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Osteoporosis and Osseointegration of
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. 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


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
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

l5 The natural form of vitamin D is cholecalciferol. ( 3 ) loss of estrogen and changes in hormonal balances at menopause cause accelerated calcium loss. (2) during pregnancy the fetus requires 400 mg calcium per day. 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. or osteoid.]. This process affects both men and women at about the same rate. Regardless of their dental status. impaired vitamin D synthesis such as liver or renal disease. found in the cells and interstitial fluid. were compared. and target cell resistance (vitamin D-resistant rickets. An accumulation of osteoid tissue replaces normal bone.” A preliminary study that compared the diets of older patients before and after the fabrication and placement of complete dentures showed that calcium deficienciespersisted. and an osteoporotic state is the net result. it is immediately mobilized from the bones to replenish the cellular supply.J i m 1993. or a glucocorticoid state associated with thyroid therapy in persons of either sex.25(OH). will not mineralize normally. They found that intestinal absorption of calcium decreased significantly with age and was lower in osteoporotic. inadequate sunlight without vitamin D supplements. The most common causes are early surgical hysterectomy in women. The remaining 1%. the diets of five different elderly 121 groups. hypogonadism in men. these patients had in common a deficiency in calcium intake. and deformity fractures can occur.25 dihydroxycholecalciferol (calcitri01) or a placebo for a period of 2 years. calcium is needed instantly.10 Numerous studies illustrate that the “average” American consumes considerably less calcium than the 1200 mg recommended daily allowance. If calcium is not available from the diet in adequate amounts. loss of bone density will result.I2 In a later study. Volume 2. The calcium levels in and around the cells are strictly controlled by parathyroid hormones.’“ Vitamin D deficiencies can result from a poor diet. iVumber 2 result is accelerated bone loss.* In type 11primary or aging-associated osteoporosis a proportionate loss of both cortical and trabecular bone is seen. and another 125 to 200 mg is lost into the digestivejuices. it is concentrated in the liver. Most cholecalciferol forms in the skin as a result of irradiation of 7-dehydrocholestero1 by ultraviolet rays from the sun. 25 dihydroxycholecalciferol [1. If this occurs over an extended period of time. It is this substance that expresses almost all the stimulatory activity of vitamin D. is vital for nerve signal transmission and blood clotting.25 dihydroxycholecalciferolwas significantly decreased in both a group of osteoporotic patients and a group of normal elderly patients. Once cholecalciferol enters the circulation. 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. and the nutritional picture of the older American is probably even worse. 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. erating functions. 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. all with varying dentitions and/or prosthetic replacements. an additional 300 mg calcium per day is required. but it is lost by the body through several mechanisms. If any of these factors are deficient. where 25 (OH) DYiis hydroxylated to form the active hormone I .14 In 1981 Gallagher et a1 reported that serum 1. which is designated as vitamin D. gastrointestinal disorders such as malabsorption syndromes. a secondary cause of osteoporosis can be identified.13 In addition to calcium. A major contributing factor to all types of osteoporosis is a deficiency of dietary calcium. and osteomalacia or rickets results. the mineralization of bone requires normal plasma concentrations of phosphate and vitamin D. Approximately 99% of the total body weight of calcium is stored in the bones of the skeleton. Whenever cellular levels decrease. during breast-feeding. aberrations of the and other bone regenparathyroid hormone (m). Any loss of calcium results in loss of calcium from the bone. where it is hydroxylated to become 25-hydroxycholecalciferol[25 (OH) DJ]. As a result of this lack of mineralization. One to two hundred mjlligrams a day is lost through normal urine output.U. The final metabolic conversion of the vitamin occurs in the kidneys. In 10% ofwomen and 40% of men presenting with spontaneous vertebral fractures. the skeleton becomes soft.y Whole-bodycalcium is normally obtained through dietary sources. the organic matrix on bone. type II).l6 .

with and without osteoporosis. and long bones.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. The overwhelming majority of their studies looked at bone resorption in the niandiblc. Von Wowern et alL8in 1979 showed in rat mandibles that after extraction of all teeth.18It has also been reported that when skeletal depletion occurs as a result of stimulation by the parathyroid gland. who had acquired 218 complete dentures. Of the osteoporotic women who had their natural teeth at age 50. in nonosteoporotic women the number was only 15%. at the premolar region just distal to the implants. a significant amount of bone loss occurred in the maxillae of ostevporotic women as cornpared with age-matched.'""" 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. In 1990 Von Wowern et a1j3 studied changes in BMC of edentulous mandiblcs with osseointegrated l T limplanls (Straumann Co.. and although no definitive conclusions can be made from any of the studies. load-relating at gonion and in the forearm bones. found that mandibular alveolar ridge height was significantlycorrelated with both total body calcium and mandibular bone mass. In 1974 Wical and Swoope attempted to relate dietarycalcium deficiency to resorption in edentulous subjects. vertebrae.20 Alveolar ridge height (or residual ridge height) and metabolic bone loss have been of interest to many researchers. MA) supporting overdetitnres. This study indicated a statistically significant correlation between mineral density of the mandible and that of the radius. suggesting that exercise may decrease age-related BMC loss in this group. They found that atrophy of alveolar bone between implant fixtures averaged 0. Kribbs et aIz5in a 1989 study or 85 postmenopausal women with osteoporosis. In 1983. 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. alveolar bone may be affected before the ribs. Measurements were made at the implant site. the findings are iinportant because they suggest a relationship between osteoporosis and resorption of the edentulous alvcolar ridge. BMC measurements were made 3 weeks postoperatively and 2 years later at a follow~-upvisit. especially in the maxilla. Perifixtural bone gradually became more radiopaque. Although the study failed to utilize a comparison group." 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. Each wornan's smoking habits and level of osteoporosis (percent cortical area) were measured at the time she acquired each denture.2!3. indicating a successive. while a nonosteoporotic control group illustrated no such parallels. These researchers noted a positive correlation between deficient calcium intake and increased mandibular rc~orption.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.9 mm after lhe first year and 0. It is well known to dentistry that bite force decreases after extraction of teeth and placement of conventional dentures. 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. normal wotnen with the same length of edentulousness. 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. a number of them2'-2' found a positive relationship between severe alveolar ridge atrophy and metabolic bone loss. 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. . Bmter and Fattore Von Wowern and WorsaacZG in 1922 reported that in a stnall study of 28 cdentulous wornen. Cambridge.122 Osteoporosis and Implants A number of studies indicate that certain forms of oral bone loss may be related to a generalized osteoporotic state. aged 60 to 69 years. these changes qualitatively affect the two parts of the skeleton the same way.05 m m annually for the next 2 years.'~ A 1983 study reported on 208 white women. They concluded that when osteoporotic changes occur.44% had required a complete denture before age 60.The differences in prosthodontic requirements between these two groups had not existed beforc age 50 but continued after age 60. Several studies have stated that osseointegrated implants significantlyincrease bite force in the edentulous patient.

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. Both are simple. Table 3. Absorptiornetry. continuing for 5 to 15 years. Diagnosis of the disease can be accomplished by the use of dual-photon absorptiometry or dual energy x-ray ahsorptiometry (DEXA). sedentary individuals. the patient is considered to be at greater risk.8 13 9. anyone with a calcium-deficient diet.1 29.~~. Number 2 Her study suggests that increased function leads to a load-related.3 10. Major Dietary Sources of Calcium ~ ~~ Milk Whole Skim Yogurt Cottage cheese Swiss cheese American cheese Ice cream Sardines (with bones) Salmon (with bones. positive bone remodeling that minimizes.”8 However.1 23. bone Table 1. Osteoporosis: Which Patients Are Most at ksk? Small-boned Caucasian women.5 38. or in some cases may counteract. or a cotnbination of two or more of these modalities. and who understand the bencjits andcomplicationJ 4th drug. uses a radioisotope point source and photon scintillation detection system. the physiological. painless procedures that can be accomplished in about an hour.~~ Which patients should one suspect enough to warrant systemic testing? The more of the following factors that hold true for the patient.34 There are a number of other factors that contribute to osteoporosis. Volumf 2. The machine is termed a “bone mineral analyzer. g?mecologists or orthopedic surgeons. as they have already experienced the period of accelerated bone loss that accompanies and follows the menopause. the greater the risk for the disease: srnall-boned Caucasian women at menopause age or older. whether menopause occurred naturally or was surgically induced. 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.7 . Furthermore. smokers. vitamin D therapy. Estrogen therapy is not indicated for women who arc more than 10 to 15years postmenopausal. calcium supplementation (Tables ‘2 and 3). Routine intraoral periapical or panoramic radiographs are not diagnostic until 40% or greater bone density is lost. younger women who have had hysterectomies or hormonal disturbances. Estrogen therapy is frequently administered to reduce bone loss and to prevent both osteoporosis and bone fractures. 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. As the number increases. who tiaut.123 June 199. sometimes called densitonietry. canncd) ‘I‘of11 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.3 24. there is no strong evidence that estrogen thcrapy rebuilds bone or replenishes bone density. exercise. and especially those with a family history of the (Table 1). 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. 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. Treatment for osteoporosis can include estrogen therapy.~~ Epidemiological studies have shown that functional delay of menopause through estrogen therapy will substantially decrease the ultimate risk of hip fracture. no ooritraindications. Estrogens have bcen shown to diminish the rate of bone loss in postmenopausal women.” The systems are accurate for both cortical and trabecular bone measurement~.1.

National Institutes of Health: Consensus Confrrenrc: Osteoporosis. radiology and histomorphometry. IIabets LLMH. Nielsen SP. Henrikson PA. Worsaae N: Bone mineral content of the maxilla estimated by dual-photon absorptioinetty alter augmentation with hone or hydroxyapatite. Urist M R Current concepts of bone metabolism. J Dent Res 1988. Astrand K. SpecCare Dent 1981. J Prosthet Dent 1983.J Oral Rehabil 1974.43-93 7. NY. van 005CP. andplan to continue itfor at least 5 to 15years (during the period ofaccelerated bone 10~s). National Academy Press. Br bled J 1990. DunsJ. Berg RL. Baxter JC: Nutrition and the geriatric edentulous patient.JDent Res 1988. Am Clin Nutr 1982. \'on Wowern K. Washington DC. &ggs EL.g. Cliu Sci l983. Wical J. . Habets LLMH. 1nt. Zachariasen R: Oral manifestations of metabolic bone diseabe: Vitamin D and osteoporosis.5 m a f m 25 or 26 d a y monthb. a controller trial.Hjorting-Hansen E. Acta Odontol Scand 1979. but the biological changes may warrant some additional caution. N Engl J hled 1986.63:541-546 28. bite force and postural mitsclc actibity in patients with osseointegrated oral implant bridges.fandibular atrophy and metabolic bonc loss. The mandible and osteoporosis (2). Kribbs YJ: Two-year changes in mandibular bone mass in an osteoporotic population. Cummings SK. Krolner B. Haraldson T.17208211 24. Diagnosis and Management. Initiute exstragen theraiy as soon as possible ajer the menopause.252:163I66 6.2:491-496 9. Lutwak L. Raven. Smith DE. et al: Physical exercise as prophylaxis against irivolutionalverlebral bone loss. Melton LJ 111 (eds): Osteoporosis: Etiology. Parfitt . pp 76-100 4.143:1700-1705 19. Black D: The future of hip fractures in thc United States: Numbers.64:729736 16. Ingendl V Muscle function during chewing and swallowing in patients with osseointegrated oral iinplarit bridges. in The Second Fifty Years: Promoting Health and Preventing Disability. Bras J.12:309-313 23. 10 mg medro~fl~gaterone) on days 12-15to days 25 or 26. in Riggs EL. J Clin Invest 1979.53-65. Seeman E.ArchInt bled 1983. References 1. Kribbs PJ. Haraldson T.63:169-170 11. Riggs BL. Wahner I W . \'on Wowern N. ct al: h. and add a progestin (eg.11:612-618 15. IntJ Oral Surg 1983. Muy A4: normal women: Effect of age and menopause status. Borgmeyer-Hoelen AhWJ:Mandibular atrophy and metabolic bone loss. hace clinicalb ecident oste(@~ro. Zarb G: A 10-year follow-up study of the masticatory system after treatment with osseointegrated implant bridges.1:259-263 13. Postgrad Med 1978. Rubiri SM. Aloria J F Determinants of bone mass in postmenopausal women. Bras J. Ingervall R: Functional state.67:6.50:576-580 26.5 17. Compend Contin Educ Dent 1990. The patient should be informed of the risks involved.37:207-216 31. Eisman J.1:47Y-481 22. et al: Changes in bone mineral density of the proximal femur and spine with aging: Differences between the postmenopausal and senile osteoporosis syndromes.300:10561060 10. Carlssori GE. Int J Oral Maxillofac Surg 1988.5l:164-168 14. An electromyoographic study. Scand.rir).8:229-233 29.JProsthet Dent I984. Haraldson T.~~ Conclusions The dentist who is considering osseointegration for a patient should be aware of any systemic diseases. nutrition Bmter and Fattore and bonc health in the elderly.JAhL4 1 984. especially those affecting bone. Stoltze K Changes in bone mass in rat mandibles after tooth extraction. Acta Odontol Scand 1979. Baylorik LlJ. Part I: Measurements of mandibular bone density. Singer FR. et al: Intcstinal calcium absorption and serum vitamin D metabolites in normal subjects and osteoporotic patients. The prognosis for integration can be improved for the osteoporotic patient who is receiving treatment by a physician.17:325-329 25. h4elton LJ 111: Involutional osteoporosis. Osteoporotic bone does not heal differently than bone with more density.369861013 12. Method for detrrruining mineral contrnt o i the mandible and radius. Chestnut C H Oral findings in osteoporosis. Wallenluis K. O f : Bone remodeling: Relationship to the amount and structure of bone.Cassells JS (eds): Osteoporosis. New York.62. 0.4lbanrse A: Calcium nutrition in the elderly. Gallagher JC.67: 1405-I408 27. Toft B.52:799-802 5. Bras J.37:195- 206 30.32:13-17 18.314:1676-1686 3. Baxter JC: Osteoporosis: Oral manifestations 01 a systemic disease. Int J Oral Maxillofac Surg 198X. Berger JS: Alveolar atrophy arid decreased skeletal mass of the radius.J Oral Surg 1979. J Prosthet Dent 1974.1:75-84 21. Ann Intern Med 1974. Swoope C: Studies of residual ridge resorption. 1988. Nordin BEC.2. J Clin Invest 1982:70:716-723 Total bone calcium in 8. J Prosthet Dent 1992. Gallagher JC. costs and potential effects ofpostmenopausal cstrogen.96:243-252 . Kosenquist JB. and the pathogenesis and prevention of fractures. J Bone Miner Res 1987.80630-644 20. Histomorphometry of iliac crest biopsies in 74 patients. Etrogen therapy may also be consideredfor older women within 5 to 15 yearr @rtmenopause who are actiwb jacturing bones (. Clin Orthop 1990. Quintessence Int 1987. IIcaney RP: Calcium supplementation of the diet: Justified by present evidence. Endocrinology. Hcaney RP. 1990. Goldgai D.. Eggs EL.18:427-4'29 2. Int J Oral Surg 1978. Baxter JC: The nutritional health of geriatric patients with varicd dentitions. von Merkesteyn JPR hlandibular atrophy and metabolic bone loss. Gallagher JC. Part IT: The relationship of dietary calcium and phosphorous to residual ridge resorption.124 Osteopmosir and Implantr Prescribe low-dose ET (eg. Insure that fhP patient u n h g m s a thorough annual physical examination yearly. Johnson CC: Calcium.

Nussbaum SR. Cann C E Long-term estrogen replacement therapy prcvents bone loss and fractures.6:799-802 37.June 1993. rt al: IT1 implants with overdentures: A prevention of bone loss in edentulous mandibles? Int J Oral Maxillofac Implants 1990. National 1nsLitutt. Int J Oral Maxillofac Surg 1986.ekholm U.15:39-52 33. I.4 3-year longitudinal prospective study.1:220225 35. IIjorting-Hanscn E. Nationd Osteoporosis Foundation: Osteoporosis: A guide to diagnosis. et al: Postmenopausal osteoporosis: Dental patients at risk. Geriatrics 1984.3916-20 39. Ann Intern Med 1985. Ettinger B.102:339-324 40. Bomberg TJ. 1.34:890-895 125 36. Rigotti NA. iVumher 2 32. Rockler B. Maryland Med J 1985. Katz RD: Recent advances in the early tliagnosis ufostcoporosis: A review. et al: Osteoporosis in women with anorexia nenrosa. N E n g l J bled 1984. Von Wowern N. Shapiro S. 1992 .5: 135-139 34. et al: Marginal tissue reactions at osseointegrated titariiurn fixtures.31:16011606 38. JAMA 1984. Volume 2. Alvioli L V Osteoporosis: Lct's look at llie I d s . Adcll R.sof Health: Consensus Conference: Osteoporosis. IIerzog DB. Gerondontics 1985. Genant HK. Benson BW. . Harder F.