John R.
Antonelli, DDS, FAAHD*’,
Timothy L. Hottel, DDS, MS, MBA, FACD2
‘Professor, Department of Prosthodontics and Director of
Fixed Prosthodontics and Discipline-Integrated
Comprehensive Care Courses; 2Professor, Department of
Prosthodontics and Associate Dean for Academic and
Financial Affairs, Nova Southeastern University, Health
Professions Division, College of Dental Medicine, 3200
South University Drive, Fort Lauderdale, FL 33328.201 8;
*Corresponding author, antonell@nova.edu
Spec Care Dentist 23(1):28-34,2003
ABSTRACT
Renal osteodystrophy, characterized by uneven
bone growth and demineralization, is described.
Oral manifestations of the disorder are described,
and the value o f dental radiographs in early
detection of renal osteodystrophy is noted. A case
report of a patient with severe oral complications,
which resulted from long-standing end-stage renal
disease and secondary hyperparathyroidism, is
presented. Giant cell lesions of
hyperparathyroidism, referred to as brown tumors
(which may be associated with pain and swelling),
are the key clinical oral manifestations and are the
most dramatic dental radiographic finding in
patients with renal osteodystrophy. Bone changes
may include loss of lamina dura, giant cell lesions
of hyperparathyroidism, and bone
demineralization. The dentist’s role in detection,
assessment, and treatment is stressed.
KEY WORDS: Renal o s t e o d y s t r o p h y ,
secondary hyperparathyroidism, brown tumor,
calcitriol.
Oral manifestations of renal
osteodystrophy: case report
and review of the literature
INTRODUCTION
R e n a l o s t e o d y s t r o p h y (RO) is a d e s c r i p t i v e term f o r t h e skeletal
complications that result from pathologic alterations in calcium, phosphate,
and bone metabolism in patients with end-stage renal disease.’ Renal
osteodystrophy that occurs during renal failure is most often caused by
secondary hyperparathyroidism associated with all four parathyroid glands. *
When the glomerular filtration rate decreases below 25% of normal,
phosphate excretion is impaired.* This results in an elevated tissue
phosphate concentration. Hyperphosphatemia leads to hypocalcemia because
an elevated tissue phosphate concentration decreases renal synthesis of
calcitriol (1,25-dihydroxyvitamin D3), the active form of vitamin D3.
Absorption of calcium in the gut depends on ~ a l c i t r i o l . ~
Hypocalcemia marks the beginning of the biochemical sequence that
culminates in renal bone disease. Hypocalcemia increases parathyroid
hormone, which is regulated by serum ionized-calcium levels rather than by
phosphate. Markedly elevated parathyroid hormone levels with secondary
hyperparathyroidism are a compensatory response to hypocalcemia in
patients with end-stage renal d i ~ e a s e . ~
Elevated parathyroid hormone levels normalize serum phosphate by
decreasing phosphate reabsorption in the proximal renal tubule (a
phosphaturic effect). With further decreases in the glomerular filtration rate,
phosphate elimination (even at the stage when no phosphate is reabsorbed by
the kidneys) is insufficient to restore equilibrium. A vicious cycle develops
eventually when an increase in parathyroid hormone causes an increase,
instead o f a decrease, in phosphate. This increase occurs because the
phosphate resorbed from bone at end-stage renal disease outweighs the level
excreted in urine. Increased parathyroid hormone promotes the synthesis of
calcitriol, which stimulates intestinal calcium a b ~ o r p t i o n Calcium .~ stores
from bone also are mobilized to satisfy the body’s calcium requirements at
the expense of the skeletal system.
A hierarchy of bone loss has been observed in dogs with secondary
hyperparathyroidism.s In decreasing order, this bone loss involves, jaw
bones, especially the alveolar bone; other skull bones; ribs; vertebrae; and
long bones. No hierarchy of bone loss in humans is mentioned in the
literature.
The resorptive effect of parathyroid hormone on bone is the physiologic
b a s i s f o r t h e h i s t o l o g i c a n d radiologic characteristics o f RO. T h e
characteristic histologic features of RO are variable and include: osteitis
f i b r o s a cystica, characterized by osteoclastic b o n e resorption a n d
replacement of marrow spaces and areas of excessive resorption with profuse
quantities of fibrous tissue; osteomalacia, o r defective mineralization
(nonspecific mineralization) of osteoid, with areas of decreased density;
osteoporosis; and osteosclerosis, characterized by an abnormal increase in
Spec Care Dentist 23(1)2003 Oral Manifestations of Renal Osteodystrophy 29

bone density that may result from a

Decreased
redistribution of mineral and may renal function
be caused by the much higher
levels of parathyroid hormone seen
in RO compared with primary
hyperparathyroidism (Figure 1).
I
Decreased conversion
i I
Decreased PO1
i Acidosis
Please provide a reference# for this from 25(OH)D3 receptor function in excretion
bone and gut
~tatement.~ Increased
Common radiographic findings
include: subperiosteal erosions,
especially in the terminal
11,1502D,I
Decreased

L------7-rJ
phalanges, long bones, distal ends
of the clavicles, and j a w s ;
osteosclerosis, often best evidenced
by enhanced bone density in the
jaws and upper and lower margins
of the vertebrae, producing the so-
called rugger-jersey spine; and
central giant-cell lesions, referred
to as brown tumors (the tumor's
brown color is caused
by hemosiderin deposit^).^,'
Radiographically, brown tumors of
the j a w s appear as well-
circumscribed, unilocular o r
Osteitis fibrosa
multilocular radiolucencies. Other
radiographic
- - alterations may
include loss O f l a m i n a dura, Figure I.Flowchart for the development of bone, phosphate, and calcium abnormalities in CRF.
trabecular pattern and bone density This material is reproduced with permission from the McGraw-Hill Companies, Inc. Fauci, A.
changes, and narrowing of dental Harrison's Principles of Internal Medicine, 14th Edition, 1998, McGraw-Hill, NY.
pulp chambers.
Although alterations in lamina dura, trabecular pattern, and
radiographic density are strikingly present in many patients
with RO, there is no statistically significant relationship of
these radiographic features with serum phosphate and
parathyroid hormone level^.^ Late signs of hyperparathyroid
bone disease are decreased bone density, loss of lamina dura,
appearance of brown tumors, and pathologic fractures.* Any of
these osteodystrophies may predominate and frequently exist
sim~ltaneousIy.~
The success of various treatment modalities for RO
depends in large part on early diagnosis. Dental radiographs
may help in early diagnosis of RO because of their high
diagnostic potential.6 In a radiographic survey of patients with
end-stage renal disease using 14 periapical exposures and a
panoramic radiograph, Spolnik et aZ.6 determined that dental
and hand radiographs alone are the safest and most efficient
means of screening patients for RO.
Either panoramic or periapical dental radiographic views
can be usefd in screening for RO. However, the radiographic
pattern of RO might resemble other entities, such as traumatic
bone cyst, central giant cell granuloma, ameloblastoma, and
odontogenic keratocyst. Thus, radiographic images and
serology (plasma biochemistry) are insufficient for diagnosis of
RO; bone biopsy is indicated for diagnosis. A definitive
diagnosis of RO requires histologic, radiologic, and serologic
evidence, as well as medical history.
CASE REPORT
A 52-year-old Caucasian female was referred for dental
I
I Osteoporosis and
bone decalcification
Increased
parathyroid hormone
secretion
Parathyroid
cystica hyperplasia
evaluation of a diffuse intraoral swelling in the premolar-molar
area of the right mandible. She was alert and cooperative. Vital
signs were as follows: blood pressure, 110/60 mm Hg; pulse,
6 0 beatdminute (min) and regular; respiratory rate, 18
breathdmin; and temperature, 98.6"Fahrenheit. When providing
her medical history, the patient reported that she had been
diagnosed with chronic, progressive renal insufficiency of
unknown etiology 10 years earlier. She reportedly had received
hernodialysis three times a week for nine years. Ten months
before her dental visit, the patient had undergone successful
renal transplantation and total hyperparathyroidectomy. A
small amount of parathyroid tissue was implanted into her
forearm.
At the time of dental evaluation, the patient was taking the
following medications: tacrolimus (an immunosuppressant to
prevent or treat organ rejection) 7 milligrams twice a day;
omeprazole (an antisecretory compound to suppress gastric acid
secretion), 20 mg/day; prednisone (a glucocorticoid to help
prevent and treat organ rejection), 7.5 mg/day; azathioprine (an
immunosuppressant), 7 5 mg/day; calcium carbonate (a
phosphate-binding agent), dose not reported;
trimethoprim/sulfamethoxazole (antibiotics for prophylaxis of
infection in renal transplant recipients), % tablevd; furosemide
(a diuretic), 40 mg/day; raloxifene hydrochloride (a selective
estrogen receptor modulator with some of the biological actions
of estrogen), 60 mg/day; folk acid (a B-vitamin for reduction
of cardiovascular disease outcomes in stable renal transplant
recipients with mild to moderate elevated total homocysteine
levels), 0.4 mg/day.
Laboratory findings at one month before the dental
30 Antonelli & Hottel
examination were: calcium, 9.1 milligramsideciliter (mgidl)
(normal range, 8.9 to 10.1 mg/dl); phosphate, 3.4 mgidl
(normal range, 2.5 to 4.5 mg/dl); parathyroid hormone N-
terminal, 300 picogramsimilliliters (pg/ml) (normal range, 230
to 630 pg/ml); creatinine, 0.7 mg/dl (normal range for women,
0.6 to 0.9 mgidl); potassium, 4.2 milliequivalent/liter (mEqi1)
(normal range, 3.5 to 5.0 mEq/l); sodium, 136 mEq/l (normal
range, 135 to 145 mEqi1); hematocrit, 41% (normal range for
women, 38% to 46%); bleeding time, 5 minutes (normal range,
2 to 8 minutes, template method); hemoglobin, 12
gramsideciliter (gidl) (normal range for women, 12 to 16 g/dl);
platelets, 255,000/millimeter3 (mm3) (normal range, 130,000 to
370,000/mm3); prothrombin time, 14 seconds (normal range,
1 1 to 15 seconds); activated partial thromboplastin time, 25
seconds (normal range, 21 to 30 seconds); white blood cell
count, 8,500/mm3 (normal range, 4,000 to 1 0,000/mm3).
Laboratory findings three years before renal transplant were
calcium, 9.2 mgidl; phosphate, 4.9 mg/dl; alkaline phosphatase,
271 international units per liter (IUIl) (normal range, 16 to 95
IU/l); creatinine, 3.6 mg/dl.
An intraoral examination revealed an expansion of the
alveolar ridge in the right mandibular premolar-molar region.
The overlying mucosa appeared reddish blue, slightly distended
and was moderately painful to palpation. The mass was firm
and caused a slight elevation of the mucobuccal fold. The
lingual cortical bone in the right mandibular premolar-molar
region was intact and not tender on palpation.
Intraoral and panoramic radiographs showed marked
evidence of altered bone density in the maxilla and mandible
(Figure 2). Alterations of trabeculae produced a finely meshed
pattern that gave the bone a “ground-glass’’ or “chalky”
radiographic appearance. The appearance was compatible with
osteitis fibrosa cystica and osteomalacia (Figure 3). Osteopenia
(diminution of bone volume) was observed radiographically.
Subperiosteal cortical bone resorption was evident as the loss
of lamina dura in the cortex of the tooth socket (Figure 4), the
loss of the cortices of the nasal floor and part of the sinus walls
(Figure 2), and the loss of distinct cortical borders of the
mandibular canal (Figure 5). The cortex was poorly outlined in
Figure 2. A panoramic radiograph, taken 10 months after renal
transplantation, illustrates multiple radiolucent lesions consistent
with brown tumors. A coarsely meshed trabecular pattern with dark
marrow spaces is seen.
Spec Care Dentist 23( 1 ) 2003
most areas of the mandible.
Localized destructive lesions were present in several areas
of both the maxilla and mandible. The lesions appeared as well-
and poorly circumscribed unilocular radiolucencies, suggestive
of brown tumors (Figure 6). A large maxillary lesion was
present in the right incisor-canine-premolar area; and the
maxillary first premolar appeared to be floating in soft tissue
instead of being embedded in bone (Figure 7). Several smaller
unilocular lesions with irregular margins were seen in the
regions of the anterior, right body, and right ascending ramus
of the mandible (Figures 5 , 7). A large, well-circumscribed
radiolucent lesion appeared in the canine-premolar-molar
region of the right mandible and extended from the root apices
to the inferior border. Jaw expansion associated with
displacement of mandibular central incisors was seen, and tooth
resorption was absent (Figure 6). Narrowing and almost
complete obliteration of pulp chambers was evident in all teeth
(Figures 2, 3, and 4). Positive dental pulp vitality tests ruled out
osseous pathology of pulpal origin.
The patient was referred to an oral surgeon for evaluation,
and during subsequent surgery, the entire mass in the
mandibular right canine-premolar-molar area was removed.
The specimen was reddish brown and measured approximately
3.0 centimeters in diameter. Histologic examination revealed
multinucleated giant cells in a fibrous connective tissue stroma
and red blood cells. The diagnosis of a brown tumor was
consistent with the histologic features and the patient’s medical
history. The patient declined follow-up oral surgery evaluation
and routine dental care. Evaluation of surgical and systemic
disease treatment of oral manifestations of RO was thus
precluded.
Figure 3. Several well-and poorly demarcated brown tumors,
loss of lamina dura, and an homogenous or ground-glass
appearance (demineralization) of bone is seen.
Spec Care Dentist 23(1) 2003 Oral Manifestations of Renal Osteodystrophy
Figure 4. A nearly homogenous trabecular pattern is seen. The
crestal bone is not well delineated. An osteosclerotic area is seen
at t h e apex of t h e distal root of t h e first molar. Dental pulp canals
are largely obliterated.
DISCUSSION
Hypocalcemia, d e c r e a s e d s e r u m calcitriol, and
hyperphosphatemia are the main factors in the pathogenesis of
secondary hyperparathyroidism associated with chronic renal
failure.’ Hypocalcemia and decreased serum calcitriol are
present w h e n t h e glomerular filtration rate falls below
80 to 60 ml/miii/I.73 m’ (the point at which parathyroid
hormone levels start to rise), while hyperphosphatemia occurs
only when the glomerular filtration rate is less than about
30 mliminil.73 m3.3,5
Secondary hyperparathyroidism is best treated by reducing
serum phosphate with a phosphate-restricted diet and oral
phosphate-binding agents (such as calcium carbonate o r
calcium acetate, which act in the gut and are taken in divided
doses with meals). Phosphate-binding agents are used to
Figure 6. A large brown tumor makes this area susceptible to
pathologic fracture.
31
Figure 5. The mandibular canal has lost most of its radiographic
cortical outline. Radiolucent areas extend into t h e coronoid
process and condyle. The inferior mandibular border is poorly
outlined. Increased bone density is seen distal to t h e mandibular
molar. indicative of osteosclerosis.
suppress secondary hyperparathyroidism and avoid or reverse
osteitis fibrosa cystica, osteomalacia, and muscle weakness.
Phosphate-binding agents are titrated to maintain a serum
phosphate level of 4.5 mg/dL and a serum calcium level of
10 mg/dL.*
Renal osteodystropliy resolves in most patients who receive
hemodialysis of adequate quality and duration. When calcium
in the dialysis fluid is sufficient to prevent a net loss of calcium
Figure 7. A brown tumor has resorbed the cortical bone delineating
portions of t h e maxillary sinus and nasal floor.
32 Antonelli 8. HotteI
from the body, it is not always sufficient to suppress the
hyperplastic parathyroid glands, and total
hyperparathyroidectomy is r e q ~ i r e d Successful .~ renal
transplantation restores normal vitamin D metabolism and leads
t o regression o f bone lesions, however, secondary
hyperparathyroidism might have achieved a degree of severity
that i s not easily ~ o r r e c t e d . ~ , ~
Persistence o f secondary hyperparathyroidism is a
significant problem that occurs in up to 50% of kidney
transplant recipient^.^ Secondary hyperparathyroidism after
renal transplantation might increase the risk of acute tubular
necrosis, hypercalcemia, hypophosphatemia, as well as
continuation of RO; total hyperparathyroidectomy might be
required. Sometimes during total hyperparathyroidectomy, a
small amount of parathyroid tissue is transplanted into the
forearm in the hope of maintaining normal parathyroid
function. The transplanted tissue is easily accessible for
removal from the forearm should hyperparathyroidism recur.
Osteoblastic and osteoclastic activity after
hyperparathyroidectomy i s regulated mostly by parathyroid
hormone.I0 Optimal parathyroid hormone serum level after
renal transplantation is not known.
The use of phosphate binders and dietary phosphate
restriction to suppress secondary hyperparathyroidism in
patients with chronic renal failure results in reduced bone
turnover; it is unlikely, however, to restore disrupted trabecular
architecture. Adverse mechanical effects associated with loss of
trabecular bone structure may result in higher fracture risk in
later life, by as much as three- to four-fold in patients with end-
stage renal d i s e a ~ e . ~ , ' ? ' 'Thinning
,'~ of the bony cortex is
responsible for the largest decrease in bone mineral content in
patients with chronic renal failure and increases fracture risk.I2
Loss of lamina dura is considered to be a manifestation of
cortical bone resorption. Cortical bone resorption is seen in the
mandible, mandibular canal, alveolar crest, palatal suture, nasal
floor, and maxillary sinus walls. Kelly et ~ 7 1 found . ~ that among
38 patients with end-stage renal disease, 17 patients (45%) had
substantial thinning and complete loss of lamina dura in some
areas, and three patients (8%) had total loss of lamina dura.
Two patients (5%) showed loss of cortices of the nasal floor
and sinus walls, and one patient (2.6%) showed loss of cortical
borders of the mandibular canal. A radiographic survey6 of 30
patients with end-stage renal disease documented 22 (73%)
patients with abnormal dental radiographs. Forty-five percent
of patients had loss of lamina dura, which supports the findings
of Kelly et aL4 Three patients (10%) showed an absence of
cortical bone outlining the maxillary sinus and mandibular
canal. The absence of cortical bone outlining these structures
could be valuable in determining the extent of bone disease.
Lamina dura may be missing in Paget's disease, Cushing's
syndrome, and fibrous dysplasia, and should not be considered
pathognomonic for any disease entity?Z6
Brown tumors are the only clinical oral manifestation and
are the most dramatic dental radiographic finding of RO. Pain
and swelling in the affected area and fracture are the most
common clinical symptoms associated with brown tumors.6
Brown tumors occur most frequently in the clavicle, pelvic
girdle, and mandible. When they occur in the maxilla, the
orbital area is affected most commonly; the ethmoid and frontal
bones may be a f f e ~ t e d .Brown ~ tumors and giant-cell
reparative granulomas cannot be differentiated
Spec Care Dentist 23(1) 2003
histopathologically. Differentiation depends on laboratory
findings that indicate metabolic alterations associated with
secondary hyperparathyroidism.
Although hemodialysis prolongs life, it also prolongs
exposure to parathyroid hormone because it does not resolve
secondary hyperparathyroidism, which in turn increases the
risk for brown tumors associated with RO. Brown tumors are
more likely to develop as the length of time maintained on
hemodialysis increases. Tumor excision and parathyroid
removal are required.
Decreased bone density, compatible with the nonspecific
demineralization of osteonialacia and/or the ground glass
appearance of osteitis fibrosa cystica, is the most common jaw
abnormality and the most common radiographic change seen in
hyperparathyroidism.',6 Decreased bone density may have
diagnostic value in the evaluation of bone disease, but it is
invalid to equate it with a histologic d i a g n o s i ~ . ' In
. ~ general,
lesions o f the medullary bone i n j a w s are not visible
radiographically unless 30% to 50% of bone mineral is l ~ s t . ' . ~ , ~
Hyperparathyroidism appears to develop relatively early in
the course of chronic renal failure and precedes the appearance
of osteomalacia. Osteomalacia is a reversible defect in the
mineralization of adult bone that is caused usually by vitamin
D deficiency. Excessive unmineralized surfaces and excessive
thickness of osteoid are observed histologically. The bones
become osteopenic and fracture. Osteopenia is the most
common cause of spontaneous fractures seen in chronic renal
failure. The histologic features of osteitis fibrosa cystica
include proliferation of osteoblasts and osteoclasts. There is an
increase in the number and depth of osteoclastic resorption
cavities in trabecular bone, indicative of increased bone
resorption.' ' , I 3
Some investigator^'^^^^ have identified a pathognomonic
triad of bone changes caused by hyperparathyroidism, which
consists of loss of lamina dura, giant cell lesions, and bone
demineralization (density changes). These changes appear to
occur together, although their relative degrees may vary.4 Other
changes include clinical expansion of alveolar ridges and root
resorption (the latter was not observed in the case described
here).
Radiographic changes become more evident with increased
disease duration. Observations during a 12-year period of
patients who are receiving dialysis suggest that most patients
on dialysis for more than six years develop quantitatively more
severe osseous change^.^.^ One patient receiving dialysis
treatments for 24 months (with renal disease for 117 months)
had five brown tumors.6
When normal renal function is restored by renal
transplantation, progression of bone disease depends on the
state of the bones at the time of transplantation.' The severe
radiographic findings and disease progression seen in the
patient in this case report is a result of nine years of
maintenance hemodialysis. In the study by Kelly et al.,4 a
significant correlation between the number of months on
dialysis and the absence of both lamina dura and normal
trabeculation was found. The duration of hemodialysis
treatment is proportional to adverse changes to jaws and other
bony structures. A study of the effects of chronic renal disease
on dental radiographic changes by GanibegoviC14 concludes
that adverse changes to jaws and other bones must be addressed
within six months of the start of hemodialysis, otherwise
Spec Care Dentist 23(1 ) 2003 Oral Manifestations of Renal Osteodystrophy
damage is irreparable by calcium supplementation and kidney
transplantation.
Hyperparathyroidism may be encountered more frequently
as more patients undergo long-term dialysis treatment and live
longer. Age-related bone loss may become an increasingly
important factor affecting bone disease in these older patients.
Age and weight are important determinants of bone mineral
density. Age-related bone loss occurs at a rate of 1% to 2% per
year after age 40 and increases to 2% to 4% for 5 to 8 years
following menopause in women. There is a negative
association between age and bone mineral density in women
with end-stage renal disease but not in men with the d i s e a ~ e . ’ ~
Taal and co-workers’* confirm the importance of parathyroid
hormone-related bone disease on bone mineral density in
patients who are receiving hemodialysis. They found that age,
weight, hormonal factors, and calcium supplementation also are
determinants of bone mineral density. Estrogen therapy slows
the loss of bone, but its benefit in women older than 75 years is
unproven.* Vitamin D replacement with oral or intravenous
calcitriol (administered between hemodialysis treatments) can
increase serum calcium and produce clinical, histologic, and
radiologic improvements in some patients by suppressing
parathyroid hyperplasia and restoring normal calcium and
phosphate balance.
Renal transplantation requires the use of both
corticosteroids and cytotoxic medication. After kidney
transplant, patients typically receive an average dose of 7,500
mg of prednisolone during the first year and approximately
36,500 mg of azathioprine annually. These drugs not only
suppress rejection but also render the patient susceptible to
infection and poor wound healing, especially in the immediate
post-transplant period (six month^).^,^^
Osteoporosis is a well-documented complication of long-
term steroid therapy that occurs primarily because of impaired
intestinal absorption of calcium, inhibition of osteoblast
function, and increased urinary calcium excretion. All of these
effects promote a state of negative calcium balance that might
stimulate parathyroid function after renal transplantation.
In tests of cortisone-treated rats, dental pulp chambers
show excessive formation of a bone-like substance.”
Narrowing of pulp chambers occurs significantly more
frequently among transplant patients than among patients on
hemodialysis, possibly because of the amount of corticosteroids
received and the total plasma prednisolone clearance of the
drug.I6 Narrowing of pulp chambers complicates endodontic
treatment.
Routine dental treatment is contraindicated during the post-
renal transplant period. Emergency dental treatment should be
as noninvasive as possible, rendered after consultation with the
patient’s physician. Before routine dental treatment can resume,
the dentist should consulted with the patient’s physician to
confirm that the graft has healed and the patient is stable.18
During the consultation with the physician, the dentist should
confirm whether the patient will require antibiotic prophylaxis
as a result of post-transplant immunosuppressive medications.
Under some circumstances, for example oral surgical
procedures, the physician may recommend steroid
supplementation to to help the patient adjust to the physical
stress of the procedure. As when treating any patient, it is
important that the dental health team use universal infection
control precautions and barrier techniques when treating
33
patients who have received renal transplants. These patients are
at particular risk of infection with hepatitis B, C, or HIV,
acquired from hemodialysis and/or blood transfusions. Patients
who are immunosuppressed also may have a risk of infection
with herpes simplex virus, cytomegalovirus, and Epstein-Barr
virus, any of which can be transmitted to dental staff and other
patients.
CONCLUSION
It is surprising that RO has received little attention in the dental
literature because this disease has many dental implications,
including: pain and swelling in the affected area, and
pathologic jaw fracture (associated with brown tumor in the
late stages); destruction of the bony architecture of jaws; loss of
tooth support; root resorption; severe narrowing of dental pulp
chambers; severe limitations on routine dental treatment
(especially in the post-renal transplant period); and increased
risk of infection.
Dental evaluation of patients with RO depends on
familiarity with disease characteristics. Early disease detection
by the dentist may alter disease progression through early
successful medical intervention.
1. Syrjanen S, Lampainen E. Mandibular changes in
panoramic radiographs of patients with end stage renal disease.
Dentomaxillofac Radio1 12:51-6, 1983.
2. F‘ishman MC.Me’tiidine. 43 ‘3 e ~ . ~ ~ ~ ~ ~ ~ ~ ~
Raven Publishers; pp 187-96, 1996.
3. Koch Nogueira PC, David L, Cochat P. Evolution of secondary
hyperparathyroidism after renal transplantation. Pediatr Nephrol
14.342-46,2000.
4. Kelly WH, Mirahmadi MK, Simon JH, Gorman JT. Radiographic
changes of the jawbones in end stage renal disease. Oral Surg
OralMed Oral Pathol50:372-81, 1980.
5. Carmichael DT, Williams CA, Aller MS. Renal dysplasia with
secondary hyperparathyroidism and loose teeth in a young dog.
J VetDent 12:143-6, 1995.
6. Spolnik KJ, Maxwell DR, Patterson SS, Kleit SA, Cockerill EM.
Dental radiographic manifestations of end-stage renal disease.
Dent Radiogr Photogr 54:21-3 1 , 198 1.
7. Eastwood JB. Renal osteodystrophy: a radiological review. CRC
Crit Rev Diagn Imaging 9:77-104, 1977.
8. Silverman S, Gordan G, Grant T, et al. The dental structures in
primary hyperparathyroidism: studies in 42 consecutive dentulous
patients. Oral Surg Oral Med Oral Pathol 15:426-36, 1962.
9 . Levine MR, Chu A, Abdul-Karim FW. Brown tumor and
secondary hyperparathyroidism. Arch Ophthalmol 109347-9,
1991.
10. Mazzaferro S, Chicca S, Pasquali M, et al. Changes in bone
turnover after parathyroidectomy in dialysis patients: role of
calcitriol administration. Nephrol Dial Transplant 15:877-82,
2000.
1 1 . Croucher PI, Wright CDP, Garrahan NJ, Kudlac H, Williams AJ,
Compston JE. Characteristics of trabecular bone resorption
cavities in patients with chronic renal failure. Bone Miner 16:139-
47, 1992.
12. Taal MW, Masud T, Green D, Cassidy MJD. Risk factors for
reduced bone density in haemodialysis patients. Nephrol Dial
Transplant 14:1922-8, 1999.
34 Antonelli & Hottel Spec Care Dentist 23(1) 2003

13. Hruska K. Pathophysiology of renal osteodystrophy. Pediatr of the dental pulp chamber in patients with renal diseases. Oral
Nephrol 14:636-40,2000. Surg Oral Med Oral Pathol59:242-6, 1985.
14. GanibegoviC M. Dental radiographic changes in chronic renal 17. Anneroth G, Bloom G. Structural changes - in the incisors of
disease. MedArch 54:115-8,2000. cortisone-treated rats. J Dent Res 45:229-35, 1966.
15. Gabay C, Ruedin P, Slosman D, Bonjoour J-P, Leski M, Rizzoli
18. Little JW, Falace D A , Miller CS, Rhodus NL. Dental
R. Bone mineral density in patients with end-stage renal failure.
A m JNenhrol 13:115-23. 1993. management of the medically compromised patient. 5th ed. St.
> - ~

16. Nasstrom K, Forsberg B, Peterson A, Westesson P-L. Narrowing Louis: Mosby; pp 576-601, 1997.