Blood Coagulation and Platelet Economy in Subjects with Primary Gout

Previous studies have suggested that there is an increased incidence of degenerative vascular disease in patients with gout and an increased rate of turnover of blood platelets in patients and animals with atherosclerosis. A disturbed uric acid metabolism and “secondary” gout have long been known to occur with bone marrow diseases. A study of platelet economy and blood clotting factors in subjects with primary gout was therefore undertaken.Twenty-two male subjects with gout but with no clinical evidence of vascular disease were studied. Half of these had a negative family history for vascular disease and half had less fortunate ancestors. The most striking differences were found when gouty patients with a negative family history for vascular disease were compared with similar control subjects. The mean platelet half-life was 2.85 days in the gouty subjects and 3.74 days in the controls. The mean platelet turnover (number/c.mm./day) was 58,750 in gouty subjects, 42,370 in controls. Platelet adhesiveness and plasma thromboplastic activity were correspondingly increased in the gouty subjects. Control subjects with a positive family history all showed relatively active clotting system and platelet turnover, similar to the values found in atherosclerotic subjects. The data indicated that there is increased platelet destruction and production in some patients with primary gout. The relation between this anomaly and the vascular disease, and disturbed urate metabolism in gouty subjects, remains to be investigated.     

Paleoepidemiolgical patterns of trauma in a prehistoric population from central California

Skeletal trauma was investigated in a large collection of human remains from central California (N = 162 aged and sexed adults). Lesions investigated included cranial and long bone fractures, projectile wounds, and dislocation. Long bone fractures were found in 10.5% of individuals; overall, incidence by element was 2.3%. In addition, cranial injuries were found in 4.4% of complete adult crania. Projectile wounds were seen unambiguously in four individuals (with embedded obsidian fragments) and strongly suggested in two other individuals with partially healed lesions. Finally, one case of traumatic hip dislocation was also observed. In both incidence and patterning of injuries, this population is similar to other archeological groups from California. This evidence further supports earlier reports indicating that interpersonal aggression was quite common in prehistoric California.     

Diagnostic value of fine needle aspiration cytology in gouty tophi: a report of 7 cases

BACKGROUND The diagnosis of gout can be problematic when the presentation is atypical and serum uric acid is borderline elevated. Demonstration of monosodium urate (MSU) crystals in fine needle aspiration (FNA) smears from nodular masses clinically suspected to be tophi establishes the diagnosis unequivocally. CASES: Of the 7 cases in this study, 4 were suspected clinically to have gouty tophi. Giant cell tumor of tendon sheath, giant cell tumor of bone and metastatic tumor with multicentric involvement of bone were the clinical diagnoses in 1 case each. Serum uric acid levels high enough to be in the diagnostic range for gout were reported in 3 cases, within normal limits in 3 cases and low in 1 chronic alcoholic patient. Bright field microscopy of FNA smears revealed singly scattered or stacks of MSU crystals with variable number of inflammatory cells, with or without foreign body giant cells in 6 cases. In 1 patient, FNA showed stacks of MSU crystals only. Characteristic birefringence of MSU crystals was observed on polarizing microscopy. CONCLUSION: FNA demonstration of MSU crystals on polarizing microscopy can easily establish the nature of the nodules in and around the joints and in soft tissue as gouty tophi and is thus an investigation differentiating this lesion from other masses clinically simulating it.     

Cytology of urate milk in gouty arthritis: a case report

BACKGROUND: Synovial fluid (SF) analysis is a useful investigative procedure in the evaluation of various types of arthritides, including gouty arthritis. Rarely, gouty arthritis may present with effusion containing thick, milky white fluid. We report a case of gouty arthritis, describing cytologic features of the urate milk. CASE: A 42-year-old man presented with pain and swelling of multiple joints of long duration. Approximately 3 mL of milky white SF was obtained for white blood cell (WBC) count, with a clinical diagnosis of septic arthritis. Due to the gross nature of the sample, the WBC count could not be performed; however, cytologic examination of the sample revealed a massive amount of classic, needle-shaped urate crystals on routinely stained May-Grünwald-Giemsa smears, favoring a cytologic diagnosis of gouty arthritis. CONCLUSION: Gouty synovitis occasionally presents with thick, milky white urate-laden synovial effusions, which clinically may be mistaken for septic arthritis. This gross nature of the specimen may interfere with the performace of a WBC count on SF samples.     

Proteomic Analysis to Examine the Role of Matrix Proteins in a Gouty Tophus from a Patient with Recurrent Gout

To examine the role of matrix proteins in the formation of gouty tophus, we analyzed the crystalline components and matrix proteins in a gouty tophus from a patient with recurrent gout. Micro-area X-ray diffraction analysis and infrared spectroscopy indicated that the tophus was composed of monosodium urate monohydrate. Proteomic analysis identified 134 proteins from the tophus as matrix proteins. Many proteins relevant to inflammation and host defense were identified, and immunoglobulin was detected in all four extracted fractions (KCl, formic acid, guanidine-HCl, and ethylenediaminetetraacetic acid) and from many spots throughout a broad molecular weight range after electrophoresis. It is thought that the process of biological defense including the immunity has occurred in the gouty tophus.     

T cells as key players for bone destruction in gouty arthritis?

The deposition of monosodium urate (MSU) crystals in synovial fluid and tissue leads to gouty arthritis frequently associated with synovial inflammation and bone erosions. The cellular mechanism that links MSU crystals to an increased number of osteoclasts has not yet been fully understood. In a recent issue of Arthritis Research & Therapy Lee and colleagues proposed that bone destruction in chronic gouty arthritis is at least in part dependent on expression by T cells of receptor activator of NF-κB ligand (RANKL). The authors showed that pro-resorptive cytokines such as IL-1β, IL-6, and TNFα are expressed within tophi and stromal infiltrates. In vitro stimulation with MSU crystals revealed monocytes as a source for these cytokines, whereas T cells produce RANKL, the major trigger of osteoclastogenesis.     

Efficacy of anakinra in gouty arthritis: a retrospective study of 40 cases

Introduction

Gout is a common arthritis that occurs particularly in patients who frequently have associated comorbidities that limit the use of conventional therapies. The main mechanism of crystal-induced inflammation is interleukin-1 production by activation of the inflammasome. We aimed to evaluate the efficacy and tolerance of anakinra in gouty patients.

Methods

We conducted a multicenter retrospective review of patients receiving anakinra for gouty arthritis. We reviewed the response to treatment, adverse events and relapses.

Results

We examined data for 40 gouty patients (32 men; mean age 60.0 ± 13.9 years) receiving anakinra. Mean disease duration was 8.7 ± 8.7 years. All patients showed contraindications to and/or failure of at least two conventional therapies. Most (36; 90%) demonstrated good response to anakinra. Median pain on a 100-mm visual analog scale was rapidly decreased (73.5 (70.0 to 80.0) to 25.0 (20.0 to 32.5) mm, P <0.0001), as was median C-reactive protein (CRP) level (130.5 (55.8 to 238.8) to 16.0 (5.0 to 29.5) mg/l, P <0.0001). After a median follow-up of 7.0 (2.0 to 13.0) months, relapse occurred in 13 patients after a median delay of 15.0 (10.0 to 70.0) days. Seven infectious events, mainly with long-term use of anakinra, were noted.

Conclusions

Anakinra may be efficient in gouty arthritis, is relatively well tolerated with short-term use, and could be a relevant option in managing gouty arthritis when conventional therapies are ineffective or contraindicated. Its long-term use could be limited by infectious complications.     

Dendritic Cells Cause Bone Lesions in a New Mouse Model of Histiocytosis

Langerhans cell histiocytosis (LCH) is a rare disease caused by the clonal accumulation of dendritic Langerhans cells, which is often accompanied by osteolytic lesions. It has been reported that osteoclast-like cells play a major role in the pathogenic bone destruction seen in patients with LCH and these cells are postulated to originate from the fusion of DCs. However, due to the lack of reliable animal models the pathogenesis of LCH is still poorly understood. In this study, we have established a mouse model of histiocytosis- recapitulating human disease for osteolytic lesions seen in LCH patients. At 12 weeks after birth, severe bone lesions were observed in our multisystem histiocytosis (Mushi) model, when CD8α conventional dendritic cells (DCs) are transformed (MuTuDC) and accumulate. Most importantly, our study demonstrates that bone loss in LCH can be accounted for the transdifferentiation of MuTuDCs into functional osteoclasts both in vivo and in vitro. Moreover, we have shown that injected MuTuDCs reverse the osteopetrotic phenotype of oc/oc mice in vivo. In conclusion, our results support a crucial role of DCs in bone lesions in histiocytosis patients. Furthermore, our new model of LCH based on adoptive transfer of MuTuDC lines, leading to bone lesions within 1–2 weeks, will be an important tool for investigating the pathophysiology of this disease and ultimately for evaluating the potential of anti-resorptive drugs for the treatment of bone lesions.     

痛风性关节炎与骨关节炎的相关性研究

目的:通过检测痛风性关节炎与骨关节炎患者膝关节液中Ⅱ型胶原羧基端端肽(C-telopeptide of type II collagen,CTX-Ⅱ)的含量,探讨痛风性关节炎与骨关节炎的相关性。方法:收集膝关节发作的痛风性关节炎患者膝关节液标本46例及骨关节炎患者膝关节液标本42例,用酶联免疫吸附试验(ELISA)法检测两组关节液中CTX-Ⅱ的含量,并研究分析痛风性关节炎膝关节液中CTX-Ⅱ的含量与影像学X线特征、单钠尿酸盐(MSU)晶体的相关性。结果:1痛风性关节炎与骨关节炎的膝关节液中CTX-Ⅱ的含量相比较无统计学差异(P=0.40);245.7%(21/46)的痛风性关节炎患者膝关节X线显示骨关节炎,与膝关节X线未显示骨关节炎的痛风性关节炎(25/46)相比较,两组CTX-Ⅱ的含量无统计学差异(P=0.84);3MSU晶体阳性的痛风性关节炎(19/46,41.3%)与MSU晶体阴性的痛风性关节炎(37/46,68.7%)患者的膝关节液CTX-Ⅱ的含量比较,前者显著高于后者,差异有统计学意义(P0.05)。结论:痛风性关节炎的受累关节存在关节软骨的退变,单钠尿酸盐(MSU)晶体在局部沉积与否与关节软骨退变的程度相关。     

Pruritic facial dermatitis in a population of free-living stitchbirds

From September 2001 to February 2005, observations of an island population of the New Zealand stitchbird (Notiomystis cincta) revealed a progressive feather-losing dermatitis, which developed during the breeding season around the birds' eyes, base of the bill, and ventral neck. The lesions were significantly more likely to develop in males (96%) than females (51%), with males exhibiting a more severe form of the condition at the end of the breeding season. Histology from a dead bird revealed the presence of ovoid burrowing mites within the lesions, and isolation of mites from skin crusts of a live bird were identified as Knemidocoptes spp. Although other factors might be involved in the expression of the condition, Knemidocoptes appears to be a likely causative agent in the development of skin lesions in this population.     

MicroRNA-155 as a proinflammatory regulator via SHIP-1 down-regulation in acute gouty arthritis

Introduction

Gout is characterized by episodes of intense joint inflammation in response to intra-articular monosodium urate monohydrate (MSU) crystals. miR-155 is crucial for the proinflammatory activation of human myeloid cells and antigen-driven inflammatory arthritis. The functional role of miR-155 in acute gouty arthritis has not been defined. Therefore, the aim of this study was to examine the role of miR-155 in pathogenesis of acute gouty arthritis.

Methods

Samples from 14 patients with acute gouty arthritis and 10 healthy controls (HCs) were obtained. Peripheral blood mononuclear cells (PBMCs) and synovial fluid mononuclear cells (SFMCs) were cultured in vitro with MSU crystals, and gene expression (human miR-155 and SHIP-1) were assessed by real-time PCR. THP-1 cells were stimulated by MSU crystals and/or miR-155 transfection and then subjected to Western blot analysis. Levels of human tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-1β in cell culture supernatants were measured by Luminex. Immunohistochemistry was performed on formalin-fixed gout tissues with anti–SHIP-1 antibody. A C57BL/6 J male mouse model of gout was used to analyze the expressions of miR-155, SHIP-1, and inflammatory cytokines.

Results

The samples from gouty arthritis were highly enriched in miR-155, with levels of expression being higher than those found in PBMC from HC. Treatment of the cells with MSU crystals strongly induced miR-155. In addition, overexpression of miR-155 in the cells decreased levels of SHIP-1 and promoted production of MSU-induced proinflammatory cytokines, such as TNF-α and IL-1β. Consistent with in vitro observations, miR-155 expression was elevated in the mouse model of gout. The production of inflammatory cytokines was markedly increased in MSU crystal induced peritonitis mice.

Conclusions

Overexpression of miR-155 in the gouty SFMC leads to suppress SHIP-1 levels and enhance proinflammatory cytokines.     

Familial, structural, and environmental correlates of MRI-defined bone marrow lesions: a sibpair study

The aim of this study was to estimate the heritability and describe the correlates of bone marrow lesions in knee subchondral bone. A sibpair design was used. T2- and T1-weighted MRI scans were performed on the right knee to assess bone marrow lesions at lateral tibia and femora and medial tibia and femora, as well as chondral defects. A radiograph was taken on the same knee and scored for individual features of osteoarthritis (radiographic osteoarthritis; ROA) and alignment. Other variables measured included height, weight, knee pain, and lower-limb muscle strength. Heritability was estimated with the program SOLAR (Sequential Oligogenetic Linkage Analysis Routines). A total of 115 siblings (60 females and 55 males) from 48 families, representing 95 sib pairs, took part. The adjusted heritability estimates were 53 ± 28% (mean ± SEM; p = 0.03) and 65 ± 32% (p = 0.03) for severity of bone marrow lesions at lateral and medial compartments, respectively. The estimates were reduced by 8 to 9% after adjustment for chondral defects and ROA (but not alignment). The adjusted heritability estimate was 99% for prevalent bone marrow lesions at both lateral and medial compartments. Both lateral and medial bone marrow lesions were significantly correlated with age, chondral defects, and ROA of the knee (all p < 0.05). Medial bone marrow lesions were also more common in males and were correlated with body mass index (BMI). Thus, bone marrow lesions have a significant genetic component. They commonly coexist with chondral defects and ROA but only share common genetic mechanisms to a limited degree. They are also more common with increasing age, male sex, and increasing BMI.     

Inflammatory gout: observations over a half-century

This is a discussion of acute gouty arthritis, seen for over 50 years of engagement. It addresses the evolution of our current understanding of the interaction between urate crystals and key cellular components of the gouty inflammatory paroxysm, with new material on pathogenesis.     

Human gouty arthritis is associated with a distinct serum trace elemental profile

Homeostatic imbalance of essential trace elements is deeply involved in many pathophysiological states, especially in joint disorders such as gout. A total of 64 elements were measured in the serum samples in three regionally independent groups of patients with gouty arthritis (n = 100) and an age-matched healthy control group (n = 40) by inductively coupled plasma-mass spectrometry (ICP-MS). A distinct elemental profile of gouty arthritis encompassing significantly altered Li, Al, Ti, Fe, Cu, Se, Sr, Ta, Hg, Bi, Th, and U was obtained with a sensitivity of 0.97 (95% confidence interval (CI): 0.92-0.99) and a specificity of 0.95 (95% CI: 0.83-0.99) for gout diagnosis. An independent group of 52 subjects (39 gout patients and 13 healthy controls) was further used to validate the elemental signature, yielding a sensitivity of 1.00 (95% CI: 0.91-1.00) and a specificity of 1.00 (95% CI: 0.75-1.00) for gout prediction. It is also noteworthy that we were able to achieve ≥95.7% correct classification rate in both discovery and validation groups using only three elemental markers, Li, Al, and U. We also observed a good correlation between Li, Zn, and Cu and the other two risk factors, age and serum urate concentration, in gout patients. Our findings underscore that gouty arthritis possesses a unique elemental expression profile regardless of many other nutritional and environmental factors.     

Can ultrasonography make identification of asymptomatic hyperuricemic individuals at risk for developing gouty arthritis more crystal clear?

Hyperuricemia is the most important risk factor for gouty arthritis. The quandary is how to predict which patient with asymptomatic hyperuricemia will develop gouty arthritis. Can ultrasonography help identify hyperuricemic individuals at risk for developing gouty arthritis? In the previous issue of Arthritis Research & Therapy, Pineda and colleagues found ultrasonography changes suggestive of gouty arthritis in 25% of hyperuricemic individuals. These were found exclusively in hyperuricemic individuals but not in normouricemic patients. Ultrasonography may serve as a noninvasive means to diagnose gouty arthritis in hyperuricemic individuals who have yet to develop symptomatic gouty arthritis.In the previous issue of Arthritis Research & Therapy, Pineda and colleagues present an interesting study evaluating the use of ultrasonography (US) to help identify hyperuricemic individuals at risk for gouty arthritis [1]. Hyperuricemia is the most important risk factor for gouty arthritis. The number of adults with hyperuricemia and gouty arthritis is increasing.The National Health and Nutrition Examination Survey (NHANES) data from 2007 to 2008 showed a hyperuricemia (serum urate ≥7 mg/dl) prevalence of 21.1% in men and 4.7% in women [2]. Most individuals with hyperuricemia, however, do not develop gouty arthritis [3]. The reported gouty arthritis prevalence in the 2007 to 2008 NHANES data was 5.9% in men and 2% in women, with an overall prevalence of 3.9% (8.3 million adults) [4]. The risk of developing gouty arthritis is dependent on the severity of hyperuricemia. In the Normative Aging Study, healthy patients with serum urate levels ≥9 mg/dl upon entry into the study had a cumulative incidence of acute flares that reached 22% after 5 years, whereas those with serum urate levels ≤7 mg/dl had an annual incidence of only 0.5% [5]. In yet another study, the 5-year prevalence of gouty arthritis was 30% in individuals with serum urate levels >10 g/dl [6]. These numbers correlate with the recently reported NHANES data.The quandary is how to predict which patient with asymptomatic hyperuricemia will develop gouty arthritis, and thus who will benefit from-long term anti-inflammatory and urate-lowering therapy. Serum urate levels and gouty arthritis prevalence are related to genetic variations in the SLC2A9, ABCG2 and SLC17A3 genes. Dehghan and colleagues developed a risk score based on variations of these three genetic loci. They suggested that their genetic risk score is associated with up to a 40-fold increased risk of developing gouty arthritis, suggesting that knowledge of the genotype may help identify hyperuricemic individuals at risk for developing gouty arthritis [7]. Can US serve as another potential method to help identify hyperuricemic individuals at risk for developing gouty arthritis?Over the past several years, there has been a growing interest in musculoskeletal US in rheumatology. US visualizes tissues as acoustic reflections. Crystalline material reflects US waves more strongly than the surrounding tissues, such as unmineralized hyaline cartilage or synovial fluid. This enables distinction of monosodium urate (MSU) crystal deposition from the less echogenic surrounding soft tissues. MSU crystals are found in cartilage, tendon sheaths, synovial fluid and subcutaneous tissue. US detects deposition of MSU crystals on cartilaginous surfaces, as well as tophaceous material and typical erosions. A hyperechoic, irregular band over the superficial margin of the articular cartilage - described as a double contour sign or icing - is found exclusively in gouty arthritis [8] and represents crystalline precipitates of MSU. In addition, the presence of hypoechoic to hyperechoic inhomogeneous material surrounded by a small anechoic rim, representing tophaceous material and erosions adjacent to tophaceous material on US, are suggestive of the diagnosis of gouty arthritis. US is superior in detecting changes of gouty arthritis compared with other imaging modalities (magnetic resonance imaging, plain X-ray scans, computed tomography and three-dimensional rendering imaging) [9].Pineda and colleagues support previous evidence that US may be useful in detecting gouty arthritis in hyperuricemic patients [1]. Puig and colleagues reported that 34% (n = 12) of their asymptomatic hyperuricemic individuals had findings suggestive of tophaceous deposits [10]. Pineda and colleagues also studied a larger cohort in a controlled fashion [1]. US images of the most commonly affected joints - knees, ankles and first metatarsophalangeals - were obtained. The double contour sign and tophi were seen ultrasonographically in the knee hyaline cartilage and the first metatarsophalangeals. Tendinous infiltrations of tophaceous material were also observed. Interestingly, tendinous tophi and enthesopathies were not a rare finding in these patients. US changes suggestive of gouty arthritis were found in 25% of hyperuricemic individuals. These changes were found exclusively in the hyperuricemic individuals but not in their control group of normouricemic individuals. The main limitation of both Puig and colleagues'' study [10] and Pineda and colleagues'' study [1] is that the US findings suggestive of gouty arthritis, tophi and the double contour sign were not proven MSU crystals. In both studies, therefore, a definite diagnosis of gouty arthritis was not established.Whether finding sonographic evidence suggestive of gouty arthritis prior to development of acute flares will influence our decision of when to initiate and commit to a long-term urate-lowering therapy and chronic anti-inflammatory treatment is still to be determined. US may serve as a noninvasive means to diagnose gouty arthritis in hyperuricemic individuals who have yet to develop symptomatic gouty arthritis. How long hyperuricemia must be present before MSU crystal deposition can be seen sonographically is currently not known. Future large, prospective, randomized controlled trials of patients with proven MSU crystal gouty arthritis are needed to further evaluate the use of US to predict the presence of asymptomatic gouty arthritis in an individual hyperuricemic patient.     

Fine needle aspiration cytology of bone lesions. Analysis of a three-year experience in rural Africa

FNA biopsies were performed on 24 patients with bone lesions. Cytology diagnosed ten of the cases as classic Burkitt's lymphomas. The cytodiagnoses in the remaining 14 cases were primary bone tumors (5 cases), bone cysts (2 cases), inflammatory lesions (4 cases) and inadequate material (3 cases). Smears of the Burkitt's lymphomas of the jaw contained starry sky macrophages and neoplastic lymphoid cells with deep basophilic cytoplasms and fine vacuolizations. Taking into consideration the load of Burkitt's lymphoma cases in Africa, FNA cytology appears to be a very simple method for getting a quick tissue diagnosis (results were available within 24 hours). For doctors working in tropical hospitals with limited facilities, FNA cytopathology is very useful for distinguishing between tumors and inflammations and for differentiating between benign and malignant tumors.     

Engagement of CD14 mediates the inflammatory potential of monosodium urate crystals

Phagocyte ingestion of monosodium urate (MSU) crystals can induce proinflammatory responses and trigger acute gouty inflammation. Alternatively, the uptake of MSU crystals by mature macrophages can be noninflammatory and promote resolution of gouty inflammation. Macrophage activation by extracellular MSU crystals involves apparent recognition and ingestion mediated by TLR2 and TLR4, with subsequent intracellular recognition linked to caspase-1 activation and IL-1beta processing driven by the NACHT-LRR-PYD-containing protein-3 inflammasome. In this study, we examined the potential role in gouty inflammation of CD14, a phagocyte-expressed pattern recognition receptor that functionally interacts with both TLR2 and TLR4. MSU crystals, but not latex beads, directly bound recombinant soluble (s) CD14 in vitro. CD14(-/-) bone marrow-derived macrophages (BMDMs) demonstrated unimpaired phagocytosis of MSU crystals but reduced p38 phosphorylation and approximately 90% less IL-1beta and CXCL1 release. Attenuated MSU crystal-induced IL-1beta release in CD14(-/-) BMDMs was mediated by decreased pro-IL-1beta protein expression and additionally by decreased caspase-1 activation and IL-1beta processing consistent with diminished NACHT-LRR-PYD-containing protein-3 inflammasome activation. Coating of MSU crystals with sCD14, but not sTLR2 or sTLR4, restored IL-1beta and CXCL1 production in CD14(-/-) BMDMs in vitro. Gain of function of CD14 directly enhanced TLR4-mediated signaling in response to MSU crystals in transfected Chinese hamster ovary cells in vitro. Last, MSU crystal-induced leukocyte influx at 6 h was reduced by approximately 75%, and local induction of IL-1beta decreased by >80% in CD14(-/-) mouse s.c. air pouches in vivo. We conclude that engagement of CD14 is a central determinant of the inflammatory potential of MSU crystals.     

Paleoepidemiological patterns of interpersonal aggression in a prehistoric central California population from CA‐ALA‐329

Interpersonal aggression is assessed paleoepidemiologically in a large skeletal population from the CA‐ALA‐329 site located on the southeastern side of San Francisco Bay, California. This comprehensive analysis included all currently recognized skeletal criteria, including craniofacial fracture, projectile injury, forearm fracture, and perimortem bone modification. Craniofacial injury is moderately common, showing an adult prevalence of 9.0% with facial lesions accounting for >50% of involvement. Clinical studies suggest that such separate evaluation of facial involvement provides a useful perspective for understanding patterns of interpersonal aggression. In this group male facial involvement is significantly greater than in females, paralleling the pattern found widely in contemporary populations as well as in African apes. When compared to other North American skeletal samples the prevalence of adult cranial vault injury (3.3%) and especially projectile injury (4.4%) are quite high. However, well documented populations from southern California show markedly higher prevalence for both types of skeletal markers of aggression. Forearm fracture is also assessed using a rigorous radiographic methodology and results suggest that these injuries are not reliable indicators of interpersonal aggression. Lastly, perimortem bone modification was not observed in this population, although it has been recorded from other (older) sites nearby. This study provides an evaluation of multiple skeletal markers of interpersonal aggression in the largest sample from a single site yet reported in North America and, joined with consideration of cultural context, helps further illuminate both geographic and temporal patterns of interpersonal aggression in California. Am J Phys Anthropol, 2009. © 2009 Wiley‐Liss, Inc.     

Skeletal manifestations of rickets in infants and young children in a historic population from England

Gross and radiographic changes characteristic of inadequate bone mineralization due to rickets are described in 21 immature skeletons from a 19th century urban population from Birmingham, England. The aims of the study are as follows: to evaluate and if possible augment existing dry-bone criteria for the recognition of rickets in immature skeletal remains; to investigate the value of radiography for the paleopathological diagnosis of rickets; and to compare and contrast the expression of rickets in this group with that previously documented for a rural agrarian population from Wharram Percy, England. Some gross skeletal signs of rickets which were not previously well-documented in paleopathological studies are noted. The worth of radiography for evaluating structural changes to both cortical and trabecular bone in the disease is demonstrated, and features useful for the interpretation of vitamin D deficiency are discussed. The pattern of skeletal elements affected and the severity of changes differs in the Birmingham group from that seen in the comparative rural population. It is emphasized that a variety of factors may influence the expression of rickets in paleopathological material, including rate of skeletal growth, age cohort affected, and intensity of vitamin D deficiency. Nevertheless, careful analysis, not only of the frequency of rickets but also of the degree of severity of lesions and the patterning with respect to skeletal elements affected, may enable more nuanced understanding of the biocultural context of the disease in earlier populations.