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Cover page of the Journal of Health Sciences

 Table of Contents  
Year : 2016  |  Volume : 9  |  Issue : 3  |  Page : 251-257

Osteoporosis: Current state and need for screening with the help of oral health physicians

1 Department of Oral and Medicine and Radiology, St.Joseph Dental College and Hospital, Eluru, Andhra Pradesh, India
2 Department of Oral Medicine and Radiology, Saraswati-Dhanwantari Dental College and Hospital and Post-Graduate Research Institute, Parbhani, Maharashtra, India
3 District Hospital, Eluru, Andhra Pradesh, India
4 Department of Oral Medicine and Radiology, Sibar Institute of Dental Sciences, Guntur, Andhra Pradesh, India

Date of Web Publication21-Dec-2016

Correspondence Address:
Dr. Abhishek Singh Nayyar
44, Behind Singla Nursing Home, New Friends' Colony, Model Town, Panipat - 132 103, Haryana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2349-5006.196340

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Osteoporosis is characterized by low bone mineral density (BMD) and deterioration of bone structure resulting in an increased susceptibility to fractures of the hip, spine and wrist. Osteoporosis contributes to a great deal of morbidity and mortality and is a large burden to the health service. In the last four decades, numerous research teams have reported oral radiographic findings associated with osteoporosis. Digital orthopantomographs (OPGs), taken for routine dental evaluations, have a significant role in screening for initial osteoporotic changes. A number of mandibular cortical indices (MCIs) have, also, been developed to allow quantification of mandibular bone mass and identification of osteoporosis. Klemetti Index (KI), mental index (MI), panoramic mandibular index (PMI), antegonial index (AI) and gonial index (GI) are, all, associated with a low bone mineral density (BMD) and of help in the initial screening of osteoporosis.

Keywords: Digital orthopantomographs, mandibular cortical indices, osteoporosis

How to cite this article:
Sindhu Y U, Nayyar AS, Siddhartha K, Kartheeki B, Bhargavi D. Osteoporosis: Current state and need for screening with the help of oral health physicians. Indian J Health Sci Biomed Res 2016;9:251-7

How to cite this URL:
Sindhu Y U, Nayyar AS, Siddhartha K, Kartheeki B, Bhargavi D. Osteoporosis: Current state and need for screening with the help of oral health physicians. Indian J Health Sci Biomed Res [serial online] 2016 [cited 2020 Jul 11];9:251-7. Available from: http://www.ijournalhs.org/text.asp?2016/9/3/251/196340

  Introduction Top

Osteoporosis is an increasing health burden for both developed and developing countries.[1] Based on a 2001 census, approximately, 163 million of Indians are above the age of 50 and this number is expected to increase to 230 million by 2015.[2] In addition, osteoporosis predominantly affects elderly females and is associated with considerable mortality and morbidity.[1],[3] In Greek, Osteos means bone and pore means porous, used to describe the porous nature of the bone. Scottish surgeon, John Hunter, (1728–1793), observed bone remodeling in the 1770s, but further explanation eluded him. French surgeon and pathologist, Jean Georges Chretien Frederic Martin Lobstein, (1777–1835), had given the term “osteoporosis” to describe the porous bones, he observed, in autopsies.[4] In the early 19th century, Sir Astley Cooper, a distinguished English surgeon, noted “the lightness and softness that the bones acquire in the more advanced stages of life” and that “this state of bone favors much the production of fractures.”[3]

  Historical Background of Osteoporosis Top

In 1940, the American physician and endocrinologist, Fuller Albright, described postmenopausal osteoporosis and proposed that it was the consequence of impaired bone formation due to estrogen deficiency.[3] However, by the mid-20th century, the only known causes of osteoporosis were atrophy and age; in other cases, the disease was termed idiopathic.[4] The process of bone formation and bone resorption continues throughout one's lifetime. In growing children and adolescents, more amount of bone is formed than resorbed. As a result, the bone density of a child is continually increasing until peak bone mass is achieved.[3] Once this peak bone mass is reached, bone formation and bone resorption continue at equal rates. In mature adults, because these functions are balanced, bone density remains the same. Human bones decrease in density and increase in porosity in approximately the third decade of life.[5] In men, bone loss starts later than in the females and progresses more slowly.[6] Skeletal fragility can result from: (a) Failure to produce a skeleton of optimal mass and strength during growth; (b) excessive bone resorption resulting in decreased bone mass and micro-architectural deterioration of the skeleton; and (c) an inadequate formative response to an increased resorption during bone remodeling phases. The bone remodeling or bone multicellular units, described years ago, by Frost and others can occur either on the surface of trabecular bone as irregular Howship's lacunae or in cortical bones as relatively uniform cylindrical Haversian systems. The process begins with the activation of hematopoietic precursors to become osteoclasts which normally requires an interaction with cells of the osteoblastic lineage. Because the resorption and reversal phases of bone remodeling are short and the period required for osteoblastic replacement of the bone is long, any increase in the rate of bone remodeling will result in a loss of bone mass. Moreover, the larger number of unfilled Howship's lacunae and Haversian canals, further, weaken the bone. Excessive resorption can, also, result in complete loss of trabecular structures, so that there is no template for bone formation. Thus, there are multiple ways in which an increase in osteoclastic resorption can result in skeletal fragility.[3],[4]

  Estrogen and Osteoporosis Top

The role of hormone estrogen has drawn the attention of skeletal researchers since the times Fuller Albright introduced a classic concept on postmenopausal osteoporosis and proposed that menopausal cessation of ovarian function and the consequent sharp reduction in circulating hormone estrogen causes bone loss that ultimately results in the condition, he termed, postmenopausal osteoporosis.[7] Subsequently, the concept that there are two forms of osteoporosis, one related to estrogen deficiency at the menopause and the other to calcium deficiency and aging of the skeleton, was proposed.[3] This has been replaced by the current concept that osteoporosis represents a continuum in which multiple pathogenic mechanisms converge to cause loss of bone mass and microarchitectural deterioration of the skeletal structures.[3] The concept that estrogen deficiency is critical to the pathogenesis of osteoporosis was based initially on the fact that postmenopausal females, whose estrogen levels naturally decline, are at the highest risk for developing this disease process. Morphologic studies and measurements of certain biochemical markers have indicated that bone remodeling is accelerated at menopause as both markers of resorption and formation are increased. Hence, contrary to the Albright's original hypothesis, an increase in bone resorption and not impaired bone formation appears to be the driving force for bone loss in the setting of estrogen deficiency.[3] However, the rapid and continuous bone loss that occurs for several years after the menopause must indicate an impaired bone formative response since in younger individuals going through the pubertal growth spurts, even faster rates of bone resorption, can be associated with an increase in bone mass. However, the increased bone formation that normally occurs in response to mechanical loading is diminished in estrogen deficiency suggesting estrogen to be both anabolic and anti-catabolic. Estrogen deficiency continues to play a role in bone loss in elderly females as evidenced by the fact that estrogen treatment rapidly reduces bone breakdown in them. Moreover, recent studies in humans have shown that the level of estrogen required to maintain relatively normal bone remodeling in elderly postmenopausal females is lower than that required to stimulate classic target tissues such as the breast and uterus. Fracture risk is inversely related to estrogen levels in postmenopausal females and as little as one-quarter of the dose of estrogen that stimulates the breast and uterus are sufficient to decrease bone resorption and increase bone mass in elderly females. This greater sensitivity of the skeleton may be age-related. Estrogen is critical for epiphyseal closure in puberty in both sexes and regulates bone turnover in males as well as females. In fact, estrogen has a greater effect than androgen in inhibiting bone resorption in males although androgen may, still, play a role. Estrogen may, also, be important in the acquisition of peak bone mass in males. Moreover, osteoporosis in elderly males is more closely associated with low estrogen than with low androgen levels. Estrogen deficiency increases and estrogen treatment decreases the rate of bone remodeling as well as the amount of bone lost with each remodeling cycle.[3] Because of a higher peak bone mass in males than in the females, a lack of menopause-like process and larger bones, the prevalence of osteoporosis is lower amongst the males than in females.[8] The concept that osteoporosis is primarily due to calcium deficiency, particularly in the elderly, was initially put forth as a counterproposal to Albright's estrogen deficiency theory.[9]

  Etiopathogenesis of Osteoporosis Top

Decreased calcium intake, impaired intestinal absorption of calcium due to aging or a systemic disease process, as well as, Vitamin D deficiency can result in secondary hyperparathyroidism. The active hormonal form, 1, 25-dihydroxycholecalciferol Vitamin D (calcitriol) is not only necessary for optimal intestinal absorption of calcium and phosphorus but also to exert a tonic inhibitory effect on the parathyroid hormone (PTH) synthesis so that there are dual pathways that can lead to secondary hyperparathyroidism. Vitamin D deficiency and secondary hyperparathyroidism can contribute not only to accelerated bone loss and increasing fragility but also to neuromuscular impairment that can increase the risk of falls. Secondary hyperparathyroidism presents when there is a relative insufficiency of Vitamin D, that is, where the levels of the circulating active form, falls below 30 ng/ml suggesting that the target for Vitamin D supplementation should be at this level or higher. The seasonal decrease in Vitamin D levels and an increase in PTH levels during the winter months is associated with an increase in fractures independent of the increase in the rate of falls. In addition, increased PTH levels are associated with increased mortality in the frail elderly independent of the bone mass and Vitamin D status.[9]

  Role of Cytokines in Osteoporosis Top

Remodeling imbalance, characterized by an impaired bone formative response to increased activation of bone remodeling, is an essential component in the pathogenesis of osteoporosis. This may be due, in part, to an age-related decrease in the capacity of osteoblasts to replicate and differentiate. However, it seems likely that specific defects in the production or activity of local and systemic growth factors will, also, contribute to impaired bone formation. Bone morphogenic proteins as well as other members of the tumor necrosis factor family have been implicated. Insulin-like growth factor, which is both a systemic and local regulator, as well as transforming growth factor-beta, can also, alter bone formation. The concept that locally produced cytokines such as interleukin-1 and prostaglandins such as prostaglandin E2 (PGE2) can affect bone in more than 30 years old individuals. Subsequently, many cytokines were found to either stimulate or inhibit bone resorption and formation. Prostaglandins have both stimulatory and inhibitory actions, however, the predominant effect of PGE2, which is the major prostaglandin produced by bone, is to stimulate both resorption and formation.[9]

  Risk Factors for Osteoporosis Top

There are several risk factors which often co-exist to increase risk for the development of osteoporosis. In the UK, the main guidance comes from the National Institute for Health and Care Excellence (NICE), the National Osteoporosis Guideline Group (NOGG) and the Scottish Intercollegiate Guidelines Network (SIGN). Various clinical risk factors which are used to assess the risk of osteoporosis include increasing age, female sex, low body mass, defined as <19 kg/m 2 by NOGG and as <18.5 kg/m 2 by NICE, parental history of hip fracture, past history of fragility fracture, especially, hip, wrist and spine fractures, corticosteroid therapy, Cushing's syndrome, alcohol intake of three or, more units per day, and/or, smoking. Secondary causes of osteoporosis include conditions such as Rheumatoid arthritis and other inflammatory arthropathies, prolonged immobilization and/or, a sedentary lifestyle, primary hypogonadism, treatment with aromatase inhibitors or, androgen deprivation therapy, primary hyperparathyroidism, hyperthyroidism, post-transplantation, chronic kidney disease, gastrointestinal disease such as Crohn's disease, ulcerative colitis and coeliac disease, untreated premature menopause (<45 years) or, prolonged secondary amenorrhoea, Type 1 diabetes mellitus, Chronic liver disease and Chronic obstructive pulmonary disease (COPD). Other than aromatase inhibitors and androgen deprivation therapy, other pharmaceutical agents which may increase the risk of fragility fractures include Proton pump inhibitors (PPIs), Enzyme-inducing anti-convulsants, long-term depot medroxyprogesterone acetate, long-term anti-depressants and Thiazolidinediones (anti-diabetic agents).[9],[10] For males, androgen deficiency and for females, estrogen deficiency, early menopause (<45 years) including surgical, cessation of menstruation for 6-12 consecutive months (excluding pregnancy, hysterectomy and/or, menopause) are considered as the important risk factors. Additional risk factors which predispose for osteoporosis secondarily include visual impairment, lack of neuromuscular co-ordination or, strength, cognitive impairment and sedative medications and alcohol apart from dementia, poor health, recent falls, low calcium intake, and low physical activity.[10] Other significant risk factors include physical characteristics of the bone such as density (mass), size, geometry, micro-architecture and composition.[11]

  Pathologic Fractures in Osteoporosis Top

Osteoporotic fractures are recognized as low-trauma, pathologic fractures, resulting from low bone mineral density (BMD). The best characterized are, by order of the related disability burden, hip fractures, vertebral fractures and the wrist fractures. There are other peripheral fractures related to low bone mineral density (BMD) or, poor quality of bone mass such as proximal humeral, pelvic, rib, proximal tibial and/or, ankle fractures.[12] Pain and disability become worse with each new fracture as does the mortality rates. Lumbar fractures have the worst impact with the spinal mobility getting impaired even in the absence of significant pain. Co-morbidity is common (kyphosis, obstructive and restrictive pulmonary diseases, etc.), in particular at advanced stages, and contributes to the burden on the quality of life (QOL) and increased mortality.[12] The fracture risk of a patient can be estimated as low (<10% in next 10 years), moderate (10-20% in next 10 years), or, high (>20% in next 10 years) using known risk factors and clinical assessment tools.[9] 93% of the females acknowledge the seriousness of osteoporosis, however, 8 out of 10 females, do not believe that they are personally at risk for it. 80% of the females with osteoporosis are not even aware of their risk before diagnosis (Osteoporosis Fact Sheet, May 2012).[13]

  Tools to Detect Osteoporosis Top

There are two tools available to calculate 10-year fracture risk rates and these include FRAX ® developed by the World Health Organization (WHO) and The Q Fracture ®, an alternative based on the UK population, calculator. The National Osteoporosis Guideline Group (NOGG) advises uses of FRAX ®, Scottish Intercollegiate Guidelines Network (SIGN) advocates use of Q Fracture ®, while the National Institute for Health and Care Excellence (NICE) advises either FRAX ® or, Q Fracture ® for the risk assessment of osteoporosis. Also, there is another index suggested by the Canadian Association of Radiologists and Osteoporosis, Canada (CAROC).[9] The FRAX ® tool was developed in 2008 by the WHO to calculate the risk of fractures in males and females from several clinical risk factors (CRF), with or, without the measurement of femoral neck bone mineral density (BMD). The clinical risk factors included in the FRAX ® algorithm are age, sex, weight, height, previous history of fracture, parental hip fracture, current smoking, glucocorticoids, rheumatoid arthritis (RA), secondary osteoporosis and alcohol intake (≥3units/day). The outputs are a 10-year probability of hip fracture and a 10-year probability of a major osteoporotic fracture (clinical spine, forearm, hip or, humerus fracture). FRAX ® was developed using baseline and follow-up data from nine prospective population-based cohorts (including Europe, Australia, Canada and Japan) and validated in 11 prospective population-based cohorts (>1 million patient years). The FRAX ® tool can be used either with or, without BMD results and is applicable to people aged between 40-90 years. Q Fracture ® was developed in 2009 and has been internally and externally validated based on large primary care populations in the UK. The algorithm is based on variables that are readily available in electronic healthcare records. It estimates an individual's 10-year risk of developing both hip and major osteoporotic fractures (including hip, spine and wrist) without BMD measurement. The clinical risk factors included in the Q Fracture ® algorithm in males and females are age, sex, body mass index (BMI), smoking, alcohol intake, glucocorticoids, asthma, cardiovascular disease, history of falls, chronic liver disease, rheumatoid arthritis (RA), Type 2 diabetes mellitus and tricyclic antidepressants. Additional factors used in females alone include hormone replacement therapy (HRT), parental history of hip fracture, menopausal symptoms, gastrointestinal malabsorption and various other endocrine disorders. Q Fracture ® is applicable to people aged between 30-85 years. The CAROC paper-based risk table takes into account age, sex, past history of fracture and glucocorticoid use secondary to any reason, to determine a 10-year absolute risk of all osteoporotic fractures, however, BMD is required to calculate this increased risk, a parameter which is optional for the use of FRAX ®.[9] The purpose of screening for osteoporosis is to identify the individuals who are likely to benefit from the treatment.[6] Low bone mineral density (BMD) is one of the major risk factors for fractures from osteoporosis.[14] The American College of Preventive Medicine (ACPM) has stated that screening with BMD testing for osteoporosis is recommended in females, aged 65 years and over, and in males, aged 70 years and over. The American College of Preventive Medicine (ACPM), also, recommends that younger post-menopausal females and males, aged 50-69 years, should undergo BMD testing if they have atleast one major or, two minor risk factors present for osteoporosis.[15]

  Novel Diagnostic Adjuncts to Detect Osteoporosis Top

Various methods for measuring the bone mineral density (BMD) include Quantitative Computed Tomography (QCT), Magnetic Resonance Imaging (MRI), Quantitative Ultrasonography (Q-USG), Single Photon Absorptiometry, Dual Photon Absorptiometry, Single X-Ray Absorptiometry, and Dual X-Ray Absorptiometry/Dual Energy X-Ray Absorptiometry (DEXA).[7] Other investigations for osteoporosis include blood tests which are useful only to establish or, to rule out secondary causes for osteoporosis.[9] Calcium, Phosphorus, Alkaline phosphatase (ALP), and active form of vitamin D evaluations can be helpful.[16] Quantitative Computed Tomography (QCT) of the lumbar spine (central QCT) is performed using conventional Computed Tomography (CT) systems. QCT of radius or, tibia (peripheral QCT) can be performed using less sophisticated equipment. QCT provides volumetric acquisitions from which BMD can be estimated. Central QCT has advantages over DEXA since it allows us to differentiate between cortical and trabecular bone masses, assess the geometry of the vertebrae, and estimate the BMD volumetrically, expressed in g/cm 3. The disadvantages of central QCT are the radiation dose and the lack of validated diagnostic criteria.[17] Quantitative Ultrasonography (Q-USG) is used for measuring BMD in the peripheral skeleton, generally at the calcaneus. Photonic Absorptiometry with Iodine-125 (I-125) was initially used to study the peripheral skeleton (radius and calcaneus). It was subsequently replaced by Dual Photonic Absorptiometry that uses Gadolinium-153 (Gd-153).[17] High resolution Magnetic Resonance Imaging (MRI) may be used for assessment of the trabecular structure of the peripheral bones (calcaneus, distal radius and phalanx). The bone architecture studied using CT or MRI, quantified in terms of scale, shape, anisotropy and connectivity, allows for the assessment of bone strength without considering the BMD. Advanced MRI techniques such as diffusion, perfusion and spectroscopy, will most likely provide useful additional information in the future.[17] BMD testing using DEXA is recognized as the best available technique for the in-vivo bone measurements.[10] DEXA is based on the variable absorption of X-ray photons by different body components and uses high and low energy X-ray photons. Depending on the equipment used, these photons can be obtained using two mechanisms. In some cases, the generator emits alternating radiation of high (140kVp) and low (70-100kVp) kilovoltage peaks while moving across the surface of the body to be examined. In others, the generator emits a constant beam while a rare-earth filter separates high energy (70keV) from low energy (40keV) photons. DEXA uses low radiation doses and generally most of these devices do not require lead shielding of the room or, special protection measures for the radiotechnicians. In the DEXA units, using pencil-beam scans, the equivalent surface dose for spine and hip examinations is approximately 20-100microSv per examination and the equivalent effective dose is 1-5microSv per examination. For fan-beam DEXA units, the dose is slightly higher, approximately 56microSv for the hip, 59microSv for the spine, and 75microSv for whole body.[17] The use of two beam energies in DEXA allows the thickness of the overlying soft tissues to be removed from consideration and the density of the bone alone to be measured. It is recommended for all post-menopausal females to reduce the incidence of osteoporotic fractures and subsequent complications, however, it is difficult in clinical practice to refer all post-menopausal females for BMD testing when considering the cost effectiveness, limited number of facilities, and trained personnels for the same.[1]

  Possible Role of Oral Health Physicians in the Initial Screening of Osteoporosis Top

Oral signs of osteoporosis offer a way to a faster and readily available tool for the diagnosis of osteoporosis. The oral health physicians could screen patients with unrecognized osteoporosis using information generally available in the dental offices. The goal of such screening is not to diagnose osteoporosis but rather to identify individuals at risk for osteoporosis and refer them appropriately.[10] It is well-known that osteoporosis results in reduced jaw bone mass, as well as, alterations of the mandibular structures, especially, the inferior border.[5] Studies done by Corten et al., Horner et al., had proved that oral radiographic changes associated with osteoporosis have focused on measures of jaw bone mass or morphology.[6] It has been shown that mandibular BMD is correlated with skeletal bone density.[10] Wowern et al. stated that a continuous sex and age-related bone loss in the mandible, as in rest of the skeleton, causes increased cortical porosity and thinning of the mandibular structures.[16]

  Mandible as a Tool in the Screening of Osteoporosis Top

The mandibular cortex is a wide area which gets influenced by various developmental, pathological, physiological and age-related changes. Taking into consideration the aforesaid changes, many researchers have concentrated on the development of specific mandibular cortical indices (MCIs). Dental radiographs, made on a large fraction of the adult population, make their potential use as a marker of skeletal health, an exciting avenue of research.[6] Orthopantomographs (OPGs) are widely used to obtain a comprehensive survey of the maxillofacial complex.[18] While any exposure to x-rays is believed to carry a risk of inducing some radiation hazard, dental radiography is generally associated with low radiation exposure and the associated risk factors. Orthopantomographs (OPGs), therefore, serve as an effective tool in the initial screening of osteoporosis.[19]

  Parameters in Mandible Sensitive to the Development of Osteoporosis Top

The most commonly studied measures of mandibular morphology in relation to osteoporosis on orthopantomographs (OPGs) include the thickness and integrity of the inferior border of mandible. Loss of alveolar bone height correlated with osteoporosis in the various cross-sectional studies conducted. Mandibular cortical porosity, buccal cortical width, inferior cortical thickness, radiographic density, and the panoramic mandibular index (PMI), have all been reported to get affected with age.[6] Numerous qualitative as well as quantitative indices have, also, been developed and these include panoramic mandibular index (PMI), morphology of mandibular inferior cortex (MIC), mandibular cortical width (MCW), and gonial index (GI), etc., for the easy assessment of the initial osteoporotic signs.[6]

Qualitative Indices

Morphology of Mandibular Inferior Cortex (MIC): Klemetti E et al.,[20] classified the morphology of mandibular inferior cortex (MIC) as follows:

  • Class I: The endosteal margin of the inferior cortex is smooth
  • Class II: The endosteal margin shows semilunar defects (lacunar resorption) with formation of endosteal cortical residues, 1 to 3 layers thick; and
  • Class III: The cortex is obviously porous with dense endosteal residues.

Quantitative Indices

  1. Mental Index: Mental index (MI) or, mandibular cortical width (MCW) is a measure of the thickness of mandibular cortex in the region of mental foramen
  2. Panoramic mandibular index: Benson BW et al.[21] defined a radiomorphometric index of mandibular cortical bone mass, the panoramic mandibular index (PMI), which is the ratio between thickness of the cortex and the distance between the margins of the mental foramen to the inferior border of the mandible
  3. Panoramic analysis: Panoramic analysis (PA) is used to measure the cortical thickness at the gonial angle and is measured at the point that bisects the angle formed by the tangent to the basal border of the mandible and the tangent to the posterior border of the mandible
  4. Antegonial index: Antegonial index (AI) as described by Ledgerton D et al.[22] is a measurement of cortical width in the region anterior to the gonion at a point identified by extending a line of 'best fit' on the anterior border of the ascending ramus down to the inferior border of the mandible. A tangent to the inferior border is drawn and a perpendicular to the tangent is plotted. The measurement of antegonion cortical thickness (antegonion index) is made along this perpendicular
  5. Gonial angle: Gonial angle (GA) is assessed by tracing a line tangent to the inferior border of the mandible and another line, tangent to the posterior border of the ramus with the intersection of these two lines identified as the mandibular or, gonial angle
  6. Antegonial angle: Antegonial angle (AA) is measured by tracing two lines parallel to the inferior border of the mandible in the antegonial region and measuring the angle of their intersection at the deepest point of the antegonial notch; and
  7. Antegonial depth: Antegonial depth (AD) is measured as the distance along a perpendicular from the deepest point of antegonial notch concavity to a line parallel to the inferior border of the mandible.

Furthermore, in all aspects of radiography, digital images have become the new way of displaying radiographic data to the observers. A growing number of dental practitioners prefer digital radiography instead of conventional film-based radiography. The advantages of digital techniques compared with film-based radiography are fast communication of images; the small storage space needed, and lower contamination of the environment. Digital radiographs can be obtained using storage phosphor plates or charge-coupled device sensors. Digital systems allow for recording of electronic patient files, are time-saving and allow for enhanced features including zooming and optimal window and level settings. Dose reduction of about 40%–70% has been reported in digital panoramic radiography compared with the conventional film-based panoramic system.[18]

  Conclusion Top

There are several risk factors which often co-exist to increase risk of development of osteoporosis substantially. Clinicians trying to improve early detection of osteoporosis and prevent fragility fractures have conflicting guidelines to follow. In such a setting, dental orthopantomographs (OPG's) serve as an effective tool in the initial screening of signs of osteoporosis. The various qualitative and quantitative indices, developed, offer a high degree of sensitivity and can help the patients, at risk, being referred for an appropriate care to stop further progression as well as to prevent the sequel which are associated with an increased morbidity and considerable decrease in the quality of life (QOL) of the affected patients.


To all the researchers and patients who contributed towards the research without whom this review would not have been feasible.

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Conflicts of interest

There are no conflicts of interest.

  References Top

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Malhotra N, Mithal A. Osteoporosis in Indians. Indian J Med Res 2008;127:263-8.  Back to cited text no. 2
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Raisz LG. Pathogenesis of osteoporosis: Concepts, conflicts, and prospects. J Clin Invest 2005;115:3318-25.  Back to cited text no. 3
Manring MM, Calhoun JH. Biographical sketch: Fuller Albright. Clin Orthop Relat Res 2011;469:2092-5.  Back to cited text no. 4
Gulsahi A, Yüzügüllü B, Imirzalioglu P, Genç Y. Assessment of panoramic radiomorphometric indices in Turkish patients of different age groups, gender and dental status. Dentomaxillofac Radiol 2008;37:288-92.  Back to cited text no. 5
White SC. Oral radiographic predictors of osteoporosis. Dentomaxillofac Radiol 2002;31:84-92.  Back to cited text no. 6
Järvinen TL, Kannus P, Sievänen H. Estrogen and bone – A reproductive and locomotive perspective. J Bone Miner Res 2003;18:1921-31.  Back to cited text no. 7
Leite AF, Figueiredo PT, Guia CM, Melo NS, de Paula AP. Correlations between seven panoramic radiomorphometric indices and bone mineral density in postmenopausal women. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2010;109:449-56.  Back to cited text no. 8
BC Guidelines: Clinical Practice Guidelines. Osteoporosis – Diagnosis, Treatment and Fracture Prevention. 2012.  Back to cited text no. 9
Dervis E. Oral implications of osteoporosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;100:349-56.  Back to cited text no. 10
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Sànchez-Riera L, Wilson N, Kamalaraj N, Nolla JM, Kok C, Li Y, et al. Osteoporosis and fragility fractures. Best Pract Res Clin Rheumatol 2010;24:793-810.  Back to cited text no. 12
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Lee K, Taguchi A, Ishii K, Suei Y, Fujita M, Nakamoto T, et al. Diagnostic efficacy of alveolar bone loss of the mandible for identifying post-menopausal females with femoral osteoporosis. Dentomaxillofac Radiol 2007;36:28-33.  Back to cited text no. 14
Taguchi A. Triage screening for osteoporosis in dental clinics using panoramic radiographs. Oral Dis 2010;16:316-27.  Back to cited text no. 15
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Lorente Ramos RM, Azpeitia Armán J, Arévalo Galeano N, Muñoz Hernández A, García Gómez JM, Gredilla Molinero J. Dual energy X-ray absorptimetry: Fundamentals, methodology, and clinical applications. Radiologia 2012;54:410-23.  Back to cited text no. 17
Ghosh S, Vengal M, Pai KM, Abhishek K. Remodeling of the antegonial angle region in the human mandible: A panoramic radiographic cross-sectional study. Med Oral Patol Oral Cir Bucal 2010;15:e802-7.  Back to cited text no. 18
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