this article is to review the
literature regarding osteoporosis and its relationship to oral bone loss.
J Prosthod 2: 120- 125. Copyright 0 1993 by the American College of Prosthodontists.

INDEX WORDS: osteoporosis, implants, osseointegration, bone, resorption

FALTHY BONE WITH normal regenerative

capacity is imperative for success in all phases


of dentistry. Bone is dynamic, and can be affected by
local or systemic conditions.' Normal bone metabolism is especially crucial for success in implant treatment, as aberrations in bone physiolqgy are likely to
compromise the prognosis for optimal integration.
Osteoporosis is a systemic condition with the potential for affecting implant treatment. The disease is
particularly alarming because of its high incidence in
the expanding older population, which contains the
greatest number of candidates for implant therapy.
Osteoporosis occurs in approximately one third of
women over 60 years of age: more than one fourth
have bone fractures caused by the disease by the age
of 60, and nearly one half have bone fractures by the
age of 75.* It is responsible for vertebral and hip
fractures, and for stress fractures in any affected part
of the body. The annual cost to the IJS health care
system is at least $10 billion.? Seventeen percent of
patients with hip fractures will dip from related
causes within 6 months, making conditions related to
this disease the twelfth leading cause of death in the
adult Caucasian patient.4 The disease appears to be
increasing epidemically in recent years. Many orthopedic researchers fear that it may become one of the

From i'tbrthiixstem Lhi?~m,ri&,


Chicago, IL.
*Asohate Projssor. Pmthodontics.
nddre.fr reprint requectr tn J. Cv.rtal Baxter. DMD, MDS, 845 N
Michigan Aue, No. 948W, Chicago,IL 60611.
Copyright 01993 bl. the American College ofPosthodontists
1059-94IXI 9310202-O008&i'.OO/ 0

120

most common problems in the health of the middleaged or older person in the f ~ t u r c . ~
Osteoporosis is the loss ofbone density that occurs
when more calcium is resorbed from the bone than is
replaced. Bone constantly undergoes apposition and
resorption. In a healthy individiial, bone apposition
would be equal to bone resorption, and bone density
w~ouldremain adequate. In the osteoporotic individual, more bone is lost than replaced, resulting in
porous bone with a swiss-cheese or moth-eaten consistcncy.6
Two categories of osteoporosis have been identified: primary and secondary. Primary osteoporosis is
by far the most common form of the condition and
includes postmenopausal osteoporosis (type I), agerelated osteoporosis (type 11),and idiopathic osteoporosis. Secondary osteoporosis is caused by an identifiable agent or disease process, and therefore can be
considered a side effect of another condition or
medication.'
Type I primary or postmenopausal osteoporosis
characteristically affects women within 10 to 15 years
after menopause. Vertebral fractures and fracture of
the distal radius are the main clinical manifestations.
In patients with this type of osteoporosis, the rate of
trabeciilar bone loss is usually 2 to 3 times normal,
although the rate of cortical bone loss is only slightly
above normal. During this accelerated phase of bone
loss, trabecular plate perforation with loss of structural trabeculae weakens the vertebrae and predisposes them to collapse.
Type I osteoporosis seems to be caused by factors
closely related to, or exacerbated by, menopause, and
therefore is a disease that affecls only women. The

Journal OJProsthodontics, Vol2, No 2 (Jum),


1993:pp 120-125

J i m

1993, Volume 2, iVumber 2

result is accelerated bone loss, aberrations of the


and other bone regenparathyroid hormone (m),
erating functions.*
In type 11primary or aging-associated osteoporosis a proportionate loss of both cortical and trabecular bone is seen. This process affects both men and
women at about the same rate.
In 10% ofwomen and 40% of men presenting with
spontaneous vertebral fractures, a secondary cause of
osteoporosis can be identified. The most common
causes are early surgical hysterectomy in women,
hypogonadism in men, or a glucocorticoid state
associated with thyroid therapy in persons of either
sex.
A major contributing factor to all types of osteoporosis is a deficiency of dietary calcium. Approximately 99% of the total body weight of calcium is
stored in the bones of the skeleton. The remaining
1%, found in the cells and interstitial fluid, is vital for
nerve signal transmission and blood clotting.
The calcium levels in and around the cells are
strictly controlled by parathyroid hormones. Whenever cellular levels decrease, calcium is needed instantly. If calcium is not available from the diet in
adequate amounts, it is immediately mobilized from
the bones to replenish the cellular supply. If this
occurs over an extended period of time, loss of bone
density will result.y
Whole-bodycalcium is normally obtained through
dietary sources, but it is lost by the body through
several mechanisms. One to two hundred mjlligrams
a day is lost through normal urine output, and
another 125 to 200 mg is lost into the digestivejuices.
Women lose additional calcium because of sevcral
factors: (1) they are more prone to go on reducing
diets with a decrease in the amounts of all nutrients
ingested, (2) during pregnancy the fetus requires 400
mg calcium per day; during breast-feeding, an additional 300 mg calcium per day is required, ( 3 ) loss of
estrogen and changes in hormonal balances at menopause cause accelerated calcium loss. Any loss of
calcium results in loss of calcium from the bone, and
an osteoporotic state is the net result.10
Numerous studies illustrate that the average
American consumes considerably less calcium than
the 1200 mg recommended daily allowance, and the
nutritional picture of the older American is probably
even worse. A preliminary study that compared the
diets of older patients before and after the fabrication and placement of complete dentures showed
that calcium deficienciespersisted.I2
In a later study, the diets of five different elderly

121

groups, all with varying dentitions and/or prosthetic


replacements, were compared. Regardless of their
dental status, these patients had in common a
deficiency in calcium intake.13
In addition to calcium, the mineralization of bone
requires normal plasma concentrations of phosphate
and vitamin D. If any of these factors are deficient,
the organic matrix on bone, or osteoid, will not
mineralize normally, and osteomalacia or rickets
results. An accumulation of osteoid tissue replaces
normal bone. As a result of this lack of mineralization, the skeleton becomes soft, and deformity fractures can occur.
Vitamin D deficiencies can result from a poor
diet, inadequate sunlight without vitamin D supplements, gastrointestinal disorders such as malabsorption syndromes, impaired vitamin D synthesis such
as liver or renal disease, and target cell resistance
(vitamin D-resistant rickets, type II). l5
The natural form of vitamin D is cholecalciferol,
which is designated as vitamin D. Most cholecalciferol forms in the skin as a result of irradiation of
7-dehydrocholestero1 by ultraviolet rays from the
sun. Once cholecalciferol enters the circulation, it is
concentrated in the liver, where it is hydroxylated to
become 25-hydroxycholecalciferol[25 (OH) DJ]. The
final metabolic conversion of the vitamin occurs in
the kidneys, where 25 (OH) DYiis hydroxylated to
form the active hormone I , 25 dihydroxycholecalciferol [1,25(OH),U,]. It is this substance that expresses almost all the stimulatory activity of vitamin
D.14

In 1981 Gallagher et a1 reported that serum 1,25


dihydroxycholecalciferolwas significantly decreased
in both a group of osteoporotic patients and a group
of normal elderly patients. They found that intestinal
absorption of calcium decreased significantly with
age and was lower in osteoporotic, patients than in
normal patients matched for either age or habitual
calcium intakei5
Kribbs in 1992 reported her findings in a prospective study of 85 postmenopausal women who were
administered 1,25 dihydroxycholecalciferol (calcitri01) or a placebo for a period of 2 years. She found that
there was no significant change in bone mass in the
mandibles of patients who received calcitriol versus a
placebo and that the drug was not effective in
preventing mandibular bone loss.
No study other than Kribbs has evaluated the
longitudinal changes in mandibular bone mass in
osteoporotic subjects or attempted to increase bone
mass in the mandible by pharmacological rneans.l6

122

Osteoporosis and Implants

A number of studies indicate that certain forms of


oral bone loss may be related to a generalized
osteoporotic state. In 1974 Wical and Swoope attempted to relate dietarycalcium deficiency to resorption in edentulous subjects. These researchers noted
a positive correlation between deficient calcium intake and increased mandibular rc~orption.'~
A 1983 study reported on 208 white women, aged
60 to 69 years, who had acquired 218 complete
dentures. Each wornan's smoking habits and level of
osteoporosis (percent cortical area) were measured
at the time she acquired each denture. Of the
osteoporotic women who had their natural teeth at
age 50,44% had required a complete denture before
age 60; in nonosteoporotic women the number was
only 15%.The differences in prosthodontic requirements between these two groups had not existed
beforc age 50 but continued after age 60.18It has also
been reported that when skeletal depletion occurs as
a result of stimulation by the parathyroid gland,
alveolar bone may be affected before the ribs, vertebrae, and long bones."
Henrikson et a1 compared the bone density of
long bones with that of edentulous mandibles to
determine the relationship of age arid sex to mineral
density and volume. This study indicated a statistically significant correlation between mineral density
of the mandible and that of the radius. They concluded that when osteoporotic changes occur, these
changes qualitatively affect the two parts of the
skeleton the same way.2o Disruption or trabecular
bone in dentate osteoporotic subjects showed a statistically significant relationship to a high incidence of
vertebral fractures in the study group, while a nonosteoporotic control group illustrated no such parallels.20
Alveolar ridge height (or residual ridge height)
and metabolic bone loss have been of interest to
many researchers. The overwhelming majority of
their studies looked at bone resorption in the niandiblc, and although no definitive conclusions can be
made from any of the studies, a number of them2'-2'
found a positive relationship between severe alveolar
ridge atrophy and metabolic bone loss.
Kribbs et aIz5in a 1989 study or 85 postmenopausal women with osteoporosis, found that mandibular alveolar ridge height was significantlycorrelated
with both total body calcium and mandibular bone
mass. Although the study failed to utilize a comparison group, the findings are iinportant because they
suggest a relationship between osteoporosis and
resorption of the edentulous alvcolar ridge.

Bmter and Fattore

Von Wowern and WorsaacZG


in 1922 reported that
in a stnall study of 28 cdentulous wornen, with and
without osteoporosis, a significant amount of bone
loss occurred in the maxillae of ostevporotic women
as cornpared with age-matched, normal wotnen with
the same length of edentulousness.
In 1983, Krolner e t aI2' reported that increased
function in the form of exercise increased the bone
mineral content (BMC) in the axial and appendicular skeleton of a group of postmenopausal women,
suggesting that exercise may decrease age-related
BMC loss in this group.
It is well known to dentistry that bite force
decreases after extraction of teeth and placement of
conventional dentures. Von Wowern et alL8in 1979
showed in rat mandibles that after extraction of all
teeth, the trabecular bone mass of the mandibles
significantly decreased as a result of what Von
l4'0ww-n suggests is a decrease in bite force.
Several studies have stated that osseointegrated
implants significantlyincrease bite force in the edentulous patient.'""" Haraldson and Zarb3' in 1987
reportcd the findings or their 10-year follow-up study
of bite force after treatment with osseointegrated
implant bridges arid found that recorded bite force
increased significantlywhen compared with baseline
findings 10 years earlier. Their results coincide with
earlier studies' findings that bite force increased and
muscle activity (EMG) normalized with the duration
of the wearing of an osseointegrated implant prosthe,is.2!3,,3O

Adell et a13?reported in 1986 the results of a small


radiographic study of patients fitted with prostheses
that were fixed to titanium implants. They found
that atrophy of alveolar bone between implant fixtures averaged 0.9 mm after lhe first year and 0.05
m m annually for the next 2 years. Perifixtural bone
gradually became more radiopaque, especially in the
maxilla, indicating a successive, load-relating remodeling.
In 1990 Von Wowern et a1j3 studied changes in
BMC of edentulous mandiblcs with osseointegrated
l
T
limplanls (Straumann Co, Cambridge, MA) supporting overdetitnres. BMC measurements were
made 3 weeks postoperatively and 2 years later at a
follow~-upvisit. Measurements were made at the
implant site, at the premolar region just distal to the
implants, at gonion and in the forearm bones. Her
results indicated that BMC changes at the implant
site and in the area distal to the implants were
significantly smaller than the BhlC changes seen in
the rorearm bones and at gonion in the mandibles.

123

June 199.1, Volumf 2. Number 2

Her study suggests that increased function leads to a


load-related, positive bone remodeling that minimizes, or in some cases may counteract, the physiological, age-related changes in the bone remodeling
processes leading to B h K
Early assessment and identification of osteoporotic patients can be accomplished by endocrinologists, g?mecologists or orthopedic surgeons. Routine
intraoral periapical or panoramic radiographs are
not diagnostic until 40% or greater bone density is
lost.34 There are a number of other factors that
contribute to osteoporosis. As the number increases,
the patient is considered to be at greater risk.
Diagnosis of the disease can be accomplished by
the use of dual-photon absorptiometry or dual energy x-ray ahsorptiometry (DEXA). Both are simple,
painless procedures that can be accomplished in
about an hour. Absorptiornetry, sometimes called
densitonietry, uses a radioisotope point source and
photon scintillation detection system. The machine is
termed a bone mineral analyzer. The systems are
accurate for both cortical and trabecular bone measurement~.~~,~~
Which patients should one suspect enough to
warrant systemic testing? The more of the following
factors that hold true for the patient, the greater the
risk for the disease: srnall-boned Caucasian women
at menopause age or older, younger women who
have had hysterectomies or hormonal disturbances,
anyone with a calcium-deficient diet, smokers, sedentary individuals, and especially those with a family
history of the
(Table 1).
Treatment for osteoporosis can include estrogen
therapy, calcium supplementation (Tables 2 and 3),
exercise, vitamin D therapy, or a cotnbination of two
or more of these modalities. Estrogens have bcen
shown to diminish the rate of bone loss in postmenopausal women, whether menopause occurred naturally or was surgically induced. Furthermore, bone

Table 1. Osteoporosis: Which Patients Are Most at


ksk?

Small-boned Caucasian women, cspecially thosc


At mcnopause ag-c or older
With a history of surgical hysterectomy
With histories of anorexia or bulimia
Persons of either sex with
Genetic history of the disease
Calcium-deficient diets
History of heavy smoking
Sedentary habits
Medical trcatmcnt involving steroid or thyroid
niedicatioris

Table 2. Major Dietary Sources of Calcium


~

~~

Milk
Whole
Skim
Yogurt
Cottage cheese
Swiss cheese
American cheese
Ice cream
Sardines (with bones)
Salmon (with bones,
canncd)

Iof11
Green leafv vegetables

290 mg/8 oz
300 mg/8 oz
400 mg/8 oz
170 mg/8 oz
270 mgloz
170 mg/oz
180 mg/8 oz
125 mg/oa

60 mg/oz
280 mg/8 oz
400 me/cup

dcnsity nieasurernenls show that estrogen therapy


limits bone loss in pseudomenopausal states such as
estrogen deficiency in premenopausal women associated with excessive exercise or anore~ia/bulimia.~~
Epidemiological studies have shown that functional
delay of menopause through estrogen therapy will
substantially decrease the ultimate risk of hip fracture.
Estrogen therapy is frequently administered to
reduce bone loss and to prevent both osteoporosis
and bone fractures.8 However, there is no strong
evidence that estrogen thcrapy rebuilds bone or
replenishes bone density, and it should not be recommended for women who have already lost considerable amounts of bone?9 Estrogen therapy should be
initiatcd in high-risk women as soon after the onset
of menopause as possible, continuing for 5 to 15
years. Estrogen therapy is not indicated for women
who arc more than 10 to 15years postmenopausal, as
they have already experienced the period of accelerated bone loss that accompanies and follows the
menopause.
The National Osteoporosis Foundation recommerids the following guidelines for estrogen therapy:
Utilizerstrogen therapy to preoent ostrojmosir in w o n m ielho
are at high ritk, who tiaut. no ooritraindications, and who
understand the bencjits andcomplicationJ 4th drug.

Table 3. Relative Calcium Loads ofVarious Salts


Salt

% Calcium

Calcium carbonate
Calcium sulfate
Uibasic calcium phosphate
Tribasic calcium phosphate
Calcium lactate
Calcium gluconate
Calcium ascorbate
Calcium citrate
Calcium citratr malate

40
36.1
29.5
38.8
13
9.3
10.3
24.1
23.7

124

Osteopmosir and Implantr

Prescribe low-dose ET (eg. 0.62.5 m a f m 25 or 26 d a y


monthb, and add a progestin (eg. 10 mg medro~fl~gaterone) on days 12-15to days 25 or 26.
Insure that fhP patient u n h g m s a thorough annual
physical examination yearly.
Initiute exstragen theraiy as soon as possible ajer the
menopause. andplan to continue itfor at least 5 to 15years
(during the period ofaccelerated bone 10~s).
Etrogen therapy may also be consideredfor older women
within 5 to 15 yearr @rtmenopause who are actiwb
jacturing bones (.g. hace clinicalb ecident oste(@~ro.rir).~~

Conclusions
The dentist who is considering osseointegration for a
patient should be aware of any systemic diseases,
especially those affecting bone. The prognosis for
integration can be improved for the osteoporotic
patient who is receiving treatment by a physician.
Osteoporotic bone does not heal differently than
bone with more density, but the biological changes
may warrant some additional caution. The patient
should be informed of the risks involved.

References
1. Baxter JC: Osteoporosis: Oral manifestations 01 a systemic

disease. Quintessence Int 1987;18:427-4'29

2. &ggs EL, h4elton LJ 111: Involutional osteoporosis. N Engl J


hled 1986;314:1676-1686
3. Berg RL,Cassells JS (eds): Osteoporosis, in The Second Fifty
Years: Promoting Health and Preventing Disability. Washington DC, National Academy Press, 1990, pp 76-100
4. National Institutes of Health: Consensus Confrrenrc: Osteoporosis.JAhL4 1 984;2.52:799-802
5. Cummings SK, Rubiri SM, Black D: The future of hip
fractures in thc United States: Numbers, costs and potential
effects ofpostmenopausal cstrogen. Clin Orthop 1990;252:163I66
6. Parfitt . O f : Bone remodeling: Relationship to the amount and
structure of bone, and the pathogenesis and prevention of
fractures, in Riggs EL, Melton LJ 111 (eds): Osteoporosis:
Etiology, Diagnosis and Management. New York, NY, Raven,

1988,43-93
7. Riggs BL, Wahner I W , Seeman E, et al: Changes in bone
mineral density of the proximal femur and spine with aging:
Differences between the postmenopausal and senile osteoporosis syndromes. J Clin Invest 1982:70:716-723
Total bone calcium in
8. Gallagher JC, Goldgai D, Muy A4:
normal women: Effect of age and menopause status. J Bone
Miner Res 1987;2:491-496
9. Nordin BEC, IIcaney RP: Calcium supplementation of the
diet: Justified by present evidence. Br bled J 1990;300:10561060
10. .4lbanrse A: Calcium nutrition in the elderly. Postgrad Med
1978;63:169-170
11. Hcaney RP, Gallagher JC, Johnson CC: Calcium, nutrition

Bmter and Fattore

and bonc health in the elderly. Am Clin Nutr 1982;369861013


12. Baxter JC: Nutrition and the geriatric edentulous patient.
SpecCare Dent 1981;1:259-263
13. Baxter JC: The nutritional health of geriatric patients with
varicd dentitions.JProsthet Dent I984;.5l:164-168
14. Zachariasen R: Oral manifestations of metabolic bone diseabe: Vitamin D and osteoporosis. Compend Contin Educ
Dent 1990;11:612-618
15. Gallagher JC, Eggs EL, Eisman J, et al: Intcstinal calcium
absorption and serum vitamin D metabolites in normal
subjects and osteoporotic patients. J Clin Invest 1979;64:729736
16. Kribbs YJ: Two-year changes in mandibular bone mass in an
osteoporotic population. J Prosthet Dent 1992;67:6.53-65.5
17. Wical J, Swoope C: Studies of residual ridge resorption, Part
IT: The relationship of dietary calcium and phosphorous to
residual ridge resorption. J Prosthet Dent 1974;32:13-17
18. Aloria J F Determinants of bone mass in postmenopausal
women.ArchInt bled 1983;143:1700-1705
19. Lutwak L, Singer FR, Urist M R Current concepts of bone
metabolism. Ann Intern Med 1974;80630-644
20. Henrikson PA, Wallenluis K, Astrand K. The mandible and
osteoporosis (2). Method for detrrruining mineral contrnt o i
the mandible and radius.J Oral Rehabil 1974;1:75-84
21. Kosenquist JB, Baylorik LlJ, Berger JS: Alveolar atrophy arid
decreased skeletal mass of the radius. Int J Oral Surg
1978;1:47Y-481
22. Bras J, van 005CP, DunsJ, ct al: h,fandibular atrophy and
metabolic bonc loss. IntJ Oral Surg 1983;12:309-313
23. Habets LLMH, Bras J, Borgmeyer-Hoelen AhWJ:Mandibular atrophy and metabolic bone loss. Endocrinology, radiology
and histomorphometry. Int J Oral Maxillofac Surg 1988;17208211
24. IIabets LLMH. Bras J, von Merkesteyn JPR hlandibular
atrophy and metabolic bone loss. Histomorphometry of iliac
crest biopsies in 74 patients. Int J Oral Maxillofac Surg
198X;17:325-329
25. Kribbs PJ, Smith DE, Chestnut C H Oral findings in osteoporosis. Part I: Measurements of mandibular bone density. J
Prosthet Dent 1983;50:576-580
26. \'on Wowern N, Worsaae N: Bone mineral content of the
maxilla estimated by dual-photon absorptioinetty alter augmentation with hone or hydroxyapatite. J Dent Res 1988;67:
1405-I408
27. Krolner B, Toft B, Nielsen SP, et al: Physical exercise as
prophylaxis against irivolutionalverlebral bone loss; a controller trial. Cliu Sci l983;63:541-546
28. \'on Wowern K,Hjorting-Hansen E, Stoltze K Changes in
bone mass in rat mandibles after tooth extraction. 1nt.J Oral
Surg 1979;8:229-233
29. Haraldson T, Carlssori GE, Ingervall R: Functional state, bite
force and postural mitsclc actibity in patients with osseointegrated oral implant bridges. Acta Odontol Scand 1979;37:195-

206
30. Haraldson T, Ingendl V Muscle function during chewing
and swallowing in patients with osseointegrated oral iinplarit
bridges. An electromyoographic study. Acta Odontol Scand
1979;37:207-216
31. Haraldson T, Zarb G: A 10-year follow-up study of the
masticatory system after treatment with osseointegrated
implant bridges. Scand,JDent Res 1988;96:243-252

June 1993, Volume 2, iVumher 2

32. Adcll R, 1,ekholm U, Rockler B, et al: Marginal tissue


reactions at osseointegrated titariiurn fixtures. I. .4 3-year
longitudinal prospective study. Int J Oral Maxillofac Surg
1986;15:39-52
33. Von Wowern N, Harder F, IIjorting-Hanscn E, rt al: IT1
implants with overdentures: A prevention of bone loss in
edentulous mandibles? Int J Oral Maxillofac Implants 1990;5:
135-139
34. Shapiro S, Bomberg TJ, Benson BW, et al: Postmenopausal
osteoporosis: Dental patients at risk. Gerondontics 1985;1:220225
35. Katz RD: Recent advances in the early tliagnosis ufostcoporosis: A review. Maryland Med J 1985;34:890-895

125

36. National 1nsLitutt.sof Health: Consensus Conference: Osteoporosis. JAMA 1984;6:799-802


37. Rigotti NA, Nussbaum SR, IIerzog DB, et al: Osteoporosis in
women with anorexia nenrosa. N E n g l J bled 1984;31:16011606
38. Alvioli L V Osteoporosis: Lct's look at llie I d s . Geriatrics
1984;3916-20
39. Ettinger B, Genant HK, Cann C E Long-term estrogen
replacement therapy prcvents bone loss and fractures. Ann
Intern Med 1985;102:339-324
40. Nationd Osteoporosis Foundation: Osteoporosis: A guide to
diagnosis. 1992