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Factors of bone resorption of the residual ridge
FACTORS HAROLD
RESORPTION
OF THE
RESIDUAL
RIDGE
R. ORTMAN, D.D.S.*
UGersity
N
OF BONE
of Buffalo, School of Dentistry, Buffalo, N. Y.
ORMAL BONE is in a constant state of flux. New bone replaces old bone. The
process of resorption to eliminate this old bone goes on in all skeletal bone. In the adult during middle life, the size and the strength of bone remain nearly constant because the activities of the bone-building processes and the bone-resorbing processes are in balance. When this activity is not in balance, bone may gain in size and strength and change shape because of more rapid apposition, as occurs during growth, or it may regress because of its more rapid loss by resorption than replacement by building elements. The prosthodontic interpretation of the term ridge resorption has come to mean the loss of volume, the change in shape, and the loss of strength of the residual alveolar ridge. Boucherl lists twenty-three unanswered questions concerning prosthodontics, the first seven of which concern the nature of the supporting structures. This tissue is the sole support for complete dentures, and its importance cannot be denied. Bone does change unpredictably and dramatically at times, so the solution to our problem lies in basic research. BASIC
CONCEPT
OF BONE
A basic concept of bone structure and its functional elements must be clear before bone resorption can be understood. The structural elements of bone are (1) the osteocytes found in the bone lacunae, (2) the intercellular substance or bone matrix consisting of fibrils and calcified cementing substance, (3) the osteoblasts, and (4) the osteoclasts. Osteocytes.-Osteocytes are cells that are responsible for the metabolic activity of bone which is essential for its normal function. Osteocytes have a limited lifespan. Since they cannot regenerate by normal mitotic division, the parts of bone containing cells nearing the end of their lifespan must be removed and replaced by bone with fresher, more vital osteocytes. Calcified Cementing Substance.-The calcified cementing substance consists mainly of polymerized glycoproteins. 2 Mineral salts, namely calcium carbonate and phosphate, are bound to these protein substances. Osteoblasfs.-Osteoblasts, by their function of forming and calcifying the intercellular substance, are the active bone-forming cells. The osteoblasts surround the bone in a continuous layer. In the course of bone formation, some osteoblasts become engulfed in the intercellular substance and become osteocytes. Presented N. Y. *Clinical
before Professor
the Greater
New
York
Academy
of Prosthodontics. 429
of Prosthodontics
Meeting
in New
York,
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ORTMAN
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Den. 1962
OsteocZusts.-Osteoclasts are the cellular components of bone that are responsible for bone resorption. Bone resorption always requires the simultaneous elimination of the organic and inorganic components of the intercellular substance.2 The exact mechanism by which bone resorption is accomplished is not completely known, The explanation believed basically correct is that the organic components of the intercellular substance are removed by proteolytic action of the osteoclasts. Then, the calcium salts (inorganic) are dissolved by a chelating action of the osteoclasts. As resorption takes place, the osteocytes released may revert to osteoblasts or become osteoclasts, depending on the physiologic and pathologic demands at that time. Histologically, bone apposition and resorption can take place in close approximation, making possible the bone balance of shape and size.2 A positive bone factor exists when, throughout the entire skeletal system, influences for formation exceed resorption. As bone resorbs, a proliferation of the adjacent connective tissue occurs by mitotic division accompanied by an increase in the capillaries in that region, This reaction gave rise to one of the beliefs that bone loss results from capillary erosion or from the invasion of bone by connective tissue. However, conditions that lead to osteoclastic activity are not completely understood. Weinman and Sicherz have proposed three possible causes of bone resorption : (1)’ aging with necrosis of the bone, (2) increase in the pressure in the adjacent tissue, namely, the periosteum and the bone marrow, and (3) direct action of the elements of the blood and tissue fluids. Attempts have been made to establish one of these factors as the sole cause for resorption. However, in the edentulous mouth supporting a denture base, any one or all three explanations appear to be logical causative factors. Basic information is indicating more and more that changes in the chemistry of the bone play a dominant part as a stimulus for fibrocytes from the connective tissue and osteocytes from the bone to metamorphose into osteoclasts and to commence resorption. PATHOLOGIC
BONE
DISORDERS
Resorption, if orderly, is physiologic. However, if resorption outruns apposition to the detriment of the organs involved or the entire skeletal system, it is pathologic and a negative bone factor exists. The three types of pathologic bone disorders to be considered are osteomalacia, osteoporosis, and osteitis fibrosa. They cannot be distinguished roentgenographically. Osteomalacia is faulty calcification of the organic matrix. This condition usually results from faulty calcium metabolism as influenced by vitamin D, the parathyroid glands, or renal excretion of calcium. Osteoporosis is due to insufficient formation of the organic matrix. This condition is fundamentally a disturbance of protein metabolism and involves vitamin, hormone, and nutritional factors. Osteoporosis is the bone disorder usually found in the edentulous mouth. Osteitis iibrosa is a bone dyscrasia in which the normal cementing substance is replaced by fibrous tissue. Osteitis fibrosa is usually a result of hyperparathyroidism.
Volume Number
12 3
FACTORS
DIAGNOSIS
OF PATHOLOGIC
OF BONE
BONE
RESORPTION
OF
RESIDUAL
RIDGE
431
DISORDERS
Laboratory findings provide little reliable evidence for the diagnosis of pathologic bone disorders. In osteoporosis, the serum calcium and phosphates are more or less normal except when there is a rapid onset and osteolysis drastically exceeds osteogenesis.3 In longstanding osteoporosis, the blood calcium-phosphorus balance is normal because it is a matrix disorder. There is no evidence that normal protein values reflect a normal bone and tissue picture in laboratory tests on serum protein. Koentgenographic findings are not specific in the diagnosis of bone disorders, especially in the early stages. At least a 30 per cent demineralization of bone must occur before it is detectable on roentgenograms .4 However, roentgenograms are still one of the prime diagnostic instruments. When gross bone loss in the maxillae and mandible is visually evident, other skeletal bones show marked demineralization on roentgenograms. One pertinent investigation5 concluded that in systemic health and disease, alveolar bone reflects the prevailing status of the entire skeletal system in terms of relative bone formation and resorption. Also, other physical symptoms are present such as fatigue, rounding of the shoulders, signs of aging of the skin, persistent backaches, and joint tenderness. B This picture is seen especially in postmenopausal osteoporosis. The lack of laboratory ‘evidence makes the treatment or control of the resorption of bone difficult because etiologic factors are masked. No one factor seems to be the prime cause of bone resorption, but a syndrome of a complex nature involving many factors is involved. OSTEOPOROSIS
Osteoporosis is the pathologic resorption of bone where a negative bone factor is present. Such conditions as disuse atrophy, pressure and tension resorption, loss of bone from hormonal causes, and loss of bone from nutritional causes such as vitamin, mineral, and protein deficiencies fall into this category. DISUSE
ATROPHY
A large protein deficit followed by metabolic derangements develops from disuse.? The deficiency is in the formation of the new protein matrix with no disturbance of calcification. Atrophy of disuse is directly proportional to the extent of the disuse. The first stage is seen in the loss of bone around a tooth with no opposing occlusion. The second stage is observed in an edentulous space where several teeth have been lost and there is a loss of more bone and soft tissue covering. The final stage is the completely edentulous mouth in which there is a total remodeling of the entire residual ridge. After the loss of the natural teeth, the bone cannot be stimulated by a denture base as the teeth did internally. A loss of closing force develops because the mucous membrane and the periosteum cannot endure the force once received by the teeth. This loss of internal stimuli and the reduction of closing force are signals for disuse atrophy and a remodeling of the bone in accordance with Wolff’s law of transforma-
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ORTMAN
tion. Wolff’s law states, briefly, that “change in form and that its change is due to alteration of its internal conformation, in accordance with mathematical laws.” Disuse atrophy does not result from the direct loss rather from the lack of replacement of bone not needed are present from the action of the denture base, but the normal. The response of the bone varies with the degree, tolerance to the stimulation. REACTION
OF BONE
TO PRESSURE
AND
J. Pros. May-June,
Den. 1962
follows change in function architecture and external of nonfunctional bone, but for function. Some stimuli nature of the stimuli is not the interval, and the tissue
TENSION
The reaction of bone to pressure seems paradoxic since it can cause both apposition and resorption. As an example, if pressure on a tooth is in direct line with the long axis of the tooth, there is a stimulus for the apposition of bone that seems in the healthy individual to be in direct proportion to the time and amount of stimulus. Pressure perpendicular to the long axis of the tooth creates bone resorption, tooth migration, and looseness as resorption occurs. An increase of pressure within the limits of tolerance leads to bone apposition. As long as pressure does not interfere with the normal blood supply, nerve supply, and drainage of the bone tissue, the pressure is resist,ed. However, whenever pressure interferes with the blood or nerve supply or with the venous drainage of the bone, resorption invariably occurs.2 Normally, the stress of pressure and tension on bone is transmitted through avascular tissue such as the teeth, the condylar articulation, the intervertebral disc, and other joints. Such structures under pressure are covered by specialized fibrous tissue, fibrocartilage, or hyaline cartilage. If the pressure is against a vascular tissue covering of the bone such as the periosteum, the blood supply to the bone is aggravated and it is a target for resorption. The denture-bearing bone has a complex blood supply from two sources. The main supply is internal from the interdental arteries that pass through canals in the interalveolar septa. After extraction, if bone loss was slight, the blood supply is not greatly disturbed ; however, if extensive surgical procedures removed large amounts of alveolar bone, the internal blood supply can be vastly altered by the bone callus. The other blood supply comes externally from the periosteum. Arteries from the periosteal network enter the bone as arterioles in the numerous Volkman canals which open from the outer surface of compact bone. Interference with the blood supply leads to bone necrosis. The interference may be due to pressure directly from the bone, or it may be of inflammatory origin. If inflammation is present, a constant internal capillary pressure acts to set up resorptive processes. The amount of blood supplied to the bone from within (intrinsic and surgical sequelae) and from without (periosteal network and denture base) can predispose little or great change in bone form. It is tempting to draw definite conclusions about this concept, but it needs further investigation. However, it does seem to offer a logical explanation as to why some patients exhibit so little bone loss and some so great a loss in a given space of time.
Volume Number
12 3
FACTORS
OF BONE
RESORPTION
OF
RESIDUAL
RIDGE
433
OSTEOPHYTES
An emergency and temporary repair of bone is attempted when there is a rapid reduction of the alveolar ridge and a low grade inflammatory response of the mucoperiosteum. Bony outgrowths called osteophytes arise from the bony surface as thin trabeculae and are perpendicular to that surface.’ The trabeculae may be connected by supporting crossbars of bone. The bone of an osteophyte is always immature, primitive, coarse, and ragged in nature. These sharp bony projections cause irritation to the overlying mucoperiosteum when even the slightest pressure is directed upon them. Surgical removal and smoothing will not permanently correct this ragged condition since the projections form once more as an attempt is again made at emergency reinforcement. These projections can be seen roentgenographically, indicate abnormal pathologic destruction of bone, and continue to form unless interceptive therapy is instituted. PHENOMENON
OF STRESS
Stress is a term used to describe a situation that causes an “alarm reaction.“” The stress may be due to a chemical, mechanical, thermal, radiation, systemic (dietary, endocrine), or emotional response to any unfavorable stimuli. Selye5 has developed the concept of a “general adaptation syndrome” in response to this alarm reaction. He concludes that the ability of tissue to adapt to changes of stress depends on what he calls “adaptation energy” and that its magnitude appears to depend largely upon genetic factors modified by local factors. Stress has an effect on skeletal bone. The alarm reaction in effect when stress is high causes a complex hormonal series of events. The anterior pituitary gland is stimulated to release adrenocorticotropic hormone (ACTH ) . This causes protein catabolism which interferes with the formation of organic bone matrix. At the same time, stress also causes a decrease in the sex hormones which have a protein anabolic effect. Therefore, a protein balance is lost by a dual effect of stress. Tissues lose their resistance to stress as aging processes occur. An increase in the effect of stress occurs because of a gradual lowering of basal metabolism and of the ability of tissue to regenerate and adapt. This creates a phase of protein catabolism. ENDOCRINE
GLANDS
The endocrine glands have a profound effect on all body functions. Diseases such as diabetes mellitus, Addison’s disease, acromegaly, myxedema, and many others are endocrine disturbances. A discussion of hormonal influences is necessary to understand their effects on bone. Pituitary Glands and Hypophy.sis.-The hypophysis is the master gland of the endocrine system. It is responsible for the production of six hormones that are (1) regulators of growth, (2) controllers of lactation, (3) androgenic, (4) estrogenie, (5) thyrotropic, and (6) adrenocorticotropic. The control of the hypophysis over the endocrine system is complex, and problems of dysfunction require the analysis of an endocrinologist. Such findings are of importance to the dentist because they involve the general health of the patient, which is reflected in the oral cavity.
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ORTMAN
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Thyroid Glands.-The thyroid glands are responsible for the regulation of the rate of metabolism. Hyperthyroidism increases the metabolic rate so that a negative nitrogen balance results. Such a balance is *equivalent to protein deficiency, which can be a direct cause of osteoporosis. Thyroxine also has a direct influence on the kidneys, causing an increased excretion of calcium and phosphorus. This depletion of calcium and phosphorus results in decreased bone apposition and increased osteoclastic activity to marshal1 these elements from the bone to compensate for their dep1etion.a Parathyroid Glands.--Basic research is not definite in disclosing the exact mechanism by which the parathyroid hormone regulates the calcium-phosphorus balance in the blood. The chief argument at present is whether the hormone acts as a direct control on the apposition and resorption of bone or primarily on the kidneys by influencing calcium resorption by the tubules. When the parathyroid hormone is injected (hyperparathyroidism), there is an immediate rise in the renal excretion of ph0sphate.s This disturbs the blood calcium :phosphorus ratio by raising the blood serum calcium level. Then, phosphates are called from the bone bank by osteoclastic activity. The parathyroid hormone has another function of maintaining the blood level of the calcium ion. The calcification of bone tissue will be retarded to preserve the blood level of the calcium ion. This is related to the action of vitamin D in an antagonistic manner. Parathormone maintains blood calcium by mobilizing it from the bones by osteoclastic activity. Vitamin D maintains blood calcium by increasing the absorption of calcium from dietary sources in the intestinal tract. Islands of Lange&am. -The failure of these glands to produce sufficient insulin for the proper utilization of glucose causes diabetes mellitus. The high blood sugar with the spillover into the urine is well known. The syndrome of poor healing, low tissue tolerance, and rapid resorption of bone associated with the diabetic patient is recognized, but the instrinsic causative factors are not. The explanation for this syndrome is that, in the absence of insulin, a relative nitrogen starvation occurs from increased gluconeogenesis with the amino acids being diverted from protein synthesis.9 A diabetic controlled by either insulin or diet is not affected by this mechanism. However, perfect control is rarely possible. Therefore, a word of caution and explanation to diabetic patients is necessary so that they can appreciate their prosthetic difficulties. Suprarenal Glands.-The adrenal cortex produces steroid hormones called corticoids. One of these, cortisone, retards osteogenesis.1° It was shown experimentally that administration of ACTH interfered with the healing of bone in rachitic rats whose treatment consisted of administration of calcium and vitamin D. Cortisone and related steroids are antianabolic, may induce the formation of glucose from noncarbohydrates, and may increase the calcium loss by direct effect on calcium excretion. The prolonged use and administration of such steroids are considered very dangerous to bone tissue. The corticoids have some local effects that may be beneficial. One such effect is to control the defense mechanism of inflammation. An example of this action is the improvement of the “denture sore mouth” with the application of 0.05 per cent
z’:K: ‘3”
FACTORS
OF BONE
RESORPTION
OF
RESIDUAL
RIDGE
435
hydrocortisone acetate.12 Related steroids with the same anti-inflammatory action but with less likelihood of systemic effects are available. Gonads.-In general, the sex hormones (androgens and estrogens j promote a protein anabolic action on all tissues including bone. A striking storage of nitrogen and calcium occurred in individuals with postmenopausal or senile osteoporosis in one study when these hormones were administered. I3 More than half of the women over 50 years of age showed roentgenographic evidence of diminishing bone mass in a study by Albright and Reifensteins Postmenopausal osteoporosis is the most common form of this condition. A moderate amount of osteoporosis accompanies senescence because of the “catabolic ascendency” reflected by atrophic and degenerative changes throughout the body.” The aging person produces less and less of the androgens and estrogens, which results in faulty protein metabolism for tissue repair. The bone matrix suffers, and normal bone loss cannot be compensated. The androgens are more effective in nitrogen retention than the estrogens.‘” However, the estrogens stimulate osteoblastic activity.‘” Recent clinical evidence indicates that a combination of both androgens (testosterone j and estrogens is superior therapeutically to either hormone administered alone. A beneficial synergistic effect is obtained without the embarrassing untoward effects of masculinization caused by the androgens when used alone. Methandriol, a weakly virilizing agent, has proved experimentally to have a high protein anabolic effect in relation to the androgenic masculinizing effect. Women under treatment showed no masculinization, yet 80 per cent showed clinical evidence of improvement of osteoporosis. lS Vitamin D and calcium may be given in combination with this treatment. Geriatric problems are increasing and need to be met with understanding. The mental attitude and general sense of well-being of the patient are improved by the carefully considered use of these hormones because the catabolic rate is slowed down by this treatment. Great caution must be exercised in the administration of sex hormones because they may have carcinogenic influences if administration is not carefully controlled. DIETARY
FACTORS
: VITAMINS,
MINERALS,
AND
PROTEIN
Nutritional disturbances are regarded by some as the primary cause of osteoporosis, but most clinicians support the hormonal causative factors.B Gastrointestinal dysfunction, defective alimentation, and glandular insufficiency in the aged person are so intricately interrelated that a single causative factor does not exist. The keystone of bone therapy is a substantial protein metabolism. The synthesis of osteoid tissue in protein-starved people is compromised and calcification is decreased since the protein matrix is embarrassed. Protein may not be available because of inadequate intake, improper assimilation, or excessive loss, as in nephrosis, or because it is utilized as caloric requirements because of hyperthyroidism, uncontrolled diabetes, or a surfeit of adrenocortical hormones from either endogenous or exogenous sources. A diet in which the protein content is less than 10 per cent of the total intake
436
ORTMAN
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can cause slowed growth of bone .’ Bone apposition cannot keep up with normal osteoclastic activity, and a negative bone factor eaists. Nutritional demands may surpass the appetite and the capability of the patient for mastication. Caloric intake is seldom inadequate, but the intake of essential elements may be deficient. The action of vitamins in many respects is the same as that of hormones. Sicher” states that the relationship of vitamins and hormones can be explained on the basis that the endocrine glands produce intrinsic hormones and the vitamins are extrinsic hormones. Vitawzin A (Carotene).-Experimental avitaminosis A in rats has resulted in the failure of new bone to form as replacement for that lost from normal metabolic activity. The explanation seems to be that extended vitamin A deficiency causes renal damage by hornification of the tubules. This damage results in the abnormal loss of phosphorus as the tubules lose the capacity for reabsorption.2 The imbalance of the calcium :phosphorus ratio leads to osteoporosis. A lowering of vitamin A also has an effect on the osteoblasts so that they engage in disorderly and uncontrolled activity .3 The cells adjacent to the bone modulate to osteoclasts and become active. There is a danger of hypervitaminosis A, but experiments are inconclusive as to the mechanism. Some reports indicate an acceleration of matrix remodeling, while others seem to conclude that excess vitamin A accelerates the activity of the osteoclasts. The general function of vitamin A in regard to bone is its influence on the activity and position of the osteoblasts and osteoclasts. Vitamin B Cow/&x.-The total effect of vitamin B complex seems to be of a regulatory nature. Hypovitaminosis B results in loss of appetite and dietary insufficiency, increase in nervous irritability resulting in lowered resistance to stress, and emotional tension. The total well-being of the individual is impaired. Vitamin B complex deficiency produces effects in bone similar to a protein deficiency. Chase3 reported degeneration of bone, enamel, and dentin in rats on a B complex-deficient diet. Osteoporosis and gingival inflammation were induced in dogs by withdrawal of nicotinic acid. This condition was corrected by addition of this part of the B complex to the diet. Vitankn C.-The effect of vitamin C seems to be clear, conclusive, and dramatic. The only animals sensitive to ascorbic acid deficiency are guinea pigs, monkeys, and man.3 The appearance of scurvy in the bones of all three is similar. The apposition of new bone slows down dramatically because osteoblastic activity is impaired. Experiments have shown that an ascorbutic diet causes a severe bone loss because of adverse effects on the osteoblasts with apparent lack of effect on the osteoclasts. Hence, bone loss is greater than bone apposition. The collagen content of bones is also reduced in vitamin C deficiency. The loosening of teeth in scurvy is due both to bone resorption and to disorganization of the periodontal fibers and membranes. The periosteum is affected in a similar way. It thickens, and the cells appear immature and resemble fibroblasts. This condition may make the periosteum more easily injured by the denture base so that inflammatory processes are triggered by the denture base at lower pressure levels. Endocrine influences affect the vitamin requirements, particularly for vitamin
FACTORS
OF
RONE
RESORI’TIOTU’
OF
RESIDIihL
RIDGE
437
C. For example, l~ypertl~yroidism producctl exl)rril~lentally:~ I)y injection showetl ali increased need of vitamiii C for the collagen content of bone to remain normal. Osteophytes” appear as a result of avitaminosis C. The rapid loss of bone and the increased inflammation of the mucoperiosteum cause the development of these bony outgrowths. v;tuGz L).-Vitamin D is necessary for the calcium-phosphorus balance to remain within tolerable limits. Vitamin D would be unnecessary if the exact required ratio of calcium and phosphorus were available in the diet. A pure vitamin ‘D deficiency rachitic condition does not exist3 but is only related to the calcium-phosphorus balance in the diet and the activity of the parathyroid glands. When bone loses its ability to calcify the matrix, administration of vitamin D will cause calcification and denser bone. The dosage of this vitamin is important and its requirements obscure. Moderate overdosage causes excessively mineralized bone, but gross overdosage causes bone resorption. VitmGzs E and K.-No direct bone changes have been found from the effects of vitamins E and K. However, their actions are related to protein metabolism, which could indirectly have some side effects on bone. iLlinerals.-The inclusion of adequate calcium and phosphorus in the diet is a necessity because the prime mineralizing substance of bone is calcium phosphate. Studies on osteoporotic patients indicated that they had a significantly low intake of calcium in the diet as compared to normal individuals.16 Individual calcium requirements were shown to vary widely, with a higher requirement for patients who develop osteoporosis. The efficacy of a high dietary calcium treatment as a method of replacing lost calcium is being tested. However, a hartnful effect of more than a modest calcium intake may be the formation of kidney and bladder stones. Other minerals are suspected to be important, but little research has been done on their relation to bone metabolism. A copper deficiency has produced osteoporosis in dogs. l3 Strontium administered in lactate form increases the production of osteoid tissue and aids its mineralization.6 AZbuvnin.--Intravenous albumin in treatment of osteoporosis produced a rise in the serum level of calcium and a decrease in urinary excretion of potassium, phosphorus, and calcium.8 The effects are similar to the action of estrogen. Also, albumin serves as an important building block for bone matrix.17 ReifensteinlO has suggested that the use of albumin in conjunction with steroid therapy would increase the rate of bone formation and control bone loss. OTIIER
CONSIDERATIONS
CONCERNING
RESORPTTON
Lammielh has proposed a hypothesis for the mechanism of ridge reduction based on the molding of the bony ridge by the external molding force of the atrophying oral mucosa. This hypothesis explains some of the changes observed in ridge contour where surgical operation has created a wound that is bound and closed by contracting mucosa. Perhaps it can explain some of the changes of disuse atrophy, but it is difficult to attribute the entire change that occurs over a period of years to a single molding force of the mucosa. The force of the tnucosa is apparently
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contradicted by the existence of exostosed areas in which the tissue is very tight and also avascular. In some edentulous mouths, extensive bone resorption has occurred in regions not covered with denture bases. The soft tissues are lose and folded over the residual ridge crest even though no hypertrophy due to inflammatory processes has taken place. Here it is difficult to explain the dramatic loss of bone by force from the atrophying mucosa. In instances in which a denture has been worn and hyperplastic tissue has replaced the lost bone to satisfy the denture contour, it is difficult to attribute a molding force to such loose, pendulous tissue. Resorption continues as the soft tissue hypertrophies. The concept that roentgenographic examination can be used as an index to future bone lose has been proposed by Sobolik .19 He states that “the rapidity of bone resorption is in inverse proportion to the uniformity of the density of the alveolar support.” In other words, dense alveolar bone as determined roentgenographically provides good foundational possibilities. In contrast, Applegate20 points out that less dense bone is less likely to show unfavorable change after the insertion of a denture base than more dense bone. His explanation is that a less highly calcified bone or a less dense bone is more organic in structure and is more conducive to a normal rate of bone maintenance because its rebuilding would be facilitated. The apparent density of bone varies with the roentgenographic technique. Relative density may vary greatly within patients whose bone stability has been good over a period of years. Therefore, roentgenographic evaluation of bone relative to its stability is unreliable. ROLE
OF THE
DENTURE
BASE
IN
RESORPTION
Available evidence is inconclusive and seems to indicate that a denture base may act either to retard or to hasten the process of bone resorption. There is no question that a residual ridge will gradually resorb after the extraction of the teeth caused by disuse atrophy and aging. The rate of change is under the influence of the remaining functional stimuli, the altered blood supply, and the body chemistry as affected by nutritional, hormonal, and emotional factors. A discussion of the effects of the denture base on resorption at present must be limited to its local effects on the supporting tissues. Fundamentally, the wearing of a denture is physiologically incompatible with the function of the ridge tissues. Nowhere in Nature’s design has pressure been directed upon bone through vascular tissue as is imposed by the prosthetic base. How well the tissues will tolerate this pressure depends upon many factors. If the mechanical factors designed into the denture by the impressions, jaw relation records, and occlusion are controlled so that pressures remain within tissue tolerance, the denture base should not contribute to a more rapid rate of resorption. Indeed, if the action of the base is favorably controlled in its adaptation to the tissues and its directed force, it could provide stimuli that retard resorptive processes. The denture base can seem to trigger the dramatic loss of bone, but the stage
Volume Number
1L’ 3
FACTORS
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BONE
RESORPTION
OF
RESIDUAL
RIDGE
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has to be properly set. Dentures seemingly perfect in tissue coverage and adaptation, jaw relations, and occlusion may fail in a short period of time because of rapid bone resorption. In contrast, dentures that are inadequate in many respects are worn, and the ridges remain apparently normal. Is it possible that ridge resorption can be completely controlled by denture procedures? The answer appears to be negative.
1. Resorption of bone is a normal process. Its balance to bone apposition may be either physiologic or pathologic and is dependent upon multiple factors. 2. Treatment of rapid (pathologic) resorption is difficult because the multiple factors are interrelated and it is impossible to evaluate clinically or roentgenographically the precise part played by each. 3. A normal bone picture requires that all known body fluids and elements, both intrinsic and extrinsic, are in proper harmony and composition. 4. When bone loss is rapid and abnormal in the residual ridges, evidence of general skeletal osteoporosis is also present. This acquits the denture base from being the sole cause in abnormal resorption. 5. Disuse atrophy occurs in the edentulous mouth whether or not a denture is worn. 6. Pressure of a denture base on the bone of the residual ridge is a violation to the natural way that bone receives pressure because it is transmitted through vascular tissue. If the pressure does not alter the blood supply to the embarrassment of the bone or cause inflammation of the mucoperiosteum so that it becomes a causative factor of resorption by creating capillary pressure, the denture base could provide stimuli for reduced resorption. 7. Stress, regardless of its cause, always produces an alarm reaction which increases the rate of bone resorption. 8. Dysfunction of the endocrine glands causes an obscure but drastic effect on the rate of bone replacement, the organic matrix, and the rate of bone resorption. Hormonal or plurihormonal administration offers great possibility for control of resorption. 9. Many people are deficient in nutritional requirements necessary for the normal metabolism of bone. Vitamins, minerals, and proteins demands have potential beneficial effects when properly oriented in the diet. A panvitamin program has prophylactic value. Adequate mineral intake must be assured for a normal bone picture. Protein is the most important nutritional factor in its effect on bone. An edentulous condition necessitat’es the protection of a high protein-low carbohydrate diet. 10. The factors influencing bone resorption in young adults are primarily those of traumatic and inflammatory nature, with pressure, tension, stress, and nutrition playing the dominant part. Control of resorption for this age group can be managed effectively by sound prosthetic procedures and adequate dietary measures. 11. As the edentulous patient ages, the geriatric problems of lower protein
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metabolism, lower resistance to stress, alimentary failure, and endocrine complications come into the picture and management becomes more complex. CONCLUSIONS
The advances made in the basic sciences are providing a broader base for the understanding and management of the foundation of bone. If we can analyze and relate the progress made in basic research to dentistry, a more competent and complete health service will be available to our patients. In this way, more and more general health problems will come to the attention of our profession. Some of the health problems will need the attention of the physician who will appreciate that his cooperation is necessary for the dental future of the edentulous patient. The dentist should be prepared to extend the limit of his treatment, treat within his ability, and refer when it goes beyond his field, but, above all, know which is which. It does not seem a nebulous hope that some day there will be control over bone resorption as there is over rickets, endemic goiter, scurvy, beri-beri, and other diseases. REFERENCES
Boucher, C. 0.: h:Weinm;:;m.F&
Current Status of Prosthodontics, J. PROS. DE?. 10:411-425, 1960. and Sicher, H.: Bone and Bones, ed. 2, St. Louis, 1955, The C. V. Mosby
3. Irving, J. T.: A Comparison of the Influences of Hormones, Vitamins and Other Dietary Factors on Bone, Dentin, and Enamel, Vitamins & Hormones 15:291-323, 1957. 4. Sante, hcR; F’rples of Roentenological Interpretation, Ann Arbor, 1957, Edwards Bros., Selye, H. I’ Stress, Montreal, 1950, Acta Inc. Medical Publishers. Schecter, D. C.: Current Concepts in the Management of Osteoporosis, J. Am. Geriatrics Sot. 6:592-613, 1958. 7. Dietrich, J. E., Whedon, G. D:, and Shorr, E.: Effects of Immobilization Upon Various Metabolic and Physiological Functions of Normal Men, Am. J. Med. 4:3, 1948. 8. Albright, F., and Reifenstein, E. C., Jr.: The Parathyroid Glands and Metabolic Bone Disease, Baltimore, 1948,. Williams and Wilkins Company, p. 145. 9. Cecil, F.6i4: Textbook of Medlcme, ed. 4, Philadelphia, 1939, W. B. Saunders Company, i:
10. Reifenstein, ‘E. C., Jr.: The Relationship of Steroid Hormones to Development and Management of Osteoporosis in Aging People, Clin. Osteop. 10:206-253, 1957. Follis, R. H., Jr. : Osteoporosis, Bull. Rheumat. Dis. 4:52, 1954. :; Collett, H. A.: Oral Conditions Associated With Dentures, J. PROS. DEN. 8:591-599, 1958. 13: Gardner, A. F.: Management of Osteoporosis-Modern Concepts, Am. Pratt. & Digest Treat. 9:767-769, 1959. 14. Banhart, R. E.: A Clmical Evaluation of Methyl Androstenediol in Treatment of Osteoporosis, Am. Pratt. & Digest Treat. 5:964, 1954. 15. Gordan, G. S., Eisenberg, M., Moon, H. D., and Sakamoto, W.: Methylandrostenediol-A Protein Anabolic Steroid With Little Androgenic Activity, J. Clin. Endocrinol. 11: 209-212, 1951. 16. Whedon, G. D.: Calcium Needs of Adults and Older People, Nutrition Neys 23:1, 1960. 17. Emerson, K., Jr., and Beckman, W. W.: Calcium Metabolism in Nephrosis, J. Clin. Invest. 24:564, 1945. Lammie, G. A.: Reduction of the Edentulous Ridges, J. PROS. DEN. 10:605-611, 1960. :; Sobolik, C. F.: Alveolar Bone Resorption, J. PROS. DEN. 10:612-619, 1960. 20: Applegate, 0. C.: An Evaluation of the Support for the Removable Partial Denture, J. PROS. DEN. 10:112-123, 1960. UNIVERSITY OF BUFFALO SCHOOL OF DENTISTRY 3435 MAIN ST. BUFFALO, N. Y.
RESORPTION
OF THE
RESIDUAL
RIDGE
R. ORTMAN, D.D.S.*
UGersity
N
OF BONE
of Buffalo, School of Dentistry, Buffalo, N. Y.
ORMAL BONE is in a constant state of flux. New bone replaces old bone. The
process of resorption to eliminate this old bone goes on in all skeletal bone. In the adult during middle life, the size and the strength of bone remain nearly constant because the activities of the bone-building processes and the bone-resorbing processes are in balance. When this activity is not in balance, bone may gain in size and strength and change shape because of more rapid apposition, as occurs during growth, or it may regress because of its more rapid loss by resorption than replacement by building elements. The prosthodontic interpretation of the term ridge resorption has come to mean the loss of volume, the change in shape, and the loss of strength of the residual alveolar ridge. Boucherl lists twenty-three unanswered questions concerning prosthodontics, the first seven of which concern the nature of the supporting structures. This tissue is the sole support for complete dentures, and its importance cannot be denied. Bone does change unpredictably and dramatically at times, so the solution to our problem lies in basic research. BASIC
CONCEPT
OF BONE
A basic concept of bone structure and its functional elements must be clear before bone resorption can be understood. The structural elements of bone are (1) the osteocytes found in the bone lacunae, (2) the intercellular substance or bone matrix consisting of fibrils and calcified cementing substance, (3) the osteoblasts, and (4) the osteoclasts. Osteocytes.-Osteocytes are cells that are responsible for the metabolic activity of bone which is essential for its normal function. Osteocytes have a limited lifespan. Since they cannot regenerate by normal mitotic division, the parts of bone containing cells nearing the end of their lifespan must be removed and replaced by bone with fresher, more vital osteocytes. Calcified Cementing Substance.-The calcified cementing substance consists mainly of polymerized glycoproteins. 2 Mineral salts, namely calcium carbonate and phosphate, are bound to these protein substances. Osteoblasfs.-Osteoblasts, by their function of forming and calcifying the intercellular substance, are the active bone-forming cells. The osteoblasts surround the bone in a continuous layer. In the course of bone formation, some osteoblasts become engulfed in the intercellular substance and become osteocytes. Presented N. Y. *Clinical
before Professor
the Greater
New
York
Academy
of Prosthodontics. 429
of Prosthodontics
Meeting
in New
York,
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ORTMAN
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Den. 1962
OsteocZusts.-Osteoclasts are the cellular components of bone that are responsible for bone resorption. Bone resorption always requires the simultaneous elimination of the organic and inorganic components of the intercellular substance.2 The exact mechanism by which bone resorption is accomplished is not completely known, The explanation believed basically correct is that the organic components of the intercellular substance are removed by proteolytic action of the osteoclasts. Then, the calcium salts (inorganic) are dissolved by a chelating action of the osteoclasts. As resorption takes place, the osteocytes released may revert to osteoblasts or become osteoclasts, depending on the physiologic and pathologic demands at that time. Histologically, bone apposition and resorption can take place in close approximation, making possible the bone balance of shape and size.2 A positive bone factor exists when, throughout the entire skeletal system, influences for formation exceed resorption. As bone resorbs, a proliferation of the adjacent connective tissue occurs by mitotic division accompanied by an increase in the capillaries in that region, This reaction gave rise to one of the beliefs that bone loss results from capillary erosion or from the invasion of bone by connective tissue. However, conditions that lead to osteoclastic activity are not completely understood. Weinman and Sicherz have proposed three possible causes of bone resorption : (1)’ aging with necrosis of the bone, (2) increase in the pressure in the adjacent tissue, namely, the periosteum and the bone marrow, and (3) direct action of the elements of the blood and tissue fluids. Attempts have been made to establish one of these factors as the sole cause for resorption. However, in the edentulous mouth supporting a denture base, any one or all three explanations appear to be logical causative factors. Basic information is indicating more and more that changes in the chemistry of the bone play a dominant part as a stimulus for fibrocytes from the connective tissue and osteocytes from the bone to metamorphose into osteoclasts and to commence resorption. PATHOLOGIC
BONE
DISORDERS
Resorption, if orderly, is physiologic. However, if resorption outruns apposition to the detriment of the organs involved or the entire skeletal system, it is pathologic and a negative bone factor exists. The three types of pathologic bone disorders to be considered are osteomalacia, osteoporosis, and osteitis fibrosa. They cannot be distinguished roentgenographically. Osteomalacia is faulty calcification of the organic matrix. This condition usually results from faulty calcium metabolism as influenced by vitamin D, the parathyroid glands, or renal excretion of calcium. Osteoporosis is due to insufficient formation of the organic matrix. This condition is fundamentally a disturbance of protein metabolism and involves vitamin, hormone, and nutritional factors. Osteoporosis is the bone disorder usually found in the edentulous mouth. Osteitis iibrosa is a bone dyscrasia in which the normal cementing substance is replaced by fibrous tissue. Osteitis fibrosa is usually a result of hyperparathyroidism.
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FACTORS
DIAGNOSIS
OF PATHOLOGIC
OF BONE
BONE
RESORPTION
OF
RESIDUAL
RIDGE
431
DISORDERS
Laboratory findings provide little reliable evidence for the diagnosis of pathologic bone disorders. In osteoporosis, the serum calcium and phosphates are more or less normal except when there is a rapid onset and osteolysis drastically exceeds osteogenesis.3 In longstanding osteoporosis, the blood calcium-phosphorus balance is normal because it is a matrix disorder. There is no evidence that normal protein values reflect a normal bone and tissue picture in laboratory tests on serum protein. Koentgenographic findings are not specific in the diagnosis of bone disorders, especially in the early stages. At least a 30 per cent demineralization of bone must occur before it is detectable on roentgenograms .4 However, roentgenograms are still one of the prime diagnostic instruments. When gross bone loss in the maxillae and mandible is visually evident, other skeletal bones show marked demineralization on roentgenograms. One pertinent investigation5 concluded that in systemic health and disease, alveolar bone reflects the prevailing status of the entire skeletal system in terms of relative bone formation and resorption. Also, other physical symptoms are present such as fatigue, rounding of the shoulders, signs of aging of the skin, persistent backaches, and joint tenderness. B This picture is seen especially in postmenopausal osteoporosis. The lack of laboratory ‘evidence makes the treatment or control of the resorption of bone difficult because etiologic factors are masked. No one factor seems to be the prime cause of bone resorption, but a syndrome of a complex nature involving many factors is involved. OSTEOPOROSIS
Osteoporosis is the pathologic resorption of bone where a negative bone factor is present. Such conditions as disuse atrophy, pressure and tension resorption, loss of bone from hormonal causes, and loss of bone from nutritional causes such as vitamin, mineral, and protein deficiencies fall into this category. DISUSE
ATROPHY
A large protein deficit followed by metabolic derangements develops from disuse.? The deficiency is in the formation of the new protein matrix with no disturbance of calcification. Atrophy of disuse is directly proportional to the extent of the disuse. The first stage is seen in the loss of bone around a tooth with no opposing occlusion. The second stage is observed in an edentulous space where several teeth have been lost and there is a loss of more bone and soft tissue covering. The final stage is the completely edentulous mouth in which there is a total remodeling of the entire residual ridge. After the loss of the natural teeth, the bone cannot be stimulated by a denture base as the teeth did internally. A loss of closing force develops because the mucous membrane and the periosteum cannot endure the force once received by the teeth. This loss of internal stimuli and the reduction of closing force are signals for disuse atrophy and a remodeling of the bone in accordance with Wolff’s law of transforma-
432
ORTMAN
tion. Wolff’s law states, briefly, that “change in form and that its change is due to alteration of its internal conformation, in accordance with mathematical laws.” Disuse atrophy does not result from the direct loss rather from the lack of replacement of bone not needed are present from the action of the denture base, but the normal. The response of the bone varies with the degree, tolerance to the stimulation. REACTION
OF BONE
TO PRESSURE
AND
J. Pros. May-June,
Den. 1962
follows change in function architecture and external of nonfunctional bone, but for function. Some stimuli nature of the stimuli is not the interval, and the tissue
TENSION
The reaction of bone to pressure seems paradoxic since it can cause both apposition and resorption. As an example, if pressure on a tooth is in direct line with the long axis of the tooth, there is a stimulus for the apposition of bone that seems in the healthy individual to be in direct proportion to the time and amount of stimulus. Pressure perpendicular to the long axis of the tooth creates bone resorption, tooth migration, and looseness as resorption occurs. An increase of pressure within the limits of tolerance leads to bone apposition. As long as pressure does not interfere with the normal blood supply, nerve supply, and drainage of the bone tissue, the pressure is resist,ed. However, whenever pressure interferes with the blood or nerve supply or with the venous drainage of the bone, resorption invariably occurs.2 Normally, the stress of pressure and tension on bone is transmitted through avascular tissue such as the teeth, the condylar articulation, the intervertebral disc, and other joints. Such structures under pressure are covered by specialized fibrous tissue, fibrocartilage, or hyaline cartilage. If the pressure is against a vascular tissue covering of the bone such as the periosteum, the blood supply to the bone is aggravated and it is a target for resorption. The denture-bearing bone has a complex blood supply from two sources. The main supply is internal from the interdental arteries that pass through canals in the interalveolar septa. After extraction, if bone loss was slight, the blood supply is not greatly disturbed ; however, if extensive surgical procedures removed large amounts of alveolar bone, the internal blood supply can be vastly altered by the bone callus. The other blood supply comes externally from the periosteum. Arteries from the periosteal network enter the bone as arterioles in the numerous Volkman canals which open from the outer surface of compact bone. Interference with the blood supply leads to bone necrosis. The interference may be due to pressure directly from the bone, or it may be of inflammatory origin. If inflammation is present, a constant internal capillary pressure acts to set up resorptive processes. The amount of blood supplied to the bone from within (intrinsic and surgical sequelae) and from without (periosteal network and denture base) can predispose little or great change in bone form. It is tempting to draw definite conclusions about this concept, but it needs further investigation. However, it does seem to offer a logical explanation as to why some patients exhibit so little bone loss and some so great a loss in a given space of time.
Volume Number
12 3
FACTORS
OF BONE
RESORPTION
OF
RESIDUAL
RIDGE
433
OSTEOPHYTES
An emergency and temporary repair of bone is attempted when there is a rapid reduction of the alveolar ridge and a low grade inflammatory response of the mucoperiosteum. Bony outgrowths called osteophytes arise from the bony surface as thin trabeculae and are perpendicular to that surface.’ The trabeculae may be connected by supporting crossbars of bone. The bone of an osteophyte is always immature, primitive, coarse, and ragged in nature. These sharp bony projections cause irritation to the overlying mucoperiosteum when even the slightest pressure is directed upon them. Surgical removal and smoothing will not permanently correct this ragged condition since the projections form once more as an attempt is again made at emergency reinforcement. These projections can be seen roentgenographically, indicate abnormal pathologic destruction of bone, and continue to form unless interceptive therapy is instituted. PHENOMENON
OF STRESS
Stress is a term used to describe a situation that causes an “alarm reaction.“” The stress may be due to a chemical, mechanical, thermal, radiation, systemic (dietary, endocrine), or emotional response to any unfavorable stimuli. Selye5 has developed the concept of a “general adaptation syndrome” in response to this alarm reaction. He concludes that the ability of tissue to adapt to changes of stress depends on what he calls “adaptation energy” and that its magnitude appears to depend largely upon genetic factors modified by local factors. Stress has an effect on skeletal bone. The alarm reaction in effect when stress is high causes a complex hormonal series of events. The anterior pituitary gland is stimulated to release adrenocorticotropic hormone (ACTH ) . This causes protein catabolism which interferes with the formation of organic bone matrix. At the same time, stress also causes a decrease in the sex hormones which have a protein anabolic effect. Therefore, a protein balance is lost by a dual effect of stress. Tissues lose their resistance to stress as aging processes occur. An increase in the effect of stress occurs because of a gradual lowering of basal metabolism and of the ability of tissue to regenerate and adapt. This creates a phase of protein catabolism. ENDOCRINE
GLANDS
The endocrine glands have a profound effect on all body functions. Diseases such as diabetes mellitus, Addison’s disease, acromegaly, myxedema, and many others are endocrine disturbances. A discussion of hormonal influences is necessary to understand their effects on bone. Pituitary Glands and Hypophy.sis.-The hypophysis is the master gland of the endocrine system. It is responsible for the production of six hormones that are (1) regulators of growth, (2) controllers of lactation, (3) androgenic, (4) estrogenie, (5) thyrotropic, and (6) adrenocorticotropic. The control of the hypophysis over the endocrine system is complex, and problems of dysfunction require the analysis of an endocrinologist. Such findings are of importance to the dentist because they involve the general health of the patient, which is reflected in the oral cavity.
434
ORTMAN
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Den. 1962
Thyroid Glands.-The thyroid glands are responsible for the regulation of the rate of metabolism. Hyperthyroidism increases the metabolic rate so that a negative nitrogen balance results. Such a balance is *equivalent to protein deficiency, which can be a direct cause of osteoporosis. Thyroxine also has a direct influence on the kidneys, causing an increased excretion of calcium and phosphorus. This depletion of calcium and phosphorus results in decreased bone apposition and increased osteoclastic activity to marshal1 these elements from the bone to compensate for their dep1etion.a Parathyroid Glands.--Basic research is not definite in disclosing the exact mechanism by which the parathyroid hormone regulates the calcium-phosphorus balance in the blood. The chief argument at present is whether the hormone acts as a direct control on the apposition and resorption of bone or primarily on the kidneys by influencing calcium resorption by the tubules. When the parathyroid hormone is injected (hyperparathyroidism), there is an immediate rise in the renal excretion of ph0sphate.s This disturbs the blood calcium :phosphorus ratio by raising the blood serum calcium level. Then, phosphates are called from the bone bank by osteoclastic activity. The parathyroid hormone has another function of maintaining the blood level of the calcium ion. The calcification of bone tissue will be retarded to preserve the blood level of the calcium ion. This is related to the action of vitamin D in an antagonistic manner. Parathormone maintains blood calcium by mobilizing it from the bones by osteoclastic activity. Vitamin D maintains blood calcium by increasing the absorption of calcium from dietary sources in the intestinal tract. Islands of Lange&am. -The failure of these glands to produce sufficient insulin for the proper utilization of glucose causes diabetes mellitus. The high blood sugar with the spillover into the urine is well known. The syndrome of poor healing, low tissue tolerance, and rapid resorption of bone associated with the diabetic patient is recognized, but the instrinsic causative factors are not. The explanation for this syndrome is that, in the absence of insulin, a relative nitrogen starvation occurs from increased gluconeogenesis with the amino acids being diverted from protein synthesis.9 A diabetic controlled by either insulin or diet is not affected by this mechanism. However, perfect control is rarely possible. Therefore, a word of caution and explanation to diabetic patients is necessary so that they can appreciate their prosthetic difficulties. Suprarenal Glands.-The adrenal cortex produces steroid hormones called corticoids. One of these, cortisone, retards osteogenesis.1° It was shown experimentally that administration of ACTH interfered with the healing of bone in rachitic rats whose treatment consisted of administration of calcium and vitamin D. Cortisone and related steroids are antianabolic, may induce the formation of glucose from noncarbohydrates, and may increase the calcium loss by direct effect on calcium excretion. The prolonged use and administration of such steroids are considered very dangerous to bone tissue. The corticoids have some local effects that may be beneficial. One such effect is to control the defense mechanism of inflammation. An example of this action is the improvement of the “denture sore mouth” with the application of 0.05 per cent
z’:K: ‘3”
FACTORS
OF BONE
RESORPTION
OF
RESIDUAL
RIDGE
435
hydrocortisone acetate.12 Related steroids with the same anti-inflammatory action but with less likelihood of systemic effects are available. Gonads.-In general, the sex hormones (androgens and estrogens j promote a protein anabolic action on all tissues including bone. A striking storage of nitrogen and calcium occurred in individuals with postmenopausal or senile osteoporosis in one study when these hormones were administered. I3 More than half of the women over 50 years of age showed roentgenographic evidence of diminishing bone mass in a study by Albright and Reifensteins Postmenopausal osteoporosis is the most common form of this condition. A moderate amount of osteoporosis accompanies senescence because of the “catabolic ascendency” reflected by atrophic and degenerative changes throughout the body.” The aging person produces less and less of the androgens and estrogens, which results in faulty protein metabolism for tissue repair. The bone matrix suffers, and normal bone loss cannot be compensated. The androgens are more effective in nitrogen retention than the estrogens.‘” However, the estrogens stimulate osteoblastic activity.‘” Recent clinical evidence indicates that a combination of both androgens (testosterone j and estrogens is superior therapeutically to either hormone administered alone. A beneficial synergistic effect is obtained without the embarrassing untoward effects of masculinization caused by the androgens when used alone. Methandriol, a weakly virilizing agent, has proved experimentally to have a high protein anabolic effect in relation to the androgenic masculinizing effect. Women under treatment showed no masculinization, yet 80 per cent showed clinical evidence of improvement of osteoporosis. lS Vitamin D and calcium may be given in combination with this treatment. Geriatric problems are increasing and need to be met with understanding. The mental attitude and general sense of well-being of the patient are improved by the carefully considered use of these hormones because the catabolic rate is slowed down by this treatment. Great caution must be exercised in the administration of sex hormones because they may have carcinogenic influences if administration is not carefully controlled. DIETARY
FACTORS
: VITAMINS,
MINERALS,
AND
PROTEIN
Nutritional disturbances are regarded by some as the primary cause of osteoporosis, but most clinicians support the hormonal causative factors.B Gastrointestinal dysfunction, defective alimentation, and glandular insufficiency in the aged person are so intricately interrelated that a single causative factor does not exist. The keystone of bone therapy is a substantial protein metabolism. The synthesis of osteoid tissue in protein-starved people is compromised and calcification is decreased since the protein matrix is embarrassed. Protein may not be available because of inadequate intake, improper assimilation, or excessive loss, as in nephrosis, or because it is utilized as caloric requirements because of hyperthyroidism, uncontrolled diabetes, or a surfeit of adrenocortical hormones from either endogenous or exogenous sources. A diet in which the protein content is less than 10 per cent of the total intake
436
ORTMAN
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Den. 1962
can cause slowed growth of bone .’ Bone apposition cannot keep up with normal osteoclastic activity, and a negative bone factor eaists. Nutritional demands may surpass the appetite and the capability of the patient for mastication. Caloric intake is seldom inadequate, but the intake of essential elements may be deficient. The action of vitamins in many respects is the same as that of hormones. Sicher” states that the relationship of vitamins and hormones can be explained on the basis that the endocrine glands produce intrinsic hormones and the vitamins are extrinsic hormones. Vitawzin A (Carotene).-Experimental avitaminosis A in rats has resulted in the failure of new bone to form as replacement for that lost from normal metabolic activity. The explanation seems to be that extended vitamin A deficiency causes renal damage by hornification of the tubules. This damage results in the abnormal loss of phosphorus as the tubules lose the capacity for reabsorption.2 The imbalance of the calcium :phosphorus ratio leads to osteoporosis. A lowering of vitamin A also has an effect on the osteoblasts so that they engage in disorderly and uncontrolled activity .3 The cells adjacent to the bone modulate to osteoclasts and become active. There is a danger of hypervitaminosis A, but experiments are inconclusive as to the mechanism. Some reports indicate an acceleration of matrix remodeling, while others seem to conclude that excess vitamin A accelerates the activity of the osteoclasts. The general function of vitamin A in regard to bone is its influence on the activity and position of the osteoblasts and osteoclasts. Vitamin B Cow/&x.-The total effect of vitamin B complex seems to be of a regulatory nature. Hypovitaminosis B results in loss of appetite and dietary insufficiency, increase in nervous irritability resulting in lowered resistance to stress, and emotional tension. The total well-being of the individual is impaired. Vitamin B complex deficiency produces effects in bone similar to a protein deficiency. Chase3 reported degeneration of bone, enamel, and dentin in rats on a B complex-deficient diet. Osteoporosis and gingival inflammation were induced in dogs by withdrawal of nicotinic acid. This condition was corrected by addition of this part of the B complex to the diet. Vitankn C.-The effect of vitamin C seems to be clear, conclusive, and dramatic. The only animals sensitive to ascorbic acid deficiency are guinea pigs, monkeys, and man.3 The appearance of scurvy in the bones of all three is similar. The apposition of new bone slows down dramatically because osteoblastic activity is impaired. Experiments have shown that an ascorbutic diet causes a severe bone loss because of adverse effects on the osteoblasts with apparent lack of effect on the osteoclasts. Hence, bone loss is greater than bone apposition. The collagen content of bones is also reduced in vitamin C deficiency. The loosening of teeth in scurvy is due both to bone resorption and to disorganization of the periodontal fibers and membranes. The periosteum is affected in a similar way. It thickens, and the cells appear immature and resemble fibroblasts. This condition may make the periosteum more easily injured by the denture base so that inflammatory processes are triggered by the denture base at lower pressure levels. Endocrine influences affect the vitamin requirements, particularly for vitamin
FACTORS
OF
RONE
RESORI’TIOTU’
OF
RESIDIihL
RIDGE
437
C. For example, l~ypertl~yroidism producctl exl)rril~lentally:~ I)y injection showetl ali increased need of vitamiii C for the collagen content of bone to remain normal. Osteophytes” appear as a result of avitaminosis C. The rapid loss of bone and the increased inflammation of the mucoperiosteum cause the development of these bony outgrowths. v;tuGz L).-Vitamin D is necessary for the calcium-phosphorus balance to remain within tolerable limits. Vitamin D would be unnecessary if the exact required ratio of calcium and phosphorus were available in the diet. A pure vitamin ‘D deficiency rachitic condition does not exist3 but is only related to the calcium-phosphorus balance in the diet and the activity of the parathyroid glands. When bone loses its ability to calcify the matrix, administration of vitamin D will cause calcification and denser bone. The dosage of this vitamin is important and its requirements obscure. Moderate overdosage causes excessively mineralized bone, but gross overdosage causes bone resorption. VitmGzs E and K.-No direct bone changes have been found from the effects of vitamins E and K. However, their actions are related to protein metabolism, which could indirectly have some side effects on bone. iLlinerals.-The inclusion of adequate calcium and phosphorus in the diet is a necessity because the prime mineralizing substance of bone is calcium phosphate. Studies on osteoporotic patients indicated that they had a significantly low intake of calcium in the diet as compared to normal individuals.16 Individual calcium requirements were shown to vary widely, with a higher requirement for patients who develop osteoporosis. The efficacy of a high dietary calcium treatment as a method of replacing lost calcium is being tested. However, a hartnful effect of more than a modest calcium intake may be the formation of kidney and bladder stones. Other minerals are suspected to be important, but little research has been done on their relation to bone metabolism. A copper deficiency has produced osteoporosis in dogs. l3 Strontium administered in lactate form increases the production of osteoid tissue and aids its mineralization.6 AZbuvnin.--Intravenous albumin in treatment of osteoporosis produced a rise in the serum level of calcium and a decrease in urinary excretion of potassium, phosphorus, and calcium.8 The effects are similar to the action of estrogen. Also, albumin serves as an important building block for bone matrix.17 ReifensteinlO has suggested that the use of albumin in conjunction with steroid therapy would increase the rate of bone formation and control bone loss. OTIIER
CONSIDERATIONS
CONCERNING
RESORPTTON
Lammielh has proposed a hypothesis for the mechanism of ridge reduction based on the molding of the bony ridge by the external molding force of the atrophying oral mucosa. This hypothesis explains some of the changes observed in ridge contour where surgical operation has created a wound that is bound and closed by contracting mucosa. Perhaps it can explain some of the changes of disuse atrophy, but it is difficult to attribute the entire change that occurs over a period of years to a single molding force of the mucosa. The force of the tnucosa is apparently
438
ORTMAN
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contradicted by the existence of exostosed areas in which the tissue is very tight and also avascular. In some edentulous mouths, extensive bone resorption has occurred in regions not covered with denture bases. The soft tissues are lose and folded over the residual ridge crest even though no hypertrophy due to inflammatory processes has taken place. Here it is difficult to explain the dramatic loss of bone by force from the atrophying mucosa. In instances in which a denture has been worn and hyperplastic tissue has replaced the lost bone to satisfy the denture contour, it is difficult to attribute a molding force to such loose, pendulous tissue. Resorption continues as the soft tissue hypertrophies. The concept that roentgenographic examination can be used as an index to future bone lose has been proposed by Sobolik .19 He states that “the rapidity of bone resorption is in inverse proportion to the uniformity of the density of the alveolar support.” In other words, dense alveolar bone as determined roentgenographically provides good foundational possibilities. In contrast, Applegate20 points out that less dense bone is less likely to show unfavorable change after the insertion of a denture base than more dense bone. His explanation is that a less highly calcified bone or a less dense bone is more organic in structure and is more conducive to a normal rate of bone maintenance because its rebuilding would be facilitated. The apparent density of bone varies with the roentgenographic technique. Relative density may vary greatly within patients whose bone stability has been good over a period of years. Therefore, roentgenographic evaluation of bone relative to its stability is unreliable. ROLE
OF THE
DENTURE
BASE
IN
RESORPTION
Available evidence is inconclusive and seems to indicate that a denture base may act either to retard or to hasten the process of bone resorption. There is no question that a residual ridge will gradually resorb after the extraction of the teeth caused by disuse atrophy and aging. The rate of change is under the influence of the remaining functional stimuli, the altered blood supply, and the body chemistry as affected by nutritional, hormonal, and emotional factors. A discussion of the effects of the denture base on resorption at present must be limited to its local effects on the supporting tissues. Fundamentally, the wearing of a denture is physiologically incompatible with the function of the ridge tissues. Nowhere in Nature’s design has pressure been directed upon bone through vascular tissue as is imposed by the prosthetic base. How well the tissues will tolerate this pressure depends upon many factors. If the mechanical factors designed into the denture by the impressions, jaw relation records, and occlusion are controlled so that pressures remain within tissue tolerance, the denture base should not contribute to a more rapid rate of resorption. Indeed, if the action of the base is favorably controlled in its adaptation to the tissues and its directed force, it could provide stimuli that retard resorptive processes. The denture base can seem to trigger the dramatic loss of bone, but the stage
Volume Number
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BONE
RESORPTION
OF
RESIDUAL
RIDGE
439
has to be properly set. Dentures seemingly perfect in tissue coverage and adaptation, jaw relations, and occlusion may fail in a short period of time because of rapid bone resorption. In contrast, dentures that are inadequate in many respects are worn, and the ridges remain apparently normal. Is it possible that ridge resorption can be completely controlled by denture procedures? The answer appears to be negative.
1. Resorption of bone is a normal process. Its balance to bone apposition may be either physiologic or pathologic and is dependent upon multiple factors. 2. Treatment of rapid (pathologic) resorption is difficult because the multiple factors are interrelated and it is impossible to evaluate clinically or roentgenographically the precise part played by each. 3. A normal bone picture requires that all known body fluids and elements, both intrinsic and extrinsic, are in proper harmony and composition. 4. When bone loss is rapid and abnormal in the residual ridges, evidence of general skeletal osteoporosis is also present. This acquits the denture base from being the sole cause in abnormal resorption. 5. Disuse atrophy occurs in the edentulous mouth whether or not a denture is worn. 6. Pressure of a denture base on the bone of the residual ridge is a violation to the natural way that bone receives pressure because it is transmitted through vascular tissue. If the pressure does not alter the blood supply to the embarrassment of the bone or cause inflammation of the mucoperiosteum so that it becomes a causative factor of resorption by creating capillary pressure, the denture base could provide stimuli for reduced resorption. 7. Stress, regardless of its cause, always produces an alarm reaction which increases the rate of bone resorption. 8. Dysfunction of the endocrine glands causes an obscure but drastic effect on the rate of bone replacement, the organic matrix, and the rate of bone resorption. Hormonal or plurihormonal administration offers great possibility for control of resorption. 9. Many people are deficient in nutritional requirements necessary for the normal metabolism of bone. Vitamins, minerals, and proteins demands have potential beneficial effects when properly oriented in the diet. A panvitamin program has prophylactic value. Adequate mineral intake must be assured for a normal bone picture. Protein is the most important nutritional factor in its effect on bone. An edentulous condition necessitat’es the protection of a high protein-low carbohydrate diet. 10. The factors influencing bone resorption in young adults are primarily those of traumatic and inflammatory nature, with pressure, tension, stress, and nutrition playing the dominant part. Control of resorption for this age group can be managed effectively by sound prosthetic procedures and adequate dietary measures. 11. As the edentulous patient ages, the geriatric problems of lower protein
440
ORTMAN
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Den. 1962
metabolism, lower resistance to stress, alimentary failure, and endocrine complications come into the picture and management becomes more complex. CONCLUSIONS
The advances made in the basic sciences are providing a broader base for the understanding and management of the foundation of bone. If we can analyze and relate the progress made in basic research to dentistry, a more competent and complete health service will be available to our patients. In this way, more and more general health problems will come to the attention of our profession. Some of the health problems will need the attention of the physician who will appreciate that his cooperation is necessary for the dental future of the edentulous patient. The dentist should be prepared to extend the limit of his treatment, treat within his ability, and refer when it goes beyond his field, but, above all, know which is which. It does not seem a nebulous hope that some day there will be control over bone resorption as there is over rickets, endemic goiter, scurvy, beri-beri, and other diseases. REFERENCES
Boucher, C. 0.: h:Weinm;:;m.F&
Current Status of Prosthodontics, J. PROS. DE?. 10:411-425, 1960. and Sicher, H.: Bone and Bones, ed. 2, St. Louis, 1955, The C. V. Mosby
3. Irving, J. T.: A Comparison of the Influences of Hormones, Vitamins and Other Dietary Factors on Bone, Dentin, and Enamel, Vitamins & Hormones 15:291-323, 1957. 4. Sante, hcR; F’rples of Roentenological Interpretation, Ann Arbor, 1957, Edwards Bros., Selye, H. I’ Stress, Montreal, 1950, Acta Inc. Medical Publishers. Schecter, D. C.: Current Concepts in the Management of Osteoporosis, J. Am. Geriatrics Sot. 6:592-613, 1958. 7. Dietrich, J. E., Whedon, G. D:, and Shorr, E.: Effects of Immobilization Upon Various Metabolic and Physiological Functions of Normal Men, Am. J. Med. 4:3, 1948. 8. Albright, F., and Reifenstein, E. C., Jr.: The Parathyroid Glands and Metabolic Bone Disease, Baltimore, 1948,. Williams and Wilkins Company, p. 145. 9. Cecil, F.6i4: Textbook of Medlcme, ed. 4, Philadelphia, 1939, W. B. Saunders Company, i:
10. Reifenstein, ‘E. C., Jr.: The Relationship of Steroid Hormones to Development and Management of Osteoporosis in Aging People, Clin. Osteop. 10:206-253, 1957. Follis, R. H., Jr. : Osteoporosis, Bull. Rheumat. Dis. 4:52, 1954. :; Collett, H. A.: Oral Conditions Associated With Dentures, J. PROS. DEN. 8:591-599, 1958. 13: Gardner, A. F.: Management of Osteoporosis-Modern Concepts, Am. Pratt. & Digest Treat. 9:767-769, 1959. 14. Banhart, R. E.: A Clmical Evaluation of Methyl Androstenediol in Treatment of Osteoporosis, Am. Pratt. & Digest Treat. 5:964, 1954. 15. Gordan, G. S., Eisenberg, M., Moon, H. D., and Sakamoto, W.: Methylandrostenediol-A Protein Anabolic Steroid With Little Androgenic Activity, J. Clin. Endocrinol. 11: 209-212, 1951. 16. Whedon, G. D.: Calcium Needs of Adults and Older People, Nutrition Neys 23:1, 1960. 17. Emerson, K., Jr., and Beckman, W. W.: Calcium Metabolism in Nephrosis, J. Clin. Invest. 24:564, 1945. Lammie, G. A.: Reduction of the Edentulous Ridges, J. PROS. DEN. 10:605-611, 1960. :; Sobolik, C. F.: Alveolar Bone Resorption, J. PROS. DEN. 10:612-619, 1960. 20: Applegate, 0. C.: An Evaluation of the Support for the Removable Partial Denture, J. PROS. DEN. 10:112-123, 1960. UNIVERSITY OF BUFFALO SCHOOL OF DENTISTRY 3435 MAIN ST. BUFFALO, N. Y.