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National Medical Policy
Subject:
Bone Mineral Density Measurement
Policy Number:
NMP141
Effective Date*:
May 2004
Updated:
June 2016
This National Medical Policy is subject to the terms in the
IMPORTANT NOTICE
at the end of this document
For Medicaid Plans: Please refer to the appropriate State's Medicaid manual(s),
publication(s), citations(s) and documented guidance for coverage criteria and
benefit guidelines prior to applying Health Net Medical Policies
The Centers for Medicare & Medicaid Services (CMS)
For Medicare Advantage members please refer to the following for coverage guidelines
first:
Use
X
X
Source
National Coverage Determination
(NCD)
National Coverage Manual Citation
Local Coverage Determination
(LCD)*
Article (Local)*
Other
Reference/Website Link
Bone (Mineral) Density Studies:
http://www.cms.gov/medicare-coveragedatabase/search/advanced-search.aspx
CMS Manual - Pub 100-04. Bone Mass
Measurements (BMMs):
http://www.cms.gov/Regulations-andGuidance/Guidance/Transmittals/downloads/R123
6CP.pdf
MLN Matters Number: MM5521. Bone Mass
Measurements (BMMs):
http://www.cms.gov/Outreach-andEducation/Medicare-Learning-NetworkMLN/MLNMattersArticles/downloads/MM5521.pdf
Bone Mineral Density Studies Jun 16
1
None
Use Health Net Policy
Instructions
 Medicare NCDs and National Coverage Manuals apply to ALL Medicare members in
ALL regions
 • Medicare LCDs and Articles apply to members in specific regions. To access your
specific region, select the link provided under “Reference/Website” and follow the
search instructions. Enter the topic and your specific state to find the coverage
determinations for your region. *Note: Health Net must follow local coverage
determinations (LCDs) of Medicare Administration Contractors (MACs) located
outside their service area when those MACs have exclusive coverage of an item or
service. (CMS Manual Chapter 4 Section 90.2)
 If more than one source is checked, you need to access all sources as, on occasion,
an LCD or article contains additional coverage information than contained in the NCD
or National Coverage Manual.
 If there is no NCD, National Coverage Manual or region specific LCD/Article, follow
the Health Net Hierarchy of Medical Resources for guidance.
Current Policy Statement
Health Net, Inc. considers bone mineral density (BMD) or Bone Mass Measurement
(BMM) studies medically necessary for any of the following:
Initial Bone Mineral Density Studies
1.
Perimenopusal and postmenopausal women who have risk factors for osteoporosis
(e.g. low body weight, prior low-trauma fracture or high risk medication) and are
willing to consider available interventions.
2.
Women age 65 and older and men age 70 and older, regardless of clinical risk
factors; or
3.
Men age 50 to 69 with specific risk factors for osteoporosis (i.e., low body weight,
weight loss, physical inactivity, use of oral corticosteroids, androgen deprivation
therapy, and previous fragility fracture)
4.
Individuals who are considering therapy for osteoporosis, if BMD testing would
facilitate their decision; or
5.
An individual with vertebral abnormalities as demonstrated by an x-ray to be
indicative of osteoporosis, osteopenia, or vertebral fracture; or
6.
An individual receiving (or expecting to receive) glucocorticoid (steroid) therapy
equivalent to 5 mg of prednisone, or greater, per day for more than three months;
or
7.
An individual with a history of long term treatment with any medication that may
reduce bone mineral density or cause osteoporosis (e.g., anti-convulsants, heparin,
gonadotropin releasing hormone therapy, cytotoxic drugs, immunosuppressants or
aromatase inhibitors or thyroid replacement therapy where the TSH level is
chronically below the normal range); or
8.
An individual with primary hyperparathyroidism; or
Bone Mineral Density Studies Jun 16
2
9.
Individuals who are known or suspected to have a condition that may relate to
osteoporosis, including but not limited to any of the following:
a.
b.
c.
d.
e.
f.
g.
h.
i.
Chronic liver disease; or
Cushing Syndrome; or
Hypercalciuria; or
Hyperthyroidism; or
Hypogonadism; or
Malabsorption syndromes
Rheumatoid arthritis
Lupus
Ankylosing spondylitis
10. In individual being monitored to assess the response to or efficacy of an FDA
approved osteoporosis drug therapy (only dual-energy x-ray absorptiometry is
considered medically necessary for this indication); or
11. An individual who has completed drug therapy for osteoporosis and is being
monitored for response to therapy; or
12. An individual with impaired renal function including chronic renal failure, renal
osteodystrophy, and other specified disorders resulting from impaired renal function
and cystic kidney disease; or
13. An individual with a history of low trauma fracture(s); or
14. Postmenopausal women discontinuing estrogen should be considered for
bone density testing
15. Anyone not receiving therapy in whom evidence of bone loss would lead
to treatment
Repeat Bone Mineral Density Studies
Health Net, Inc follows Medicare policy for repeat bone mineral density measurement for
members once every 2 years (if at least 23 months have passed since the month the
last bone mass measurement was performed). A member may have a BMD
measurement more frequently than every two years if medically necessary
Note: DEXAs should not be done more often than yearly, as to do so leads to errors of
reliability, i.e., the potential technical error is more than the expected change in bone
mass. If someone needs to be monitored for bone loss over a period of less than a year,
it should be done with bone turnover markers, such as a resorption marker (urinary Ntelopeptide) or a formation marker (bone alkaline phosphatase).
Examples of situations where more frequent BMD studies may be performed are:
1. Monitoring patients on long-term glucocorticoid (steroid) therapy equivalent to
5.0 mgs of glucocorticosteriod (steroid) or greater per day for more than 3
months; and
2. Allowing for a baseline central bone mineral density to permit monitoring of
patients in the future if the initial test was performed with a technique that is
different from the monitoring method. More specifically, women who have low
Bone Mineral Density Studies Jun 16
3
bone density scores found on screening ultrasound densitometry or peripheral
DEXA scan should receive a central DEXA scan (including both spine and hip
density measurements) both to confirm the findings of the screening test and to
serve as a baseline study against which future DEXA scan results can be
compared.
3. Monitoring individuals on FDA-approved osteoporosis drug therapy, to assess
response and efficacy of therapy, until a response to such therapy has been
documented over time and condition is stabilized.
4. Follow up bone mineral density testing after discontinuation of therapy, until a
response to such therapy has been documented.
5. Men with prostate cancer undergoing hormonal manipulation
Note: In rare instances, both axial and peripheral bone mineral density (BMD) studies
may be medically necessary on the same date of service, or within thirty days of each
other. These instances include any of the following:
1. Hip or spine cannot be measured (Reason must be documented in the medical
record).
2. Hyperparathyroidism
3. Obese patient over the weight limit of the DEXA exam table.
4. Extreme arthritic changes that precludes accurate measurement.
Codes Related To This Policy
NOTE:
The codes listed in this policy are for reference purposes only. Listing of a code in this
policy does not imply that the service described by this code is a covered or non-covered
health service. Coverage is determined by the benefit documents and medical necessity
criteria. This list of codes may not be all inclusive.
On October 1, 2015, the ICD-9 code sets used to report medical diagnoses and inpatient
procedures have been replaced by ICD-10 code sets.
ICD-9 Codes
193
242-242.91
246.0
252.00-252.08
255.0
255.3
256.2
256.31
256.39
257.2
259.3
259.5
259.9
Malignant neoplasm of thyroid gland
Thyrotoxicosis with or without goiter
Disorders of thyrocalcitonis secretion
Hyperparathyroidism
Cushing’s syndrome
Other corticoadrenal overactivity
Postablative ovarian failure
Premature menopause
Other ovarian failure
Other testicular hypofunction
Ectopic hormone secretion, not elsewhere classified
Androgen insensitivity syndrome
Unspecified endocrine disorder
Bone Mineral Density Studies Jun 16
4
262
263-263.9
268.2
268.9
275.4-275.49
555-555.9
556-556.9
579-579.9
585-585.9
588.0-588.89
626.0
627.2
627.4
731.0
733.00-733.09
733.10- 733.19
733.7
733.90
733.93
733.94
733.95
753.12
753.13
753.14
753.15
753.16
753.17
753.19
756.50
756.51
758.6
781.91
793.7
793.91
793.99
805-805.9
806-806.9
808-808.9
813.4-813.47
813.5-813.54
820-820.9
995.20
E932.0
V45.77
V49.81
V50.42
V58.61
V58.63
V58.65
V58.69
Other severe, protein-calorie malnutrition
Other and unspecified protein-calorie malnutrition
Osteomalacia, unspecified
Unspecified vitamin D deficiency
Disorders of Calcium metabolism
Regional enteritis
Ulcerative Colitis
Intestinal malabsorption
Chronic kidney disease
Disorders resulting from impaired renal function
Absence of menstruation
Symptomatic menopausal or female climacteric states
Symptomatic states associated with artificial menopause
Osteitis deformans without mention of bone tumor
Osteoporosis
Pathologic fracture
Algoneurodystrophy
Disorder of bone and cartilage, unspecified
Stress fracture of tibia or fibula
Stress fracture of the metatarsals
Stress fracture of other bone
Polycystic kidney, unspecified type
Polycystic kidney, autosomal dominant
Polycystic kidney, autosomal recessive
Renal dysplagia
Medullary cystic kidney
Medullary sponge kidney
Other specified cystic kidney disease
Osteodystrophy, unspecified
Osteogenesis imperfecta
Gonadal dysgenesis
Loss of height
Nonspecific abnormal findings on radiological and other examinations of
body structure
Other image test inconclusive due to excess body fat
Nonspecific abnormal findings on radiological and other examinations of
body structure
Fracture of vertebral column without mention of spinal cord injury
Fracture of vertebral column with spinal cord injury
Fracture of pelvis
Lower end, closed
Lower end, open
Fracture of neck of femur
Unspecified adverse effect of unspecified drug, medicinal and biological
substance
Adrenal cortical steroids (causing adverse effects)
Acquired absence of genital organs
Asymptomatic postmenopausal status (age-related) (natural)
Prophylactic organ removal, ovary
Long-term (current) use of anticoagulants
Long-term (current) use of antiplatelets/antithrombotics
Long-term (current) use of steroids
Long-term (current) use of other medications
Bone Mineral Density Studies Jun 16
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V67.51
V67.59
V82.81
Note:
Following completed treatment with high-risk medication, NEC
Following other treatment, other
Screening for osteoporosis
Central DXA of the hip and/or spine is the preferred measurement for
definitive diagnosis. Bone density measured at the femoral neck by DXA is
the best predictor of hip fracture. DXA is the gold standard method for the
noninvasive diagnosis of osteoporosis.
ICD-10 Codes
C73
E05.00-E05.91
E07.0
E21.0-E21.5
E24.0-E24.9
E27.0
E28.310-E28.319
E28.39
E29.1
E34.2
E34.50-E34.52
E34.9
E43
E44.0-E44.1
E55.9
E83.50-E83.59
E89.40-E89.6
K50.00-K50.919
K51.00-K51.919
K90.0-K90.9
M83.9
M80.00-M80.88
M81.0-M81.8
M94.361-M84.369
M84.371-M94.379
M84.38
M84.40-M84.68
M88.9
M89.00-M89.09
M89.9
M94.9
N18.1–N18.9
N25.0-N25.9
N91.2
N95.1
N95.8
Q61.02
Q61.19
Q61.2
Q61.3
Q61.4
Q61.5
Q61.8
Malignant neoplasm of thyroid gland
Thyrotoxicosis (hyperthyroidism)
Hypersecretion of calcitonin
Hyperparathyroidism and other disorders of parathyroid gland
Cushing’s syndrome
Other adrenocortical overactivity
Premature menopause
Other primary ovarian failure
Testicular hypofunction
Ectopic hormone secretion, not elsewhere classified
Androgen insensitivity syndrome
Endocrine disorder, unspecified
Unspecified severe protein-calorie malnutrition
Protein-calorie malnutrition of moderate and mild degree
Vitamin D deficiency, unspecified
Disorders of calcium metabolism
Postprocedural ovarian failure
Crohn’s disease (regional enteritis)
Ulcerative colitis
Intestinal malabsorption
Adult osteomalacia, unspecified
Age-related osteoporisis with current pathological fracture
Osteoporosiswithout current pathological fracture
Stress fracture, tibia and fibula
Stress fracture, ankle, foot and toes
Stress fracture, other sites
Pathological fracture, not elsewhere classified
Osteitis deformans of unspecified bone
Algoneurodystrophy
Disorder of bone, unspecified
Disorder of cartilage, unspecified
Chronic kidney disease (CKD)
Disorders resulting from impaired renal function
Amenorrhea, unspecified
Menopausal and female climacteric states
Other specified menopausal and perimenopausal disorders
Congenital multiple renal cysts
Other polycystic kidney, infantile type
Polycystic kidney, adult type
Polycystic kidney, unspecified
Renal dysplasia
Medullary cystic kidney
Other cystic kidney diseases
Bone Mineral Density Studies Jun 16
6
Q78.0
Q78.9
Q96.0-Q96.9
R29.890
R93.6
R93.7
R93.8
R93.9
S20.000-S22.089
S12.00-S12.691
S32.000-S32.399
S52.501-S52.516
S72.001-S72.099
T50.905
Z13.820
Z40.02
Z78.0
Z79.01
Z79.02
Z79.51
Z79.52
Z79.89-Z79.899
Z90.71-Z90.79
Osteogenesis imperfecta
Osteochondrodysplasia, unspecified
Turner’s syndrome
Loss of height
Abnormal findings on diagnostic imaging of limbs
Abnormal findings on diagnostic imaging of other parts of
musculoskeletal system
Abnormal findings on diagnostic imaging of other specified body
structures
Diagnostic imaging inconclusive due to excess body fat of patient
Fracture of thoracic vertebra
Fracture of cervical vertebra and other parts of the neck
Fracture of lumbar sine and pelvis
Fracture of lower end of radius
Fracture of head and neck of femur
Adverse effect of unspecified drugs, medicaments and biological
Substances
Encounter for screening for osteoporosis
Encounter for prophylactic removal of ovary
Asymptomatic menopausal state
Long term (current) use of anticoagulants
Long term (current) use of antithrombotics/antiplatelets
Long term (current) use of inhaled steroids
Long term (current) use of systemic steroids
Other long term (current) therapy
Acquired absence of genital organ(s)
CPT Codes
76977
77078
77080
77081
77082
77086
Ultrasound bone density measurement and interpretation, peripheral
site(s), any method
Computed tomography, bone mineral density study, one or more sites;
axial skeleton (eg, hips, pelvis, spine)
Dual energy x-ray absorptiometry (DEXA), bone density study, one or
more sites; axial (central) skeleton (e.g., hips, pelvis, spine)
Dual energy absorptiometry (DEXA), bone density study, one or more
sites; appendicular (peripheral) skeleton (e.g., radius, wrist, heel)
Dual energy x-ray absorptiometry (DXA) bone density study, one or more
sites, vertebral fracture assessment (code deleted 12/2014)
Vertebral fracture assessment via dual-energy X-ray absorption (DXA)
HCPCS Codes
G0130
Single energy x-ray absorptiometry (SEXA) bone density study, one or
more sites; appendicular skeleton (peripheral) (e.g., radius, wrist, heel)
Codes not Covered by Medicare (February 2008)
78350
78351
Bone density (bone mineral content) study, one or more sites, single
photon absorptiometry
Bone density (bone mineral content) study, dual photon absorptionmetry,
one or more sites
Scientific Rationale – Update June 2016
Bone Mineral Density Studies Jun 16
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Wu et al (2016) investigated the osteoporosis risk in patients with peptic ulcer disease
(PUD) using a nationwide population-based dataset. This Taiwan National Health
Insurance Research Database (NHIRD) analysis included 27,132 patients aged 18 years
and older who had been diagnosed with PUD (International Classification of Diseases,
Ninth Revision, Clinical Modification [ICD-9-CM] codes 531-534) during 1996 to 2010.
The control group consisted of 27,132 randomly selected (age- and gender)-matched
patients without PUD. The association between PUD and the risk of developing
osteoporosis was estimated using a Cox proportional hazard regression model.During
the follow-up period, osteoporosis was diagnosed in 2538 (9.35 %) patients in the PUD
group and in 2259 (8.33 %) participants in the non-PUD group. After adjusting for
covariates, osteoporosis risk was 1.85 times greater in the PUD group compared to the
non-PUD group (13.99 vs 5.80 per 1000 person-years, respectively). Osteoporosis
developed 1 year after PUD diagnosis. The 1-year follow-up period exhibited the highest
significance between the 2 groups (hazard ratio [HR]=63.44, 95% confidence interval
[CI]=28.19-142.74, P<0.001). Osteoporosis risk was significantly higher in PUD patients
with proton-pump-inhibitors (PPIs) use (HR=1.17, 95% CI=1.03-1.34) compared to PUD
patients without PPIs use. The authors concluded this study revealed a significant
association between PUD and subsequent risk of osteoporosis. Therefore, PUD patients,
especially those treated with PPIs, should be evaluated for subsequent risk of
osteoporosis to minimize the occurrence of adverse events.
Scientific Rationale – Update June 2015
Monadi et al (2015) reported the results of studies which addressed the impact of
inhaled corticosteroid (ICS) therapy on BMD of patients with asthma are conflicting. A
case-control study aimed to compare BMD status in ICS user with asthma with healthy
controls according to age. BMD at the lumbar spine (LS), femoral neck (FN) was
measured by dual energy X-ray absorptiometry (DEXA). Patients and controls were
compared according to BMD gr/cm2, BMD T-score, BMD Z-score, frequency of
osteoporosis (defined as BMD T-score ≤-2.5), and frequency of patients with BMD Zscore <-1 at LS and FN with regard to age <50 and ≥50 years old. Forty-four ICS user
patients (females 63.6 %) with median treatment duration of 6.5 years and 50 controls
(females, 69.4 %) with respective mean age of 49.2±9.5 and 47.4±10.5 years
(p=0.38 and p=0.35) entered the study. Overall LS-BMD and FN-BMD gr/cm2 in total
patients were lower than in controls by 6 % (p=0.065) and 5.9 % (p=0.09),
respectively. In patients <50 years, mean LS-BMD gr/cm2 was lower than controls by
11.3 % (p=0.013) and FN-BMD by 8.8 % (p=0.044). Mean BMD T-score and BMD Zscore in both measurement sites were also lower than controls (p=0.013 and 0.01,
respectively. Frequency of osteoporosis did not differ but frequency of patients with BMD
Z-score <-1 was significantly higher in patients (odds ratio (OR)=6.57 95 % CI, 1.823.9, p=0.004). In age group ≥50 years old, reduction of BMD in both measurement
sites did not reach to a significant level. The authors concluded the study indicates that
BMD reduction in ICS user with asthma is dependent on age and appears that younger
patients are at greater risk of BMD loss. These findings suggest preventive measures
particularly in patients <50 years.
Benetti-Pinto et al (2015) sought to analyze long-term variation in bone mineral density
among young women with primary ovarian insufficiency. A cohort study evaluated bone
mineral density in 72 women with primary ovarian insufficiency who were receiving
estrogen + progesterone therapy. Bone mineral density was evaluated every 2 years for
8 years. The women were young, with a mean (SD) age of 34.1 (6.7) years and had a
bone density measurement at baseline. The mean (SD) time between the last
menstruation and the beginning of hormone treatment was 2.9 (4.2) years. The initial
mean (SD) bone mineral density was 1.03 (0.17) and 0.91 (0.16) g/cm for the lumbar
Bone Mineral Density Studies Jun 16
8
spine and femoral neck, respectively. The mean (SD) T score was -1.03 (1.39) and –
0.29 (1.09) for the lumbar spine and femoral neck, respectively. Bone mineral density
measurements after a follow-up period of 2, 4, 6, and 8 years did not differ from bone
mineral density at baseline. Osteopenia and osteoporosis were observed at the lumbar
spine and femoral neck in 46% and 25% of women at the time of diagnosis, with no
difference in the percentage of affected women across time. The authors concluded
although women with primary ovarian insufficiency who are receiving estrogen +
progesterone therapy maintain stable bone mass throughout an 8-year follow-up period,
this treatment is not sufficient to decrease the number of women who experience some
level of low bone density. Therapeutic regimens should be reviewed, probably with
resumption of discussions about the need for other therapeutic strategies.
Scientific Rationale – Update June 2013
Tuchendler and Bolanowski (2013) evaluated the effects of hyperthyroidism and
hypothyroidism on osseous tissue metabolism in premenopausal women. 38 women
with hyperthyroidism, 40 with hypothyroidism and 41 healthy women participated in this
study. Initially after 6 and 12 months, each patient underwent selected hormonal,
immunological and biochemical tests, measurement of concentrations of bone turnover
markers and densitometry were also performed. On initial evaluation, lower cortical
bone density was found in patients with hyperthyroidism (femoral neck). After 12
months, an increase in BMD was seen, but it was still lower than in the control group.
Statistically significantly higher concentrations of bone turnover markers, decreasing
from the sixth month of treatment, were noted only in the group with hyperthyroidism.
Statistically significant differences were not noted in the femoral neck nor in the lumbar
spine BMD in patients with hypothyroidism. Authors concluded hyperthyroidism poses a
negative effect on bone metabolism. Hypothyroidism in premenopausal females does not
have any influence on bone density.
Ulu et al (2012) sought to evaluate bone loss in the early- and late-stage ankylosing
spondylitis (AS) patients using posteroanterior (PA) and lateral lumbar and femoral bone
mineral density (BMD) measurement methods. Eighty-six AS patients and 50 control
subjects were enrolled. PA spine, lateral spine, and femur BMD values of patients and
controls were measured. The presence of any syndesmophytes or compression fractures
was determined. Patients were divided as early (<10 years) and late stage (≥10 years)
according to the onset of the inflammatory pain. Mean PA spinal BMD was similar in
patients and controls (p = 0.460). Femoral and lateral spine BMD values were
significantly lower in patients (p = 0.012 and p = 0.001). When comparing early- and
late-stage AS groups, mean PA spinal BMD was found to be lower in the early group (p
= 0.005), while femoral and lateral spinal values were lower (although statistically not
significant) in the late group. At least one compression fracture was present in 28 % of
patients. Although not statistically significant, mean PA spinal BMD was higher in those
with fractures. Femoral and lateral spinal BMD values were significantly lower in the
fracture group (p = 0.034 and p = 0.004). Lateral spinal BMD values were significantly
lower in patients with syndesmophytes (p = 0.004). Bone loss is increased in AS
compared with control subjects. The BMD measurement at the lateral lumbar spine
reflects bone loss and fracture risk better than PA spine and femoral measurements.
Scientific Rationale – Update October 2010
van der Weijden et al (2010) sought to determine the prevalence and risk factors of low
bone mineral density (BMD) in patients with spondylarthropathies (SpA) at an early
stage of disease. In this cross-sectional study, the BMD of lumbar spine and hips was
measured in 130 consecutive early SpA patients. The outcome measure BMD was
defined as osteoporosis, osteopenia, and normal bone density. Logistic regression
Bone Mineral Density Studies Jun 16
9
analyses were used to investigate relations between the following variables: age,
gender, disease duration, diagnosis, HLA-B27, erythrocyte sedimentation rate (ESR), Creactive protein (CRP), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI),
Bath Ankylosing Spondylitis Functional Index (BASFI), Bath Ankylosing Spondylitis
Metrology Index (BASMI), extra-spinal manifestations and medication, with outcome
measure low BMD (osteopenia and/or osteoporosis). The SpA population had a median
time since diagnosis of 6.6 months and a disease duration of 6.3 years. In total, 9% of
the early SpA patients had osteoporosis, 38% osteopenia, and 53% normal BMD. On
univariate analyses, male gender, diagnosis of ankylosing spondylitis, increased CRP,
high BASFI, and high BASMI were significantly associated with low BMD. Factors
showing a relation with low BMD in the multivariate model were male gender, high
BASMI and high BASFI. In early SpA patients, a high frequency (47%) of low BMD in
femur as well as in lumbar spine was found. Low BMD was associated with male gender
and decreased functional capacity. The authors concluded the findings emphasize the
need for more alertness for osteoporosis and osteopenia in spondylarthropathy patients
at an early stage of the disease.
Alibhai et al (2010) used linked administrative databases in Ontario, Canada, and
matched 19,079 men 66 years old or older with prostate cancer with at least 6 months
of continuous androgen deprivation therapy or bilateral orchiectomy with men with
prostate cancer who had never received androgen deprivation. Matching variables were
age, prior cancer treatment, diagnosis year, co morbidity, medication, prior fractures
and socioeconomic variables. Primary outcomes were a typical fragility fracture of the
spine, hip or wrist and any fracture. Independent predictors of fracture outcomes were
assessed with Cox proportional hazards models. At a mean 6.47-year follow-up
androgen deprivation therapy was associated with an increased risk of fragility fracture
and any fracture. Independent predictors of fragility and any fracture were increasing
age, prior bone thinning medications, chronic kidney disease, prior dementia, prior
fragility fracture and prior osteoporosis diagnosis or treatment. The authors concluded
continuous androgen deprivation therapy for at least 6 months is associated with an
increased risk of fracture. Increasing age, prior osteoporotic fracture and dementia are
important clinical factors that may warrant greater consideration of anti-osteoporotic
therapy in these men.
Scientific Rationale – Update September 2009
The advent of potent acid suppressive medications such as proton pump inhibitors
(PPI’s) has revolutionized the management of acid-related diseases such as
gastroesophageal reflux disease (GERD). However, it is important that PPIs are only
given for appropriate indications and that, whenever possible, they are used in the
lowest effective dose. Many individuals have been using these medications on a
continuous or long-term basis, which could result in untoward symptoms.
Proton pump inhibitors may affect bone mineral metabolism. This class of drugs inhibits
the production and intragastric secretion of hydrochloric acid, which is believed to be an
important mediator of calcium absorption in the small intestine. A significant decreased
secretion of hydrochloric acid, known as hypochlorhydria, has been noted, particularly
among the elderly population, who may have decreased PPI clearance.
These individuals may be more likely to have hypochlorhydria at baseline due to higher
prevalence of Helicobacter pylori infection, which could theoretically result in calcium
malabsorption. Studies have shown that PPI therapy may decrease insoluble calcium
absorption or bone density. The PPI’s may also reduce bone resorption through inhibition
Bone Mineral Density Studies Jun 16
10
of osteoclastic vacuolar proton pumps. Long-term PPI therapy, particularly at high
doses, may be associated with an increased risk of hip fracture.
Recent studies have suggested that the use of proton pump inhibitors for 1 or more
years may be associated with hip fracture and other osteoporotic fractures; however,
there is limited data on additional risk beyond 4 years exposure. Because proton pump
inhibitors are commonly prescribed to control and prevent symptoms of chronic
unrelenting conditions, it is likely that many patients will use these medications for more
than 4 years.
Osteoporosis is a common condition throughout the developed world, affecting up to
16% of women and 7% of men aged 50 years and older. The presence of underlying
osteoporosis is a major risk factor for the development of fractures of the hip, proximal
femur, spinal vertebra and forearm. In 2000, the estimated number of people with
fractures worldwide was 56 million, and about 9 million new osteoporotic fractures occur
each year. This number is predicted to increase to 88,124 by the year 2041. Moreover,
the case-fatality rate for hip fractures can exceed 20%, and all osteoporosis-related
fractures can lead to substantial long-term disability and decreased quality of life.
Many risk factors for the development of osteoporosis-related fracture have been
identified, including white ethnic background, low body mass index, physical inactivity
and female sex. There are also a number of medication classes, including corticosteroids
and serotonin selective reuptake inhibitors, whose use has been linked to higher rates of
osteoporosis.
Studies
Insogna (2009) Two recent studies have reported increased hip fracture rates with longterm proton pump inhibitor (PPI) use raising concerns about adverse effects of this class
of drugs on mineral metabolism. One plausible mechanism by which PPIs could affect
calcium economy and skeletal homeostasis is by impairing intestinal calcium absorption.
In the long term, this could potentially lead to a negative whole body calcium balance,
resulting in higher rates of bone loss and a greater risk of fragility fractures.
Kate et al (2008) performed a two phase matched nested case-control study. Phase 1
identified 4414 case patients (aged 50–79 yrs) with an incident hip fracture between
1995 and 2005. Phase 2 included the 1098 case patients identified as having no major
medical risk factors for hip fracture (as assessed in phase 1) and a new set of 10,923
controls without major risk factors for hip fracture. The relative risk (RR) for hip fracture
among patients who received any PPI prescription was 0.9 (95% confidence interval
0.7–1.1) compared with those with no PPI prescription. We found no evidence of an
increased risk of hip fracture with increased PPI use. The RR estimates were similar in
both sexes and in all age subgroups. No specific PPI was associated with an increased
risk of hip fracture. Use of PPIs does not increase the risk of hip fracture in patients
without major risk factors. The difference in results between our study and that of
another, which indicated that PPI use increases the risk of hip fracture, may be due to
residual confounding or effect modification in the latter study.
Targownik et al (2008) completed a retrospective matched cohort study, using data
from Population Health Research Data Repository in Canada. The authors matched
15,792 cases of osteoporosis related fractures with 47,289 controls. No significant
association between overall risk of an osteoportic fracture and use of proton pump
inhibitors was noted for durations of 6 years or less. However, exposure of 7 or more
years was associated with increased risk of an osteoporosis-related fracture. This study
Bone Mineral Density Studies Jun 16
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also found an increased risk of hip fracture after five or more years of exposure to highdose PPI’s.
Yang et al (2006) completed a nested case control study using data from the General
Practice Research Database (1987-2003), from the U.K. Study included 13,556 hip
fracture cases and 135,386 controls. The study noted that risk of hip fracture was
increased among patients prescribed long-term, high-dose PPIs, > 5years of medication
treatment. Short-term use of PPI’s did not appear to increase the fracture risk.
In summary, all of the studies note that additional research is necessary to examine the
effect of acid inhibition on calcium absorption and bone mineral metabolism, to
determine the effect of acid inhibition on bone mineral density over time.
The National Osteoporosis Foundation guidelines do not include PPI therapy as a risk
factor for increased bone loss.
Scientific Rationale – Update March 2009
According to the National Osteoporosis Foundation (NOF), the decision to perform bone
density assessment should be based on an individual’s fracture risk profile and skeletal
health assessment. The NOF states that measurement of bone density is not indicated
unless the results will influence the patient’s treatment decision. Dual energy x-ray
absorptiometry (DXA) is the most widely used method for measuring BMD because it
gives very precise measurements at clinically relevant skeletal sites.
According to the NOF guidelines, the following bone mass measurement technologies are
capable of predicting both site-specific and overall fracture risk. When performed
according to accepted standards, these densitometric techniques are accurate and highly
reproducible:



Central or peripheral dual-energy x-ray absorptiometry (pDXA)
Quantitative computed tomography (QCT) and peripheral QCT (pQCT)
Quantitative ultrasound densitometry (QUS)
According to the NOF, central DXA assessment of the hip or spine is currently the “gold
standard” for serial assessment of BMD and may be used to monitor the effectiveness of
treatment. QCT, trabecular BMD of the lumbar spine can also be used to monitor age-,
disease- and treatment-related BMD changes in men and women. Precision of
acquisition should be established by phantom data and analysis precision by re-analysis
of patient data. The NOF notes that in postmenopausal women, QCT measurement of
spine trabecular BMD can predict vertebral fractures whereas pQCT of the forearm at the
ultra distal radius predicts hip, but not vertebral fractures. They note there is lack of
sufficient evidence for fracture prediction in men.
Quantitative computed tomography (QCT) is based on the differential absorption of
ionizing radiation by calcified tissue. Standard CT scanners are used, and attenuation
measurements are compared with a standard reference to calculate bone mineral
equivalents. Unlike other techniques, 3-dimensional BMD is directly calculated. QCT
uniquely allows for the separate estimation of cancellous and cortical bone in the
vertebral body. A focused examination of cancellous bone may be useful in assessing
response to therapy (e.g., teriparatide therapy). QCT measures volumetric trabecular
and cortical bone density at the spine and hip, whereas peripheral QCT (pQCT)
measures the same at the forearm or tibia. It is important to note that QCT and pQCT
are associated with greater amounts of radiation exposure than central DXA or pDXA.
Bone Mineral Density Studies Jun 16
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Quantitative ultrasound densitometry (QUS) does not measure BMD directly but rather
speed of sound (SOS) and/or broadband ultrasound attenuation (BUA) at the heel, tibia,
patella and other peripheral skeletal sites. A composite parameter using SOS and BUA
may be used clinically. Validated heel QUS devices predict fractures in postmenopausal
women (vertebral, hip and overall fracture risk) and in men 65 and older (hip and nonvertebral fractures). QUS is not associated with any radiation exposure.
The NOF notes that peripheral skeletal sites (e.g. peripheral DXA, pQCT and QUS) do not
respond in the same magnitude as the spine and hip to medications and thus are not
appropriate for monitoring response to therapy at this time.
Scientific Rationale - Update February 2008
As of February 20, 2008 Medicare has expanded the number of beneficiaries qualifying
for BMM by reducing the dosage requirement for glucocorticoid (steroid) therapy from
7.5 mg of prednisone per day to 5.0 mg. It also changed the definition of BMM by
removing coverage for a single-photon absorptiometry as it is not considered reasonable
and necessary under the Social Security Act (Section 1862 (a)(1)(A)) Finally, it requires
in the case of monitoring and confirmatory baseline BMMs, that they be performed with
a dual-energy x-ray absorptiometry (axial) test. Medicare also requires a valid ICD-9M
diagnosis code indicating the reason for the test is postmenopausal female, vertebral
fracture, hyperparathyroidism, or steroid therapy. (MLN Matters MM5847)
Initial Scientific Rationale
Osteoporosis, or porous bone, is a disease characterized by low bone mass and
structural deterioration of bone tissue, leading to bone fragility and an increased
susceptibility to fractures of the hip, spine, and wrist. Peak bone mass is reached around
age 30; after this age, bone resorption slowly begins to exceed bone formation.
Osteoporosis develops when bone resorption occurs too quickly or if replacement occurs
too slowly. In women, bone loss is most rapid in the first few years after menopause
but persists into the postmenopausal years
The National Institute of Health reports that in the in the U.S. today, 10 million
individuals already have osteoporosis and 34 million more have low bone mass, placing
them at increased risk for this disease. One out of every two women and one in four
men over 50 will have an osteoporosis-related fracture in their lifetime. Osteoporosis is
responsible for an estimated 300,000 hip fractures annually. More than 2 million
American men suffer from osteoporosis, and millions more are at risk. Men account for
about 25 percent of hip fractures
Bone mineral density (BMD) is a key component used by physicians to determine the
need for pharmacologic therapy to treat osteoporosis. The most widely used method to
measure bone mineral density is the Dual Energy X-ray Absortiometry, or DEXA
scanning. The scanner utilizes two sources of x-ray energy at a set frequency in an
alternating fashion which greatly improves the precision and accuracy as compared to
the more traditional radioisotope studies (such that would be used for a bone scan).
Also, when compared with radiographic absortiometry or single energy x-ray
absortiometry, DEXA scanning more precisely documents small changes in bone mass
and can be used to examine both the spine and the extremities. DEXA scanning of the
spine, hip or the total body requires only one, two or four minutes respectively.
Quantitative computed tomography (QCT) is the only technique that can directly
measure bone density and volume as well as distinguishing trabecular from cortical
Bone Mineral Density Studies Jun 16
13
bone. DEXA scanning is less expensive, exposes the patient to less radiation and is more
sensitive and accurate at measuring subtle changes in bone density over time or in
response to drug therapy than is QCT.
Reports from the various BMD technologies provide a comparison of the patient’s bone
mineral density values with those of young normal women (T score) to age matched
normal women (Z score). By comparing a patient’s bone density against the peer group,
it can be determined if the patient is at risk for fracture and if the bone mass is typical
for his/her age and sex. The T-score is expressed in standard deviations (SD). For each
standard deviation below the mean, the risk of fracture increases significantly. The
World Health Organization (WHO) defines osteopenia as a T score -1 to -2.5 standard
deviations below the mean and osteoporosis as -2.5 or more standard deviations below
the mean. Each one standard deviation in BMD below the young adult normal represents
an increased risk of fracture.
Bone mineral density measurements as a method to monitor response to treatment
generally do not need to be repeated within two years since changes in bone density
occur slowly. In addition, changes in bone mineral density at central sites (i.e., hip and
spine) are often not reflected by changes in bone mineral density at peripheral sites, so
it is recommended that peripheral measurement not used to monitor treatment
response.
Review History
May 11, 2004
June 28, 2005
August 30,2005
May 2006
July 2006
March 2007
February 2008
September 2008
March 2009
September 2009
October 2010
July 2011
June 2012
June 2013
June 2014
June 2015
June 2016
Medical Advisory Council, initial approval
Update
Update
Update to include Medicare criteria related repeat studies and steroid
dose of >= 7.5 mg per day
Update – no revisions
Coding update
Changed glucocortiosteriod dose from 7.5 mgs per day to 5.0 per
day. Removed 78350 and G0130 from Medicare covered codes.
Updated policy to comply with Medicare criteria related to BMD for
monitoring response to treatment and additional indications for more
frequent studies. Coding updates.
Updated scientific rationale with bone mass measurement
technologies accepted by the NOF as capable of predicting both sitespecific and overall fracture risk.
Added continuous or long-term therapy ‘Proton Pump Inhibitors’
(PPI’s) (> 5 years), as a criteria for Initial Bone Mineral Density
Studies.
Revised wording in criteria #1, added criteria #3, 14 and 15. Added
Medicare table, links to NCD and benefit policy.
Update. Added Revised Medicare Table. No Revisions.
Update. No Revisions.
Update – no revisions. Code updates.
Update – no revisions. Code updates
Update – no revisions. Code updates
Update – no revisions. Code updates
This policy is based on the following evidence-based guidelines:
Bone Mineral Density Studies Jun 16
14
1. National Osteoporosis Foundation. Clinician’s Guide to Prevention and Treatment of
Osteoporosis. 2008.
2. Hodgson SF, Watts NB, Bilezikian JP, et al. American Association of Clinical
Endocrinologists medical guidelines for clinical practice for the prevention and
treatment of postmenopausal osteoporosis: 2001 edition, with selected updates for
2003. Endocr Pract 2003 Nov-Dec; 9(6): 544-64.
3. American College of Obstetricians and Gynecologists (ACOG). Osteoporosis.
Washington (DC): American College of Obstetricians and Gynecologists (ACOG);
2004 Jan. 14 p. (ACOG practice bulletin; no. 50).
4. Qaseem A, Snow V, Shekelle P. et al. Screening for Osteoporosis in Men: A Clinical
Practice Guideline from the American College of Physicians. Ann Intern Med 2008
May 6;148(9):680-4. Available at:
http://www.annals.org/content/148/9/680.full
5. National Osteoporosis Foundation (NOF). Clinician’s guide to prevention and
treatment of osteoporosis. 2010.
6. American College of Radiology (ACR) Appropriateness Criteria Osteoporosis and bone
mineral density. Revised 2010.
7. American Association of Clinical Endocrinologists (AACE) Menopause Guidelines
Revision Task Force. American Association of Clinical Endocrinologists medical
guidelines for clinical practice for the diagnosis and treatment of menopause. 2010.
Available at: https://www.aace.com/files/osteo-guidelines-2010.pdf
8. Nelson H; Haney E, et al. Screening for Osteoporosis: An Update for the U.S.
Preventative Services Task Force. Annals of Internal Medicine 2010 July; 153(2):113.
9. U.S. Preventive Services Task Force. Screening for osteoporosis: U.S. preventive
services task force recommendation statement. Ann Intern Med. 2011;154(5):356.
10. National Osteoporosis Foundation (NOF). Clinician’s guide to prevention and
treatment of osteoporosis. 2013. Update Apr 2014
11. The American Congress of Obstetricians and Gynecologists. Osteoporosis. Practice
Bulletin Number 129. Sept 2012. Reaffirmed 2014
References – Update June 2016
1.
2.
3.
4.
Chen SJ, Chen YJ, Cheng CH, et al. Comparisons of Different Screening Tools for
Identifying Fracture/Osteoporosis Risk Among Community-Dwelling Older People.
Medicine (Baltimore). 2016 May;95(20):e3415.
Lloyd JT, Alley DE, Hochberg MC, et al. Changes in bone mineral density over time
by body mass index in the health ABC study. Osteoporos Int. 2016 Jun;27(6):210916.
Pavel OR, Popescu M, Novac L, et al. Postmenopausal osteoporosis - clinical,
biological and histopathological aspects. Rom J Morphol Embryol. 2016;57(1):12130.
Wu CH, Tung YC, Chai CY, et al. . Increased Risk of Osteoporosis in Patients With
Peptic Ulcer Disease: A Nationwide Population-Based Study. Medicine (Baltimore).
2016 Apr;95(16):e3309.
References – Update June 2015
1.
2.
3.
Benetti-Pinto CL, Ferreira VB, Yela DA. Long-term follow-up of bone density in
women with primary ovarian insufficiency. Menopause. 2015 Mar 9.
Heidari B, Hosseini R, Javadian Y, et al. Factors affecting bone mineral density in
postmenopausal women. Arch Osteoporos. 2015 Dec;10(1):217.
López E, Casajús JA, Ibarz E, et al. Application of a model based on dual-energy Xray absorptiometry and finite element simulation for predicting the probability of
Bone Mineral Density Studies Jun 16
15
4.
osteoporotic hip fractures to a sample of people over 60 years. Proc Inst Mech Eng
H. 2015 May;229(5):369-85
Monadi M, Javadian Y, Cheraghi M, et al. Impact of treatment with inhaled
corticosteroids on bone mineral density of patients with asthma: related with age.
Osteoporos Int. 2015 Apr 10.
References – Update June 2014
1.
2.
Imai K. Recent methods for assessing osteoporosis and fracture risk. Recent Pat
Endocr Metab Immune Drug Discov. 2014 Jan;8(1):48-59.
Kurtoglu-Aksoy N, Akhan SE, Bastu E, et al. Implications of premature ovarian
failure on bone turnover markers and bone mineral density. Clin Exp Obstet
Gynecol. 2014;41(2):149-53.
References – Update June 2013
1.
Adams JE. Advances in bone imaging for osteoporosis. Nat Rev Endocrinol. 2013
Jan;9(1):28-42
2. Briot K. DXA parameters: Beyond bone mineral density. Joint Bone Spine. 2013
Apr 23.
3. Chevalley T, Bonjour JP, van Rietbergen B, et al. Fracture history of healthy
premenopausal women is associated with a reduction of cortical microstructural
components at the distal radius. Bone. 2013 May 6.
4. Friis-Holmberg T, Rubin KH, Brixen K, et al. Fracture Risk Prediction Using
Phalangeal Bone Mineral Density or FRAX-A Danish Cohort Study on Men and
Women. J Clin Densitom. 2013 Apr 23.
5. Ikegami S, Kamimura M, Uchiyama S, et al. Unilateral vs Bilateral Hip Bone Mineral
Density Measurement for the Diagnosis of Osteoporosis. J Clin Densitom. 2013 May
15.
6. Liu X, Qian ZY, Feng YS, Li HL, Xu YJ. Comparison of differences between hip and
lumbar bone mineral density in dual energy X-ray absorptiometric data. Zhonghua
Yi Xue Za Zhi. 2013 Jan 15;93(3):191-4.
7. Rozental TD, Deschamps LN, Taylor A, et al. Premenopausal women with a distal
radial fracture have deteriorated trabecular bone density and morphology compared
with controls without a fracture. J Bone Joint Surg Am. 2013 Apr 3;95(7):633-42.
8. Runarsdottir RG, Thorsteinsdottir G, Indridason OS, Sigurdsson G. Bone mineral
density of young women with history of anorexia nervosa. Laeknabladid. 2012
Oct;98(10):523-9.
9. Tuchendler D, Bolanowski M. Assessment of bone metabolism in premenopausal
females with hyperthyroidism and hypothyroidism. Endokrynol Pol. 2013;64(1):404.
10. Ulu MA, Cevik R, Dilek B. Comparison of PA spine, lateral spine, and femoral BMD
measurements to determine bone loss in ankylosing spondylitis. Rheumatol Int.
2012 Dec 29.
References Update – June 2012
1.
2.
3.
Gourlay ML, Fine JP, Preisser JS, et al. Bone-density testing interval and transition
to osteoporosis in older women. N Engl J Med 2012; 366:225
Kleerekoper M. Screening for Osteoporosis. UpToDate. March 28 2012.
Leslie WD, Morin SN, Lix LM, for the Manitoba Bone Density Program. Rate of Bone
Density Change Does Not Enhance Fracture Prediction in Routine Clinical Practice. J
Clin Endocrinol Metab 2012.
References Update – July 2011
Bone Mineral Density Studies Jun 16
16
1.
Jamal SA. Bone mass measurements in men and women with chronic kidney
disease. Curr Opin Nephrol Hypertens. 2010;19(4):343-348.
References Update – October 2010
1.
2.
3.
4.
Abarado C, Mahon SM. Androgen-deprivation bone loss in patients with prostate
cancer. Clin J Oncol Nurs. 2010 Apr;14(2):191-8.
Alibhai SM, Duong-Hua M, Cheung AM, et al. Fracture types and risk factors in men
with prostate cancer on androgen deprivation therapy: a matched cohort study of
19,079 men. J Urol. 2010 Sep;184(3):918-23.
Khosla S. Update in male osteoporosis. J Clin Endocrinol Metab. 2010 Jan;95(1):310
van der Weijden MA, van Denderen JC, Lems WF, et al. Low bone mineral density is
related to male gender and decreased functional capacity in early
spondylarthropathies. Clin Rheumatol. 2010 Aug 10
References Update – September 2009
1.
2.
3.
4.
5.
6.
7.
Insogna KL. The Effect of Proton Pump-Inhibiting Drugs on Mineral Metabolism. Am
J Gastroenterol 2009; 104:S2–S4.
Targownik LE, Lix LM, Metge CJ, et al. Use of proton pump inhibitors and risk of
osteoporosis-related fractures. CMAJ. August 12, 2008; 179 (4).
doi:10.1503/cmaj.071330. Available at:
http://www.cmaj.ca/cgi/content/full/179/4/319
Kaye JA, Jick H. Proton Pump Inhibitor Use and Risk of Hip Fractures in Patients
without Major Risk Factors. Pharmacotherapy 2008;28(8):951–959.
Vestergaard P, Rejnmark L, Mosekilde L. Proton pump inhibitors, histamine h(2)
receptor antagonists, and other antacid medications and the risk of fracture. Calcif
Tissue Int. 2006;79:76-83.
Yang YX, Lewis JD, Epstein S, et al. Long-term Proton Pump Inhibitor Therapy and
Risk of Hip Fracture. JAMA. 2006;296:2947-2953. Available at: http://jama.amaassn.org/cgi/content/full/296/24/2947
O’Connell MB, Madden DM, Murray AM, et al. Effects of proton pump inhibitors on
calcium carbonate absorption in women: a randomized crossover trial. Am J Med.
2005;118:778-781.
Jacobson BC, Ferris TG, Shea TL, et al. Who is using chronic acid suppression
therapy and why? Am J Gastroenterol. 2003;98:51-58.
References Update – March 2009
2.
3.
4.
5.
Khoo BC, Brown K, Cann C, et al. Comparison of QCT-derived and DXA-derived
areal bone mineral density and T scores. Osteoporos Int. 2008 Dec 24.
Imai K, Ohnishi I, Matsumoto T et al. Assessment of vertebral fracture risk and
therapeutic effects of alendronate in postmenopausal women using a quantitative
computed tomography-based nonlinear finite element method. Osteoporos Int.
2008 Sep 18.
Zanchetta JR, Bogado CE, Ferretti JL et al. Effects of teriparatide [recombinant
human parathyroid hormone (1-34)] on cortical bone in postmenopausal women
with osteoporosis. J Bone Miner Res. 2003 Mar; 18(3): 539-43.
Lane NE, Sanchez S, Modin GW et al. Parathyroid hormone treatment can reverse
corticosteroid-induced osteoporosis. Results of a randomized controlled clinical trial.
Clin Invest. 1998 Oct 15; 102(8): 1627-33
References Update – October 2008
Bone Mineral Density Studies Jun 16
17
1. Centers for Medicare & Medicaid Services. LCD for Bone Mineral Density (BMD)
Studies (L20800). Effective 1/1/2007.
2. HighMark Medicare Services. Provider bulletin. Effective Jan 2007.
3. Centers for Medicare & Medicaid Services. LCD for Bone Mineral Density (BMD)
Studies (L5829) Effective 1/1/2007.
References Initial
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
The Relationship Between Bone Mineral Density and Ultrasound in Postmenopausal
and Osteoporotic Women, Yeap, SS; Pearson, D; Cawte, SA; Hosking, DJ.
Osteoporosis International 1998; 8 (2): 141-146.
Bone Densitometry: Patients Receiving Prolonged Steroid Therapy. Health
Technology Assessment, No. 9, September 1996, AHCPR Pub. No. 96-0058.
Bone Densitometry: Patients with End-Stage Renal Disease. Health Technology
Assessment, No. 8, AHCPR Pub. No. 96-0040.
Screening for Postmenopausal Osteoporosis, Wallace, Tonner and Atkins, Guide to
Clinical Preventive Services, report of the U.S. Preventive Services Task Force,
Williams and Wilkins, 1996, pp. 509-516.
U.S. Department of Health and Human Services, Center for Medicare and Medicaid
Services (CMS). Medicare Program; Medicare Coverage and Payment for Bone Mass
Measurements. 42 CFR Part 410, 63 Fed. Reg. 121, pp. 34320-34328; June 24,
1998. No authors listed.
Osteoporosis prevention, diagnosis, and therapy. NIH Consens Statement.
2000;17(1):1-45
American Academy of Orthopaedic Surgeons/American College of Obstetricians and
Gynecologists/American Geriatrics Society/American College of Radiology/American
College of Rheumatology/American Academy of Physical Medicine and
Rehabilitation/American Association of Clinical Endocrinologists/National
Osteoporosis Foundation/The Endocrine Society/American Society for Bone and
Mineral Research. Physician's guide to prevention and treatment of osteoporosis.
Belle Mead (NJ): Excerpta Medica, Inc.; 1999.
Bone Densitometry, Erlichman and Holohan, in Nuclear Medicine: Diagnosis and
Therapy, edited by Harbert, Eckelman and Neurnann; New York: Thieme Medical
Publishers, Inc., 1996, pp. 865-880.
American College of Obstetricians and Gynecologists, Committee on Gynecologic
Practice. Bone density screening for osteoporosis. ACOG Committee Opinion No.
270. Washington, DC: ACOG; 2002. No authors listed.
Management of postmenopausal osteoporosis: Position statement of The North
American Menopause Society. Menopause. 2002;9(2):84-101.
The Effect of Age on the Association Between Body-Mass Index and Mortality, J.
Stevens et. Al., New England Journal of Medicine, Volume 338, Number 1; Jan 1,
1998.
U.S. Preventive Services Task Force. Screening for Osteoporosis in Postmenopausal
Women. In: Guide to Clinical Preventive Services: Report of the U.S. Preventive
Services Task Force. 3rd ed. Rockville, MD: Agency for Healthcare Research and
Quality, 2000-2002. Available at:
http://www.ahrq.gov/clinic/3rduspstf/osteoporosis/osteorr.htm. Accessed May 3,
2004
Miller PD, Njeh CF, Jankowski LG, et al. What are the standards by which bone mass
measurement at peripheral skeletal sites should be used in the diagnosis of
osteoporosis. J Clin Densitom. 2002;5 Suppl:S39-S45.
Cummings SR, Bates D, Black DM. Clinical use of bone densitometry: Scientific
review. JAMA. 2002;288(15):1889-1897.
Bone Mineral Density Studies Jun 16
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15. Espallargues M, Sampietro-Colom L, Estrada MD, et al. Identifying bone-massrelated risk factors for fracture to guide bone densitometry measurements: A
systematic review of the literature. Osteoporos Int. 2001;12:811-822.
16. Homik J, Hailey D. Selective testing with bone density measurement. Edmonton,
Alberta, Canada: Alberta Heritage Foundation for Medical Research; 1999.
17. Bone Mineral Density at Distal Forearm Can Identify Patients with Osteoporosis at
Spine or Femoral Neck. Jones T., Davie MW; British Journal Rheumatology, 1998
May; 37 (5): 539-543.
18. Nelson HD, Helfand M. Screening for postmenopausal osteoporosis. Rockville, MD:
Agency for Healthcare Research and Quality (AHRQ); 2002.
19. Agency for Healthcare Research and Quality (AHRQ).Osteoporosis in
postmenopausal women: Diagnosis and monitoring. Rockville, MD: AHRQ; 2001.
20. Kanis JA, Brazier JE, Stevenson M, et al. Treatment of established osteoporosis: A
systematic review and cost-utility analysis. Health Technol Assess. 2002;6(29).
Institute for Clinical Systems Improvement (ICSI)
21. Densitometry as a diagnostic tool for the identification and treatment of
osteoporosis in women. Bloomington, MN: ICSI; 2000. Canadian Coordinating Office
for Health Technology Assessment (CCOHTA).
22. Bone mineral density screening. Ottawa, Canada: CCOHTA; 2003. International
Society of Clinical Densitometry (ISCD). Bone mineral density testing. Official
Positions. West Hartford, CT: ISCD; November 1, 2003.
23. Miller PD. Bone mass measurements. Clin Geriatr Med. 2003;19(2):281-297, vi.
24. Review of Bone Density Measurement; Evidence that Radiographic Osteopenia
Predicts Low Bone Mass. Ahmed Al: Ilic, D; Blake, GM; Ryner, JM; Fogel, I.
Radiology 1998 Jun; 207 (3): 619-624.
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a particular procedure, drug, service or supply is not based upon the Policies, but rather is subject to the facts
of the individual clinical case, terms and conditions of the member’s contract, and requirements of applicable
laws and regulations. The contract language contains specific terms and conditions, including pre-existing
conditions, limitations, exclusions, benefit maximums, eligibility, and other relevant terms and conditions of
coverage. In the event the Member’s contract (also known as the benefit contract, coverage document, or
evidence of coverage) conflicts with the Policies, the Member’s contract shall govern. The Policies do not
replace or amend the Member’s contract.
Policy Limitation: Legal and Regulatory Mandates and Requirements
The determinations of coverage for a particular procedure, drug, service or supply is subject to applicable legal
and regulatory mandates and requirements. If there is a discrepancy between the Policies and legal mandates
and regulatory requirements, the requirements of law and regulation shall govern.
Reconstructive Surgery
CA Health and Safety Code 1367.63 requires health care service plans to cover reconstructive surgery.
“Reconstructive surgery” means surgery performed to correct or repair abnormal structures of the body caused
by congenital defects, developmental abnormalities, trauma, infection, tumors, or disease to do either of the
following:
(1) To improve function or
(2) To create a normal appearance, to the extent possible.
Reconstructive surgery does not mean “cosmetic surgery," which is surgery performed to alter or reshape
normal structures of the body in order to improve appearance.
Requests for reconstructive surgery may be denied, if the proposed procedure offers only a minimal
improvement in the appearance of the enrollee, in accordance with the standard of care as practiced by
physicians specializing in reconstructive surgery.
Reconstructive Surgery after Mastectomy
California Health and Safety Code 1367.6 requires treatment for breast cancer to cover prosthetic devices or
reconstructive surgery to restore and achieve symmetry for the patient incident to a mastectomy. Coverage
for prosthetic devices and reconstructive surgery shall be subject to the co-payment, or deductible and
coinsurance conditions, that are applicable to the mastectomy and all other terms and conditions applicable to
other benefits. "Mastectomy" means the removal of all or part of the breast for medically necessary reasons,
as determined by a licensed physician and surgeon.
Policy Limitations: Medicare and Medicaid
Policies specifically developed to assist Health Net in administering Medicare or Medicaid plan benefits and
determining coverage for a particular procedure, drug, service or supply for Medicare or Medicaid members
shall not be construed to apply to any other Health Net plans and members. The Policies shall not be
interpreted to limit the benefits afforded Medicare and Medicaid members by law and regulation.
Bone Mineral Density Studies Jun 16
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