Pattern Of Bone Loss Research Articles

Genetic Background Influences Cortical Bone Response to Ovariectomy

Peak bone mass is genetically determined, but little is known about the heritability of bone loss. Inbred mice were ovariectomized at 16 weeks of age and killed at three time-points after surgery. We found that the variation in estrogen deficit-related cortical bone loss is genetically determined. Variability in adult bone morphology and composition among three inbred mouse strains-A/J, C57BL/6J (B6), and C3H/HeJ (C3H)-suggests that they gain bone in different ways during growth. In this study, we tested the hypothesis that these strains would also lose bone differently after estrogen deprivation. Female A/J, B6, and C3H mice (N = 70/strain) were either ovariectomized (OVX) or sham-operated at 16 weeks of age and killed at 4, 8, and 16 weeks after surgery. Cortical bone histomorphometry was performed on right femoral mid-diaphyseal cross-sections. Mechanical properties were determined by loading left femoral mid-diaphyses to failure in four-point bending. Both OVX-A/J and OVX-B6 mice showed a 7-8% decrease in cortical area and width because of an 8-10% marrow expansion at 16 weeks after OVX. This bone loss did not affect mechanical properties in OVX-A/J femurs, but maximum load and stiffness in OVX-B6 decreased slightly (9%) at 4 and 8 weeks, and markedly (14-19%) at 16 weeks after OVX. In contrast, OVX-C3H showed a significant decrease in cortical area and width (6-7%) at 4 weeks after OVX and a slight decrease in the subperiosteal area (4%) at 8 weeks after OVX, although marrow area remained unchanged. Surprisingly, intracortical resorption spaces, which were present in sham-C3H mice, were greatly increased (+195%) in OVX-C3H mice at 8 weeks after OVX. Bone strength and stiffness in OVX-C3H mice decreased markedly (12-14%) at 4 weeks but slightly (8-10%) at 8 weeks after OVX. All indices except intracortical pore area in OVX-C3H mice returned to sham levels at 16 weeks after OVX. The magnitude, timing, and location of cortical bone loss after OVX varied significantly among A/J, B6, and C3H mice. The subsequent changes in mechanical properties after OVX depended on the variable bone patterns as well as the size and shape of the adult bone. Our results suggest that patterns of estrogen deficit-associated cortical bone loss are genetically determined.

Multiple factors associated with HA-coated implants had more marginal bone loss but greater survival rates at 12 years than pure titanium implants

Original Article Schwart-Arad D, Mardinger O, Levin L, Kozlovsky A, Hirshberg A. Marginal bone loss pattern around hydroxyapatite-coated versus commercially pure titanium implants after up to 12 years of follow-up. Int J Oral Maxillofac Implants 2005;20:238-44. Level of Evidence 2b Purpose/Question The purpose of this study was to compare the marginal bone loss (MBL), complications, and 12-year survival rates of commercially pure titanium (cpTi) and hydroxyapatite (HA)–coated implants placed in the maxilla. Source of Funding None listed Type of Study/Design Systematic review

Osteoporosis after spinal cord injury

Osteoporosis is a known consequence of spinal cord injury (SCI) and occurs in almost every SCI patient. It manifests itself as an increase in the incidence of lower extremity fractures. The pattern of bone loss seen in SCI patients is different from that usually encountered with endocrine disorders and disuse osteoporosis. In general, there is no demineralization in supralesional areas following SCI. Several factors appear to have a major influence on bone mass in SCI individuals, such as the degree of the injury, muscle spasticity, age, sex and duration after injury. At the lumbar spine, bone demineralization remains relatively low compared to that of the long bones in the sublesional area. A new steady state level between bone resorption and formation is reestablished about 2 years after SCI. SCI may not only cause bone loss, but also alter bone structure and microstructure. Trabecular bone is more affected than cortical bone in the SCI population. Numerous clinical series have reported a high incidence ranging from 1 to 34% of lower extremity fractures in SCI patients. The pathogenesis of osteoporosis after SCI remains complex and perplexing. Disuse may play an important role in the pathogenesis of osteoporosis, but neural factors also appear to be important. SCI also leads to impaired calcium and phosphate metabolism and the parathyroid hormone (PTH)-vitamin D axis. Pharmacologic intervention for osteoporosis after SCI includes calcium, phosphate, vitamin D, calcitonin and biphosphonates. However, the concomitant prescription of bone-active drugs for the prevention and treatment of osteoporosis remains low, despite the availability of effective therapies. Functional stimulated exercises may contribute to the prevention of bone loss to some extent. In addition, many unanswered questions remain about the pathogenesis of osteoporosis and its clinical management.

Ovariectomy-Induced Bone Loss Varies Among Inbred Strains of Mice

There is a subset of women who experience particularly rapid bone loss during and after the menopause. However, the factors that lead to this enhanced bone loss remain obscure. We show that patterns of bone loss after ovariectomy vary among inbred strains of mice, providing evidence that there may be genetic regulation of bone loss induced by estrogen deficiency. Both low BMD and increased rate of bone loss are risk factors for fracture. Bone loss during and after the menopause is influenced by multiple hormonal factors. However, specific determinants of the rate of bone loss are poorly understood, although it has been suggested that genetic factors may play a role. We tested whether genetic factors may modulate bone loss subsequent to estrogen deficiency by comparing the skeletal response to ovariectomy in inbred strains of mice. Four-month-old mice from five inbred mouse strains (C3H/HeJ, BALB/cByJ, CAST/EiJ, DBA2/J, and C57BL/6J) underwent ovariectomy (OVX) or sham-OVX surgery (n = 6-9/group). After 1 month, mice were killed, and microCT was used to compare cortical and trabecular bone response to OVX. The effect of OVX on trabecular bone varied with mouse strain and skeletal site. Vertebral trabecular bone volume (BV/TV) declined after OVX in all strains (-15 to -24%), except for C3H/HeJ. In contrast, at the proximal tibia, C3H/HeJ mice had a greater decline in trabecular BV/TV (-39%) than C57BL/6J (-18%), DBA2/J (-23%), and CAST/EiJ mice (-21%). OVX induced declines in cortical bone properties, but in contrast to trabecular bone, the effect of OVX did not vary by mouse strain. The extent of trabecular bone loss was greatest in those mice with highest trabecular BV/TV at baseline, whereas cortical bone loss was lowest among those with high cortical bone parameters at baseline. We found that the skeletal response to OVX varies in a site- and compartment-specific fashion among inbred mouse strains, providing support for the hypothesis that bone loss during and after the menopause is partly genetically regulated.

Metacarpal radiogrammetry: a useful indicator of bone loss throughout the skeleton?

Metacarpal radiogrammetry has received increasing interest in recent studies of archaeological human bone in facilitating the identification of age-related cortical bone loss and osteoporosis risk in the past. The technique is relatively simple and non-destructive, and existing comparative clinical data is an advantage in its application to archaeological samples. In order for metacarpal radiogrammetry to be useful in identifying individuals that could have been at risk of fracture in the past, cortical bone loss as measured at the second metacarpal is assumed to be reflective of bone loss occurring throughout the skeleton and across the metabolically different cortical and trabecular bone. Archaeological studies have frequently relied on literature reviews of clinical data to justify the technique as valid and useful. However, the present study has examined whether cortical bone loss measured in the second metacarpal is similar to bone loss measured at specific skeletal sites that are more frequently affected by osteoporosis-related fracture. Skeletons from two post-medieval collections from London, UK, Redcross Way and Farringdon Street (lower burial ground of St. Bride's Church) were studied. The results of the present study demonstrate that the second metacarpal is useful in identifying age-related bone loss at sites that are predilected to osteoporotic fracture, most notably the distal radius, which is prone to Colles' fractures. Metacarpal radiogrammetry also correlates well with bone loss in skeletal sites that are primarily composed of trabecular bone, including the fourth lumbar vertebra (a site of compression fractures) and the iliac crest (the location for clinical biopsies). The present study also confirms previous findings of significant differences between the pattern of cortical bone loss between the metacarpal and the femur. The poor relationship between these two areas is most likely attributable to mechanical loading.

Tibial cancellous bone changes in patients with knee osteoarthritis. A short-term longitudinal study using Fractal Signature Analysis

To quantify tibial cancellous bone changes over 24 months in patients with medial compartment knee osteoarthritis (OA) subdivided into those with slow or detectable joint space narrowing (JSN). Digitised macroradiographs (4x) were obtained at baseline and 24 months from 40 patients (F:26) and subdivided by computerised measurement of minimum medial compartment joint space width (JSW) into those with slow JSN (<0.2 mm/year, n=66) or detectable JSN (>or=0.2 mm/year, n=14) and who had a mean (range) JSW at baseline of 3.89 (1.66-5.48) mm and 3.73 (2.49-5.74) mm, respectively. Fractal Signature Analysis measured longitudinal change in bone structure at four regions of interest (ROI): medial and lateral subchondral (Sc) and subarticular (Sa) regions. Mean (range) JSN for slow and detectable groups was 0.01 (-0.31-0.18) mm/year and 0.44 (0.20-1.01)mm/year, respectively. All ROIs in both groups had significant (P<0.05) decrease in fractal dimension (FD) at most trabecular sizes (vertical: 0.36-1.14 mm; horizontal: 0.36-1.14 mm, excluding the lateral Sa region) over 24 months. There were no between-group differences except at a few trabecular sizes within the Sa regions where the detectable JSN group had significantly (P<0.05) greater decrease in FD compared to the slow JSN group (medial: horizontal sizes 0.54-0.72 mm, 1.02-1.08 mm; lateral: vertical sizes 0.90-1.02 mm). Bone loss occurred in all knees with medial compartment OA. Decrease in FD of vertical and horizontal trabeculae was consistent with decrease in trabecular number associated with loss. The pattern of bone loss was similar in knees with slow and detectable JSN.

Classification, reproducibility and prevalence of root proximity in periodontal patients

The primary aim of this study is to define and classify root proximity. The secondary aim is to examine the reproducibility of the measurement tools, to study the prevalence per inter-dental area and to examine whether the distance from the cemento-enamel junction (CEJ) to the bone crest (BC) differs between sites with root proximity and their contra-lateral sites without root proximity. In order to indicate the location of root proximity, a modification of the Shei ruler was developed, dividing the roots into three equal parts. A radiographic template was used to measure the distance between the roots, in this way determining the severity of the root proximity. The reproducibility of the measurement tool was tested, the prevalence was calculated and the distances CEJ-BC for root proximity sites and contra-lateral sites were recorded. A two-digit classification was obtained dividing the root into three locations [apical (A), between (B) and coronal (C)], with each location having the possibility of three different severities of root proximity. The described modification of the Shei ruler and the measurement tool for the severities can be considered as reproducible measurement tools. Root proximity was most prevalent in maxillary molars and between central and lateral incisors in the maxilla and mandible. There was no difference in CEJ-BC distance between the root proximity sites and their contra-lateral sites. We can conclude that a two-digit classification for root proximity was established. Root proximity in untreated periodontal patients has no influence on the distance CEJ-BC. However, the location of root proximity becomes important from the moment that periodontal disease has been established at that site. The severity of root proximity is important for choosing treatment options. There is a striking similarity between bone loss patterns and tooth loss and the location of inter-dental spaces where root proximity is most prevalent.

Retinoid-induced bone thinning is caused by subperiosteal osteoclast activity in adult rodents

Excess of Vitamin A (retinol) and related compounds (retinoids) induces bone fragility and is associated with increased hip fracture incidence in humans. Yet, their impact on the adult skeleton has been studied in relatively little detail. It is assumed that they induce generalized bone loss and decrease long-bone thickness due to reduction of radial bone growth. Here we characterized early skeletal responses of adult rodents to retinoid treatment, revealing novel aspects of retinoid action on the mature skeleton. The retinoid Ro 13-6298, given subcutaneously for 4 days, induced bone loss in the hind limbs of 12- and 56-week-old rats and of 15-week-old mice. In vivo monitoring of bone mass and geometry changes by peripheral quantitative computed tomography demonstrated that bone mass decline was due to subperiosteal cortical bone loss, which induced a shrinkage of bone diameter, whilst cancellous bone mass was preserved. We observed that the native retinoic acid isomer all- trans RA induced an identical pattern of bone loss. Histomorphometric evaluation revealed that increased subperiosteal osteoclastic bone resorption caused the cortical bone destruction. Interestingly, bone resorption was suppressed in cancellous bone, which was in agreement with reduced in vitro formation of osteoclasts from bone marrow cells that were derived from the proximity of cancellous bone. The retinoid-induced increase in subperiosteal bone resorption could be blocked by bisphosphonate as direct potent inhibitor of osteoclast action, but not by estradiol. Retinoid treatment induced a reduction of bone-forming surfaces at the subperiosteal site, but not in cancellous bone. In vitro osteoblast performance was also reduced or unchanged, depending on the cellular system used and assay type/duration. In conclusion, our studies revealed that the impact of retinoids on bone is highly bone-compartment-specific at early treatment phases. Furthermore, we showed that bone diameter shrinks in the adult skeleton after retinoid treatment due to subperiosteal osteoclastic bone resorption. Thus, retinoid-induced bone thinning is not only due to reduced radial bone growth as previously assumed. Our findings might explain why high intake of retinol is associated with increased hip fracture risk in the elderly and suggest a therapy to prevent such potential negative effects.

Sexual dimorphism and age dependence of osteocyte lacunar density for human vertebral cancellous bone

The sexual dimorphism in age-related loss of human vertebral cancellous bone is not fully understood and could be related to dimorphism in the bone cell populations. The objective of this study was to investigate age- and gender-related differences in the osteocyte population and its relationship with bone volume fraction for human vertebral cancellous bone. Histomorphometric techniques were used to quantify osteocyte lacunae (a measure of osteocyte population) and bone volume fraction in male and female human T12 vertebrae, the most common site of vertebral fracture. Two measures of osteocyte population [number of osteocytes per bone area (OtLcDn) and number of osteocytes per total area (OtLcN/TA)] and their relationships with age and bone volume fraction were found to be sexually dimorphic. Dimorphism in osteocyte density may explain the dimorphic patterns of bone loss in human vertebrae due to the sensory and signal communication functions that osteocytes perform.

Getting the Dog Moving After Surgery

Getting the Dog Moving After Surgery

Bed rest and other determinants of bone loss during pregnancy

The purpose of this study was to evaluate patterns of bone loss during pregnancy and potential influences. This was a prospective study of 181 women receiving prenatal care at Magee-Womens Hospital or its auxiliary clinics in Pittsburgh, Pennsylvania, between 1992 and 1995. Bone mineral density was measured at approximately 16 and 36 weeks' gestation. Trabecular, but not cortical, bone loss occurred during pregnancy. Mean ultra-distal bone mineral density loss was 1.9% (95% CI 1.2-2.5) during the 20-week period. Women prescribed bed rest had an adjusted mean loss of 4.6% compared with 1.5% for women not prescribed bed rest ( P = .001) and 6-fold higher odds ( P = .001) of bone loss > or =5% during the 20-week period. Nulliparity, calcium intake < 2 000 mg/day, low weight gain, and maternal age < 21 or >30 years were more modestly associated with greater bone loss. Substantial trabecular bone loss may occur during pregnancy, particularly in women prescribed bed rest. Study of postpartum bone recovery in such women is needed.

Intra‐oral pattern of tooth and periodontal bone loss between the age of 50 and 60 years. A longitudinal prospective study

Objective: In a 10‐year prospective study we analyzed (i) the intra‐oral pattern of and (ii) potential risk factors for tooth and periodontal bone loss in 50‐year‐old individuals. Methods: A randomized subject sample of 50‐year‐old inhabitants in the County of Värmland, Sweden, was examined at baseline and after 10 years. Data from full‐mouth clinical and radiographic examinations and questionnaire surveys of 309 (72%) of the individuals who were dentate at baseline were available for analysis. Non‐parametric tests and binary logistic multiple regression models were used for statistical analysis of the data. Results: 4.1% of the 7,101 teeth present at baseline, distributed among 39% of the subjects, were lost during the 10‐year interval. The incidence of tooth loss was highest among mandibular molars (7.5%) and lowest among canines (1.8%). The relative risk (RR) for tooth loss for endodontically compromised teeth was 4.1 and for furcation‐involved molars 2.4–6.5, depending on tooth position. Logistic regression analysis identified baseline alveolar bone level (ABL), endodontic conditions, CPITN score (Community Periodontal Index of Treatment Needs), tooth position, caries, and educational level as risk factors for tooth loss. The overall mean 10‐year ABL change was −0.54 mm (S.E. 0.01). On a tooth level the ABL change varied between −0.35 mm (mandibular molars) and −0.79 mm (mandibular incisors). Smokers experienced a greater (20–131% depending on tooth type) mean bone loss than non‐smokers. The logistic regression model revealed that tooth position, smoking, and probing pocket depth ≥4 mm were risk factors for bone loss of >1 mm. No pertinent differences were observed with respect to risk factors for ABL change in the subgroup of non‐smokers compared to the results of the analysis based on the entire subject sample. Conclusion: Tooth loss was more common in the molar than in the anterior tooth regions, while periodontal bone loss had a random distribution in the dentition. The predominant risk factors identified with regard to further radiographic bone loss were ‘probing pocket depth ≥6 mm’ and ‘smoking’.

Normal Acquisition and Loss of Bone Mass

The natural patterns of bone mass accumulation and loss with age represent the templates of individual life cycle periods that are distinguished by marked, physiologically and genetically identifiable, changes in bone mass. During the third trimester of pregnancy, maternal calcium absorption increases and the fetus accumulates about two-thirds of the total bone mass of the term infant. In early infancy, human milk calcium is derived primarily from maternal bone stores, which incur substantial bone losses that are quickly replenished during and after weaning. At puberty, a marked increase in bone mass occurs in conjunction with the initial physical and hormonal changes that characterize this stage. Calcium absorption and bone calcium deposition rates peak in females shortly before menarche. At that time, the bone calcium deposition rate is approximately five times that of adulthood. Skeletal bone mass reaches over 90% of its maximum by age 18 (earlier in females) but does not peak until age 25–30. At some point in mid-life, women experience perimenopause, the 3- to 5-year period prior to menopause during which estrogen levels begin to drop and there are marked increases in bone resorption and loss. Throughout adulthood, calcium absorption efficiency from the diet gradually declines.

Osteopenia and osteoporosis in patients with end-stage liver disease caused by hepatitis C and alcoholic liver disease: Not just a cholestatic problem

Although best characterized in chronic cholestatic liver disease, osteopenic bone disease and fracturing are well-recognized complications of cirrhosis, particularly after liver transplantation. We sought to compare the prevalence of osteopenia and osteoporosis, to assess the effect of orthotopic liver transplantation (OLT) on bone density, and to determine fracture rates before and after OLT in three groups of patients with advanced cirrhosis: patients with cirrhosis from hepatitis C virus (HCV) alone, from alcohol abuse (ALD), and from HCV in conjunction with alcohol abuse (HCV+ALD). Between 1991 and 2001, 207 consecutive patients who underwent OLT for HCV (68 patients), ALD (66), and HCV+ALD (73) were assessed clinically, biochemically, radiologically, and by bone densitometry. The baseline mean T score was lower in the HCV group than in the ALD group (-1.43 versus -0.87, P =.048) despite ALD patients having more advanced liver disease; patients with HCV+ALD had intermediate T scores. The pattern of significant bone loss at 4 months and 12 months was similar for all three groups. The baseline fracture rate was lowest in the HCV group and highest in the ALD group, despite the latter having the highest bone density. Fractures occurred in 17% of patients in the first year after transplantation, the majority being vertebral compression fractures. Patients with cirrhosis caused by HCV, ALD, or a combination of both should be screened for osteopenia, especially before OLT.

Understanding prosthodontics — where did it all go wrong?

This paper addresses the anatomical and physiological effects of tooth loss on the patient and, further, audits the teaching of prosthodontics over the last 30 years. There is an abundance of evidence to outline changes that occur post-extraction related to morphological changes in the maxilla, the mandible and combined changes in inter-maxillary relations. In addition to the knowledge of patterns of bone loss, we are also now well aware that there is evidence to suggest that planned retention of roots and/or the placement of implants can help reduce post-extraction bone loss. Awareness by clinicians of the anatomical, physiological and psychological effects of edentulousness, is essential if empathy is to be struck with the patient. Equally, patients being rendered edentulous must be made aware of these factors if true informed consent is to be gained. New graduates are now less well equipped to practice complete denture prosthodontics than, say, 10 years ago and this is a consequence of three factors: crowded curricula, diminution in laboratory hours and the time a dental student spends in clinical prosthodontics.

Medieval trabecular bone architecture: The influence of age, sex, and lifestyle

Osteoporosis has become a growing health concern in developed countries and an extensive area of research in skeletal biology. Despite numerous paleopathological studies of bone mass, few studies have measured bone quality in past populations. In order to examine age- and sex-related changes in one aspect of bone quality in the past, a study was made of trabecular bone architecture in a British medieval skeletal sample. X-ray images of 5-mm-thick coronal lumbar vertebral bone sections were taken from a total of 54 adult individuals divided into three age categories (18-29, 30-49, and 50+ years), and examined using image analysis to evaluate parameters related to trabecular bone structure and connectivity. Significant age-related changes in trabecular bone structure (trabecular bone volume (BV/TV), trabecular number (Tb.N), trabecular separation (Tb.Sp), and anisotropic ratio (Tb.An)) were observed to occur primarily by middle age with significant differences between the youngest and two older age groups. Neither sex showed continuing change in trabecular structure between the middle and old age groups. Age-related changes in bone connectivity (number of nodes (N.Nd) and node-to-node strut length (Nd.Nd)) similarly indicated a change in bone connectivity only between the youngest and two older age groups. However, females showed no statistical differences among the age groups in bone connectivity. These patterns of trabecular bone loss and fragility contrast with those generally found in modern populations that typically report continuing loss of bone structure and connectivity between middle and old age, and suggest greater loss in females. The patterns of bone loss in the archaeological samples must be interpreted cautiously. We speculate that while nutritional factors may have initiated some bone loss in both sexes, physical activity could have conserved bone architecture in old age in both sexes, and reproductive factors such as high parity and extended periods of lactation could have played a key role in female bone maintenance in this historic population. The study of qualitative elements (such as trabecular architecture) is vital if we are to understand bone maintenance and fragility in the past.

Bone development and age-related bone loss in male C57BL/6J mice

The objective of this study was to examine changes in the long bones of male C57BL/6J mice with growth and aging, and to consider the applicability of this animal for use in studying Type II osteoporosis. Male C57BL/6J mice were aged in our colony between 4 and 104 weeks ( n = 9–15/group). The right femur and humeri were measured for length and subjected to mechanical testing (3-point flexure) and compositional analysis. The left femurs were embedded and thick slices at the mid-diaphysis were assessed for morphology, formation indices, and bone structure. In young mice, rapid growth was marked by substantial increases in bone size, mineral mass, and mechanical properties. Maturity occurred between 12 and 42 weeks of age with the maintenance of bone mass and mechanical properties. From peak levels, mice aged for 104 weeks experienced decreased whole femur mass (12.1 and 18.6% for dry and ash mass, respectively), percentage mineralization (7.4%), diminished whole bone stiffness (29.2%), energy to fracture (51.8%), and decreased cortical thickness (20.1%). Indices of surface-based formation decreased rapidly from the onset of the study. However, the periosteal perimeter and, consequently, the cross-sectional moments of inertia continued to increase through 104 weeks, thus maintaining structural properties. This compensated for cortical thinning and increased brittleness due to decreased mineralization and stiffness. The shape of the mid-diaphysis became increasingly less elliptical in aged mice, and endocortical resorption and evidence of subsequent formation were present in 20–50% of femurs aged ≥78 weeks. This, combined with the appearance of excessive endocortical resorption after 52 weeks, indicated a shift in normal mechanisms regulating bone shape and location, and was suggestive of remodeling. The pattern of bone loss at the femoral mid-diaphysis in this study is markedly similar to that seen in cortical bone in the human femoral neck in Type II osteoporosis. This study has thus demonstrated that the male C57BL/6J mouse is a novel and appropriate model for use in studying endogenous, aging-related osteopenia and may be a useful model for the study of Type II osteoporosis.

Periodontal bone loss associated with an improper flossing technique: a case report

This article documents a case in which soft tissue and bone damage was associated with a long-standing habit of improper flossing. A 33-year-old patient with excellent oral hygiene presented with gingival clefting and an unusual pattern of moderate angular bone loss at several sites. Previous radiographs suggested that some bony lesions had been present for more than 13 years. Examination revealed no evidence that the osseous defects were related to chronic periodontitis or occlusal trauma. The focus of treatment for these chronic injuries was teaching the patient an atraumatic flossing technique. As the lesions had gone undiagnosed for many years, this case underscores the need to look for clinical signs of floss-induced damage during periodic examinations.

A theoretical analysis of the changes in basic multicellular unit activity at menopause

Bone loss at menopause is an important contributor to the development of osteoporosis in women. Although alterations in bone remodeling are the implied process through which bone is lost at menopause, how menopause influences basic multicellular units (BMUs), the teams of cells that perform bone remodeling, is not completely clear. In this analysis we utilize a computer simulation of BMU activity to evaluate the changes that occur at menopause. Transient and maintained changes in both the rate of bone turnover (expressed as the BMU birthrate or origination frequency) and the focal bone balance (differences between the amount of bone formed and resorbed at each remodeling site) are considered. The magnitude of the change in BMU activity is determined parametrically through comparison to lumbar spine bone mineral density data present in the literature. We find that a change in bone turnover that is maintained after menopause, a transient change in focal bone balance at menopause, or a combination of the two is consistent with bone loss patterns seen clinically. Understanding the changes in BMU activity that occur at menopause could lead to improved strategies to treat and prevent postmenopausal osteoporosis.

Strategies of stem fixation and the role of supplemental bone graft in revision total knee arthroplasty.

Bone loss is commonly encountered at the time of revision total knee arthroplasty because of loosening of the implant, osteolysis, infection, or difficulty with removal of the original implant. Regardless of the etiology of the bone loss, its location and magnitude may compromise adequate fixation, alignment, and ligamentous stability of the revision prosthesis. In the setting of bone stock deficiency, or when an implant with a constrained articulation is used, it is prudent to use a longer stem to effect stress transition that protects weak or newly grafted proximal bone1. Successful stabilization of the implant construct can be achieved with a variety of fixation strategies: cementing the condylar surfaces of the implant while using a cementless press-fit stem2,3, fixation of the entire construct without cement4, or fixation of the entire construct with cement. All have been used with success5-7. Because patterns of bone loss can vary so extensively, a classification of the bone loss that is encountered during revision total knee arthroplasty is useful when selecting patients for bone graft procedures. The classification system of the Anderson Orthopaedic Research Institute (AORI) provides guidelines for bone defect management at the time of revision total knee arthroplasty8( Table I). Type-1 defects can be restored either with local autologous bone grafts that are obtained during the revision or with particulate allograft. Type-2 defects are associated with damaged metaphyseal bone that requires either cement, metal augments, or a bone graft to restore the joint line. Type-2 defects may be subdivided into Type-2A defects (involving only one condyle) or Type-2B defects (involving both condyles). Structural and particulate bone graft may be used for Type-2 defects depending on the need for structural support of the prosthesis. Type-3 defects are characterized by deficient …