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Oral roentgenographic findings in osteitis fibrosa generalisata associated with chronic renal disease
Oral roentgenographic findings in osteitis fibrosa generalisata associated with chronic renal disease Robert F. Walsh, D.D.X.,” and Xortimer Bronx, N. Y. VETERAN5
ADMINISTRATION
Kamniol, D.D.S.,‘K’*
HOSPITAL
P
atients who have long-standing, severe, chronic renal insufficiency with azotemia may exhibit demineralizing changes in the skeletal system.l These changes have been called renal ost,eitis fibrosa gencralisata, and they are indistinguishable, roentgenogra,phically and histologically, from those seen in the osteitis fibrosa that may accompany primary hyperparathyroidism.’ While it is known that the parathyroid glands undergo hyperplasia in the course of chronic renal disease, it is by no means certain that, the demineralizing skeletal changes accompanying this disease are produced by this “secondary hpperparathyroidism.“l ROENTGENOGRAPHIC
FINDINGS
Osteitis fibrosa generalisata is a metabolic bone disease characterized by an increased rate of bone resorption. Hence, the entire skeleton is affected by this demineralization, resulting in a generalized reduction in radiographic density, Subperiosteal bone resorption, most readily seen along the margins of the middle phalanges, is the most important and dependable roentgenographic evidence of osteitis fibrosa. Loss of the lamins dura is a frequently sought radiographic sign of osteitis fibrosa; this is another instance of subperiosteal resorption, since the periodontal membrane is a specialized periosteum. In addition, the normal trabecular pattern is altered and the trabeculae appear indistinct, often producing a ground-glass appearance. Although osteitis fibrosa is a generalized skeletal disorder, the radiographic changes are more evident in some bones than in others. The skull often takes on *Assistant Chief, Dental **Chief, Dental Service.
Service.
273
a characteristic mot&d or ground-glass appearance. Circumscribed ra(liolucentics or “cysts” may occur in t,h(b ton g bones ant1 the jaws. These cysts, however, are rare in renal osteitis fibrosa gencra1isata.l Intraora,l radiographs of osteitis fibrosa gencralisata reveal a generalized radiolucency with blurring of the normal twabecular pattern. Depending on thr severity of the disease, the lamina dura may be partially or completely absent. Anatomic landmarks, such as the mental foramen, the mandibular canal, and the floor of the maxillary sinus, may become indistinct. The cortical bone of thr alveolar crest and the inferior border of the mandible may appear thinned or absent. Xultiple radiolucencies or “cysts,” not associated with tooth apices, may be seen in severe cases of ostcitis fibrosa gencralisata due to primary hypcrparathyroidism. These arc evidence of gross rcplacemcnt of bone by soft tissue.” The teeth themselves are nnaffeetcd hp the generalized denrincrwlization. However, they may appear to be more radiopaque t,han normal as a result of the loss of adjacent lamina durn and the decreased density of the surrounding bone. For the sarnc reasons, the roots of the teeth may also give the illusion of being spindle shapetLt PATHOGENEM
Osteitis fibrosa generalisata may occur in primary hyperparathyroidism as well as in chronic severe azotemie renal disease. In primary hypcrparathyroidism, the bone disease, when it occurs, is ascribed to the increased amounts of parathormone present. In chronic azotemic renal disease, both the excess hormone produced by the secondary parathyroid hyperplasia and the accompanying metabolic abnormalities hare been implicated as the cause of the identical bone changes.1 Primary
hyperparathyroidism
In primary hyperparathyroidism, there is an overproduction of hormone as a result of adenoma, primary hyperplasia, or carcinoma of the parathyroid glands. The excess hormone causes a phosphate diuresis by decreasing t,he renal tubular reabsorption of inorganic phosphorus. As a result, the serum phosphorus level falls, causing a, relative undersaturation in the extracellular fluids with regard to the normal solnbility product of calcium and phosphorus ions. The ion product is restored to the normal saturation of the solubility product by the addition of more calcium ions. The additional calicum is obtained from the diet or, where dietary intake is insufficient, from the skeleton. In the latter instance, osteitis fibrosa generalisata results. However, the ingestion of as little as one gra.m of calcium daily (equivalent to that contained in one quart of milk) can prevent skeletal demineralization even in t,he presence of severe parathyroid hyperfunction. The elevated serum calcium level that results from this mobilization of calcium from the diet or the skeleton produces a hypercalciuria. The serum alkaline phosphatase is elevated where there is bone demineralization.” A direct effect of parathormone on bone has been demonstrated. However, this effect, if it were always operable, would not explain the many cases of primary hyperparathyroidism without bone change8.l
Volume 28 ITumber 2
Osteitis
fibrosa
generai’imta
rind
renal
disease
275
Primary hyperpa,rathyroidism, unless effectively treated, may lead to renal lithiasis, nephrocalcinosis, and eventually severe renal impairment. This renal dysfunction may result in a rise in serum phosphorus, a fall in serum calcium, and a fall in urinary calcium, so that the biochemical signs become more difficult, to interpret.l Chronic
renal
disease
Chronic azotemic renal disease is marked by a rise in the serum phosphorus level, which is caused by the inability of the kidney to excrete phosphorus. This results in a tendency to a low serum calcium level in order to sat.isfy the calciumphosphorus solubility product relationship. Since hypocalcemia and/or hyperphosphst’emia are stimuli for increased parathyroid hormone production, the parathyroid glands undergo hyperplasia ; hence, we have a “secondary hyperparathyroidism. ’ ‘2, G At the same time, other metabolic abnormalities occur in renal failure and result in a severe acidosis. Renal osteitis fibrosa generalisata is thought by some to be t.he result of this continuous state of acidosis rather than the result of the increased parathormone level produced by the secondary parathyroid hyperplasia.5 Biochemical signs are a low or normal serum calcium, elevated serum phosphorus, and elevated serum alkaline phosphatase. CASE
REPORTS
In the two ca.ses of long-sta.nding azotemic renal disease which follow, there were striking radiographic changes in the jaws. In the first case, the bone changes were the result of primary renal disease. The second case illustrates the difficulty sometimes encountered in determining whether the bone changes are the result of primary hyperparathyroidism or of primary azotemic renal disease. Regardless of the etiology, the bone disease produced is osteitis fibrosa generalisata. CASE
1
A 35.year-old white man with a 16.year history of progressive renal disease was admitted to the Veterans Administration Hospital, Bronx, New York, for inclusion in the renal dialysis program. The serum calcium level ranged from 8 to 10 mg. per cent and t.he serum phosphorus level from 10 to 16.6 mg. per cent. The blood urea nitrogen level had been as high as 232 mg. per cent, but fell to 73 after repeated dialyses. A skeletal survey at this time revealed a granular appearance of the skull with small radio-lucencies intermingled with areas of increased density, subperiosteal erosion of the proximal and middle phalanges and of the ribs, and calcification of the femoral vessels. It was concluded that the bone changes were the result of the azotemic renal disease (renal osteitis fibrosa generalisata). Fig. 1 shows the intraoral radiographs of this patient. CASE 2
A 44.year-old white man with an l&year history of renal disease and a 13.year history of hypertension was admitted to this hospital with azotemia (blood urea nitrogen, I40 to 194 mg. per cent) and slight acidosis. The serum calcium level ranged from 10 to 12 mg. per cent, and the serum phosphorus level ranged between 10 and 17 mg. per cent. Numerous metastatic calcifications, band keratopathy, subperiosteal resorption in the hands, and a very high parathormone level were found. In addition, the clavicles mere demineralized and deformed. There was some question as to whether this represented (1) primary hyperparathyroidism with secondary renal failure due to nephrocalcinosis or (2) chronic azotemie
276
OS., OX & O.P. Auguust~, 1969
Volume 28 Number 2
Osteitis
fibrosa
generalisa~ta
0:nd renal
&se ‘ase
277
O.S., O.M. & O.P. August, 1969 renal disease with secondzcry parathyroitl hyperplasia. Surgical exploration revealed two large parathyroid glands, xv-hich were rcmovwl and were found to be hyperplastic on histologic examination. It was tentatively c~~ncluclcd that the pnrathyroid hpperplasia was sccondnry to the chronic renal discnse. Since remission of symptoms was only temporary following the surgical procedure and was followed by severe elevation of the parat~hormone level, along with crippling metastatic. calcifications, the patient underwent further surgical exploration 22 months later, at which time a large parathyroid adenoma wu removed. This finding tended to support a diagnosis rather t,lmn the previous of primary hyperparathyroidism with secondary renal failure, impression of parathyroid hyperplasia secondary to chronic renal disease. Fig. 2 sl~ows this patient’s intraoral radiographs. Intraoral
radiographs
The most notable feature of the x-ray series of both patients (Figs. 1 and 2) is the generalized radiolucency of the jaws. The bone appears more homogeneous
Fig. 3. Case 1. Maxillary canine area illustrating ground-glass appearance of lamma dura, absence of radiopaque alveolar crestal border, and floor of sinus.
Fig. 4. Case 2. Mandibular molar area demonstrating usually denotes inferior border of mandible.
absence of radiopaque
of
bone, 10s~
zone
which
Volume Number
28 2
Pig. 5. Case 1. Mandibular
Fig.
6. Case 1. Mandibular
Osteitis
fibrosa
molar region
showing
generalis&.
irregular
canine area demonstrating
and
radioluccnt
widened,
rcna,l
disease
279
areas.
irregular
nutrient
canal.
than normal as a result of alteration of the trabecular pattern ; the fine lacelike trabeculae produce a ground-glass appearance. Closer inspection reveals complete loss of the lamina dura. The floors of the maxillary sinuses, which usually appear as thin, sharply defined, radiopaque lines, are fuzzy and indistinct. The radiopaque zone that normally denotes the cortical bone of the alveolar crest is absent (Fig. 3). Similarly, the mandibular canals and mental foramina cannot be seen. The enlarged reproduction of the right mandibular molar area in Case 2 (Fig. 4) demonstrates loss of the wide radiopaque zone which is normally characteristic of the inferior border of the mandible. The median maxillary suture appears as an unusually broad radiolucent zone.
In addit,ion, the radiographs of Case 1 (Vi g. 1) reveal many small, irregular radioluccnt. areas (for esamplc, in the right. maxillary and mandibular molar regions) which are evidence of gross boric resorption. An enlargement, of one of these areas is shown in Fig. 5. The nutrient canals appear wider than normal and have irregular margins. This is particularly evident in the mandibular incisor-canine area (Figs. 1 and 6). DISCUSSION
The demineralizing skeletal changes of osteitis fibrosa generalisata may be produced by primary hyperparathyroidism and by chronic azotemic renal diease. It is sometimes difficult to determine whether the ost,eitis fibrosa generalisata in a uremic patient is the result of primary hyperparathyroidism with secondary renal failure or is primarily due to the azotemic renal diseasc7 Primary hyperparathyroidism is marked by an eleva.ted serum calcium level and a lowered serum phosphorus level, while azotemic renal disease is accompanied by a low or normal serum calcium and an elevated serum phosphorus. The appearance of secondary renal failure as a complication of primary hyperparathyroidism blurs this distinction by causing a fall in serum calcium and a rise in serum phospl1orus.l The osteitis fibross generalisata of primary hyperparathyroidism is generally held to be caused by the increased parathormone level. It has been thought by some investigators that renal osteitis fibrosa generalisata is also produced by excess parathormone, since chronic renal disease is almost invariably accompanied by secondary hyperplasia of the parathyroid glands; hence, the name Others, however, believe that renal osteitis seconfhy hyperpa.rathyroidism. fibrosa generalisata is the result of the disordered metabolism of chronic renal disease, particularly the severe, long-standing acidosis.” Loss of lamina dura occurs not only in the osteitis fibrosa generalisata of primary hyperparathyroidism and chronic azotemic renal disease, but. it may also occur in Paget’s disease, osteomalacia, fibrous dysplasia., sprue, and Cushing’s syndrome. Thereforc, the absence of lamina dura as a diagnostic sign of osteitis fibrosa becomes more reliable when considered in conjunction with the other altered changes in the surrounding bone, namely, generalized radiolucency, trabecular pattern, and loss of anat,omic landmarks.” It should be emphasized that the early stages of the disorder may be detected histologically without the presence of definitive radiographic changes ; dependable radiographic evidence of bone disease appears only after approximately 30 per cent of the mineral salts have been lost.” A technique for determination of parathyroid hormone level by radioimmunoassay has been developed.R This may become a valuable diagnostic tool, since it gives a direct measurement of parathyroid gla,nd activity. SUMMARY
Two cases demonstrating the oral roentgenographic changes in osteitis fibrosa generalisata associated with chronic azotemic renal disease have been presented. The oral radiographs demonstrated the characteristic changes of osteitis fibrosa,
Volume Number
28 2
Osteitis
fibrosa
generalisata
and renal disease
281
including generalized demineralization, altered trabecular pattern, loss of lamina dura, and blurring of bony anatomic landmarks. The cause of the bone changes in renal osteitis fibrosa generalisata was discussed with reference to parathyroid fun&on and the disordered metabolism of chronic azotcmic renal disease. REFERENCES
1. Cecil, R. L., and Loeb, R. F.: A Textbook of Medicine, ed. 11, Philadelphia, 1963, W. B. Saunders Company, pp. 814-819, 1434-1436, 1505-1507. Glands and Metabolic Bone 2. Albright, F., and Riefenstein, E. C., Jr.: The Parathyroid Disease (Selected Studies), Baltimore, 1948, Williams & Wilkins Company, pp. 115116. 3. Pugh, D. G.: Roentgenographie Diagnosis of Disease of Bone, New York, 1951, Thomas Nelson & Sons, pp. 19-26. 4. Stafne, E. C.: Oral Roentgenographic Diagnosis, ed. 2, Philaclelphia, 1963, W. B. Saunders Company, pp. 263-264. 5. Williams, R. H.: Textbook of Endocrinology, ed. 2, Philadelphia, 1955, W. B. Saunders Company, pp. 483-576. 6. Black, B. Marden: Hyperparathyroidism, Springfield, Ill., 1953, Charles C Thomas, Publisher, pp. 43-47. 7. Schreiner, G. E., and Maher, J. F. : Uremia: Biochemistry, Pathogenesis Treatment, Springfield, Ill., 1961, Charles C Thomas, Publisher, pp. 348-353. 8. Berson, S. A., Yalow, R. S., Aurbach, G. D., and Potts, J. T., Jr.: Immunoassay of Bovine and Human Parathyroid Hormone, Proc. Nat. Aead. SC. 49: 613.617, 1963.
ADMINISTRATION
Kamniol, D.D.S.,‘K’*
HOSPITAL
P
atients who have long-standing, severe, chronic renal insufficiency with azotemia may exhibit demineralizing changes in the skeletal system.l These changes have been called renal ost,eitis fibrosa gencralisata, and they are indistinguishable, roentgenogra,phically and histologically, from those seen in the osteitis fibrosa that may accompany primary hyperparathyroidism.’ While it is known that the parathyroid glands undergo hyperplasia in the course of chronic renal disease, it is by no means certain that, the demineralizing skeletal changes accompanying this disease are produced by this “secondary hpperparathyroidism.“l ROENTGENOGRAPHIC
FINDINGS
Osteitis fibrosa generalisata is a metabolic bone disease characterized by an increased rate of bone resorption. Hence, the entire skeleton is affected by this demineralization, resulting in a generalized reduction in radiographic density, Subperiosteal bone resorption, most readily seen along the margins of the middle phalanges, is the most important and dependable roentgenographic evidence of osteitis fibrosa. Loss of the lamins dura is a frequently sought radiographic sign of osteitis fibrosa; this is another instance of subperiosteal resorption, since the periodontal membrane is a specialized periosteum. In addition, the normal trabecular pattern is altered and the trabeculae appear indistinct, often producing a ground-glass appearance. Although osteitis fibrosa is a generalized skeletal disorder, the radiographic changes are more evident in some bones than in others. The skull often takes on *Assistant Chief, Dental **Chief, Dental Service.
Service.
273
a characteristic mot&d or ground-glass appearance. Circumscribed ra(liolucentics or “cysts” may occur in t,h(b ton g bones ant1 the jaws. These cysts, however, are rare in renal osteitis fibrosa gencra1isata.l Intraora,l radiographs of osteitis fibrosa gencralisata reveal a generalized radiolucency with blurring of the normal twabecular pattern. Depending on thr severity of the disease, the lamina dura may be partially or completely absent. Anatomic landmarks, such as the mental foramen, the mandibular canal, and the floor of the maxillary sinus, may become indistinct. The cortical bone of thr alveolar crest and the inferior border of the mandible may appear thinned or absent. Xultiple radiolucencies or “cysts,” not associated with tooth apices, may be seen in severe cases of ostcitis fibrosa gencralisata due to primary hypcrparathyroidism. These arc evidence of gross rcplacemcnt of bone by soft tissue.” The teeth themselves are nnaffeetcd hp the generalized denrincrwlization. However, they may appear to be more radiopaque t,han normal as a result of the loss of adjacent lamina durn and the decreased density of the surrounding bone. For the sarnc reasons, the roots of the teeth may also give the illusion of being spindle shapetLt PATHOGENEM
Osteitis fibrosa generalisata may occur in primary hyperparathyroidism as well as in chronic severe azotemie renal disease. In primary hypcrparathyroidism, the bone disease, when it occurs, is ascribed to the increased amounts of parathormone present. In chronic azotemic renal disease, both the excess hormone produced by the secondary parathyroid hyperplasia and the accompanying metabolic abnormalities hare been implicated as the cause of the identical bone changes.1 Primary
hyperparathyroidism
In primary hyperparathyroidism, there is an overproduction of hormone as a result of adenoma, primary hyperplasia, or carcinoma of the parathyroid glands. The excess hormone causes a phosphate diuresis by decreasing t,he renal tubular reabsorption of inorganic phosphorus. As a result, the serum phosphorus level falls, causing a, relative undersaturation in the extracellular fluids with regard to the normal solnbility product of calcium and phosphorus ions. The ion product is restored to the normal saturation of the solubility product by the addition of more calcium ions. The additional calicum is obtained from the diet or, where dietary intake is insufficient, from the skeleton. In the latter instance, osteitis fibrosa generalisata results. However, the ingestion of as little as one gra.m of calcium daily (equivalent to that contained in one quart of milk) can prevent skeletal demineralization even in t,he presence of severe parathyroid hyperfunction. The elevated serum calcium level that results from this mobilization of calcium from the diet or the skeleton produces a hypercalciuria. The serum alkaline phosphatase is elevated where there is bone demineralization.” A direct effect of parathormone on bone has been demonstrated. However, this effect, if it were always operable, would not explain the many cases of primary hyperparathyroidism without bone change8.l
Volume 28 ITumber 2
Osteitis
fibrosa
generai’imta
rind
renal
disease
275
Primary hyperpa,rathyroidism, unless effectively treated, may lead to renal lithiasis, nephrocalcinosis, and eventually severe renal impairment. This renal dysfunction may result in a rise in serum phosphorus, a fall in serum calcium, and a fall in urinary calcium, so that the biochemical signs become more difficult, to interpret.l Chronic
renal
disease
Chronic azotemic renal disease is marked by a rise in the serum phosphorus level, which is caused by the inability of the kidney to excrete phosphorus. This results in a tendency to a low serum calcium level in order to sat.isfy the calciumphosphorus solubility product relationship. Since hypocalcemia and/or hyperphosphst’emia are stimuli for increased parathyroid hormone production, the parathyroid glands undergo hyperplasia ; hence, we have a “secondary hyperparathyroidism. ’ ‘2, G At the same time, other metabolic abnormalities occur in renal failure and result in a severe acidosis. Renal osteitis fibrosa generalisata is thought by some to be t.he result of this continuous state of acidosis rather than the result of the increased parathormone level produced by the secondary parathyroid hyperplasia.5 Biochemical signs are a low or normal serum calcium, elevated serum phosphorus, and elevated serum alkaline phosphatase. CASE
REPORTS
In the two ca.ses of long-sta.nding azotemic renal disease which follow, there were striking radiographic changes in the jaws. In the first case, the bone changes were the result of primary renal disease. The second case illustrates the difficulty sometimes encountered in determining whether the bone changes are the result of primary hyperparathyroidism or of primary azotemic renal disease. Regardless of the etiology, the bone disease produced is osteitis fibrosa generalisata. CASE
1
A 35.year-old white man with a 16.year history of progressive renal disease was admitted to the Veterans Administration Hospital, Bronx, New York, for inclusion in the renal dialysis program. The serum calcium level ranged from 8 to 10 mg. per cent and t.he serum phosphorus level from 10 to 16.6 mg. per cent. The blood urea nitrogen level had been as high as 232 mg. per cent, but fell to 73 after repeated dialyses. A skeletal survey at this time revealed a granular appearance of the skull with small radio-lucencies intermingled with areas of increased density, subperiosteal erosion of the proximal and middle phalanges and of the ribs, and calcification of the femoral vessels. It was concluded that the bone changes were the result of the azotemic renal disease (renal osteitis fibrosa generalisata). Fig. 1 shows the intraoral radiographs of this patient. CASE 2
A 44.year-old white man with an l&year history of renal disease and a 13.year history of hypertension was admitted to this hospital with azotemia (blood urea nitrogen, I40 to 194 mg. per cent) and slight acidosis. The serum calcium level ranged from 10 to 12 mg. per cent, and the serum phosphorus level ranged between 10 and 17 mg. per cent. Numerous metastatic calcifications, band keratopathy, subperiosteal resorption in the hands, and a very high parathormone level were found. In addition, the clavicles mere demineralized and deformed. There was some question as to whether this represented (1) primary hyperparathyroidism with secondary renal failure due to nephrocalcinosis or (2) chronic azotemie
276
OS., OX & O.P. Auguust~, 1969
Volume 28 Number 2
Osteitis
fibrosa
generalisa~ta
0:nd renal
&se ‘ase
277
O.S., O.M. & O.P. August, 1969 renal disease with secondzcry parathyroitl hyperplasia. Surgical exploration revealed two large parathyroid glands, xv-hich were rcmovwl and were found to be hyperplastic on histologic examination. It was tentatively c~~ncluclcd that the pnrathyroid hpperplasia was sccondnry to the chronic renal discnse. Since remission of symptoms was only temporary following the surgical procedure and was followed by severe elevation of the parat~hormone level, along with crippling metastatic. calcifications, the patient underwent further surgical exploration 22 months later, at which time a large parathyroid adenoma wu removed. This finding tended to support a diagnosis rather t,lmn the previous of primary hyperparathyroidism with secondary renal failure, impression of parathyroid hyperplasia secondary to chronic renal disease. Fig. 2 sl~ows this patient’s intraoral radiographs. Intraoral
radiographs
The most notable feature of the x-ray series of both patients (Figs. 1 and 2) is the generalized radiolucency of the jaws. The bone appears more homogeneous
Fig. 3. Case 1. Maxillary canine area illustrating ground-glass appearance of lamma dura, absence of radiopaque alveolar crestal border, and floor of sinus.
Fig. 4. Case 2. Mandibular molar area demonstrating usually denotes inferior border of mandible.
absence of radiopaque
of
bone, 10s~
zone
which
Volume Number
28 2
Pig. 5. Case 1. Mandibular
Fig.
6. Case 1. Mandibular
Osteitis
fibrosa
molar region
showing
generalis&.
irregular
canine area demonstrating
and
radioluccnt
widened,
rcna,l
disease
279
areas.
irregular
nutrient
canal.
than normal as a result of alteration of the trabecular pattern ; the fine lacelike trabeculae produce a ground-glass appearance. Closer inspection reveals complete loss of the lamina dura. The floors of the maxillary sinuses, which usually appear as thin, sharply defined, radiopaque lines, are fuzzy and indistinct. The radiopaque zone that normally denotes the cortical bone of the alveolar crest is absent (Fig. 3). Similarly, the mandibular canals and mental foramina cannot be seen. The enlarged reproduction of the right mandibular molar area in Case 2 (Fig. 4) demonstrates loss of the wide radiopaque zone which is normally characteristic of the inferior border of the mandible. The median maxillary suture appears as an unusually broad radiolucent zone.
In addit,ion, the radiographs of Case 1 (Vi g. 1) reveal many small, irregular radioluccnt. areas (for esamplc, in the right. maxillary and mandibular molar regions) which are evidence of gross boric resorption. An enlargement, of one of these areas is shown in Fig. 5. The nutrient canals appear wider than normal and have irregular margins. This is particularly evident in the mandibular incisor-canine area (Figs. 1 and 6). DISCUSSION
The demineralizing skeletal changes of osteitis fibrosa generalisata may be produced by primary hyperparathyroidism and by chronic azotemic renal diease. It is sometimes difficult to determine whether the ost,eitis fibrosa generalisata in a uremic patient is the result of primary hyperparathyroidism with secondary renal failure or is primarily due to the azotemic renal diseasc7 Primary hyperparathyroidism is marked by an eleva.ted serum calcium level and a lowered serum phosphorus level, while azotemic renal disease is accompanied by a low or normal serum calcium and an elevated serum phosphorus. The appearance of secondary renal failure as a complication of primary hyperparathyroidism blurs this distinction by causing a fall in serum calcium and a rise in serum phospl1orus.l The osteitis fibross generalisata of primary hyperparathyroidism is generally held to be caused by the increased parathormone level. It has been thought by some investigators that renal osteitis fibrosa generalisata is also produced by excess parathormone, since chronic renal disease is almost invariably accompanied by secondary hyperplasia of the parathyroid glands; hence, the name Others, however, believe that renal osteitis seconfhy hyperpa.rathyroidism. fibrosa generalisata is the result of the disordered metabolism of chronic renal disease, particularly the severe, long-standing acidosis.” Loss of lamina dura occurs not only in the osteitis fibrosa generalisata of primary hyperparathyroidism and chronic azotemic renal disease, but. it may also occur in Paget’s disease, osteomalacia, fibrous dysplasia., sprue, and Cushing’s syndrome. Thereforc, the absence of lamina dura as a diagnostic sign of osteitis fibrosa becomes more reliable when considered in conjunction with the other altered changes in the surrounding bone, namely, generalized radiolucency, trabecular pattern, and loss of anat,omic landmarks.” It should be emphasized that the early stages of the disorder may be detected histologically without the presence of definitive radiographic changes ; dependable radiographic evidence of bone disease appears only after approximately 30 per cent of the mineral salts have been lost.” A technique for determination of parathyroid hormone level by radioimmunoassay has been developed.R This may become a valuable diagnostic tool, since it gives a direct measurement of parathyroid gla,nd activity. SUMMARY
Two cases demonstrating the oral roentgenographic changes in osteitis fibrosa generalisata associated with chronic azotemic renal disease have been presented. The oral radiographs demonstrated the characteristic changes of osteitis fibrosa,
Volume Number
28 2
Osteitis
fibrosa
generalisata
and renal disease
281
including generalized demineralization, altered trabecular pattern, loss of lamina dura, and blurring of bony anatomic landmarks. The cause of the bone changes in renal osteitis fibrosa generalisata was discussed with reference to parathyroid fun&on and the disordered metabolism of chronic azotcmic renal disease. REFERENCES
1. Cecil, R. L., and Loeb, R. F.: A Textbook of Medicine, ed. 11, Philadelphia, 1963, W. B. Saunders Company, pp. 814-819, 1434-1436, 1505-1507. Glands and Metabolic Bone 2. Albright, F., and Riefenstein, E. C., Jr.: The Parathyroid Disease (Selected Studies), Baltimore, 1948, Williams & Wilkins Company, pp. 115116. 3. Pugh, D. G.: Roentgenographie Diagnosis of Disease of Bone, New York, 1951, Thomas Nelson & Sons, pp. 19-26. 4. Stafne, E. C.: Oral Roentgenographic Diagnosis, ed. 2, Philaclelphia, 1963, W. B. Saunders Company, pp. 263-264. 5. Williams, R. H.: Textbook of Endocrinology, ed. 2, Philadelphia, 1955, W. B. Saunders Company, pp. 483-576. 6. Black, B. Marden: Hyperparathyroidism, Springfield, Ill., 1953, Charles C Thomas, Publisher, pp. 43-47. 7. Schreiner, G. E., and Maher, J. F. : Uremia: Biochemistry, Pathogenesis Treatment, Springfield, Ill., 1961, Charles C Thomas, Publisher, pp. 348-353. 8. Berson, S. A., Yalow, R. S., Aurbach, G. D., and Potts, J. T., Jr.: Immunoassay of Bovine and Human Parathyroid Hormone, Proc. Nat. Aead. SC. 49: 613.617, 1963.