Is osteoarthritis a systemic disorder of bone?

Objective

To describe the osteologic findings associated with osteoarthritis (OA) of a variety of joints.

Methods

We performed visual examination of 563 skeletons of which ≥80% of the skeleton was available, from an archaeologic site in England. The surfaces and margins of several different joints (shoulders, elbows, wrists, hips, hands, knees, and ankles) were studied for evidence of eburnation and osteophytes, respectively, and the entire skeleton was examined for evidence of generalized enthesophyte formation. Associations between changes in different joint sites and between enthesophyte formation and evidence of OA were sought.

Results

Eburnation and osteophyte formation at the hand, hip, and knee were strongly associated with eburnation and osteophytes at other joint sites not commonly thought to be prone to OA, including the elbow and wrist. Only the ankle was rarely involved. There was also a strong relationship between both bone eburnation and osteophytes and generalized enthesophyte formation. These findings remained statistically significant after adjustment for the age, sex, and historical period of the skeletons.

Conclusion

Our findings indicate that skeletal OA is more widespread in the body than is apparent from clinical studies and are consistent with other data suggesting that OA is a disease that is primarily dependent on systemic predisposition to a particular type of bone response to mechanical stress.

     

Is atherosclerosis a mitochondrial disorder?

There is increasing evidence that damage to the vascular environment from oxidative stress plays a major role in the pathogenesis of atherosclerosis in addition to classical risk factors, such as age, arterial hypertension, diabetes, dyslipidemia, smoking, vascular wall inflammation, or genetic predisposition. Oxidative stress results from the endogenous or exogenous generation of reactive oxidative or nitrogen species, generated by the respiratory chain or enzymatic sources. Oxidative stress results in lipid peroxidation, damage of mitochondrial components including mitochondrial DNA, mitochondrial dysfunction, damage of endothelial cells, vascular smooth muscle cells, and erythrocytes, and lastly apoptosis via either the receptor-mediated pathway or the mitochondria-mediated pathway and activation of the caspase cascade. Though re-balancing of the redox homeostasis by various agents is clinically hardly effective, various trials with experimental agents are promising in this respect. Overall, atherosclerosis appears to be the endpoint of various different pathogenetic mechanisms, of which oxidative stress and disturbed mitochondrial metabolism and function are key factors.     

Is anorexia nervosa a cultural disorder?

Several epidemiological studies as well as clinicians' experience indicate that during the last four decades anorexia nervosa, perfectly described in the 19th century, has become increasingly frequent in industrial societies. In contrast, the disease is said to be extremely rare in traditional societies where it appears only when the life style has been "occidentalized". As a pathology of starvation in a society of abundance, anorexia nervosa lies at the cross-roads of biology and society by referring to two sectors with strong cultural determinations: the ideal body shape and the moral value of food. In a more subtle way, the ever growing incidence of the disease might also coincide with the expansion of such occidental moral values as self-control and individualism and with changes in family structure. Anorexia nervosa may be regarded as a culturally determined illness that "shapes" in a stereotyped mould psychological or even neuroendocrine disorders which vary from one patient to another. This brings it very close to the "culture-bound syndromes" or "ethnic disorders" described by ethnopsychiatrists.     

Is sickle cell disease-related neurotoxicity a systemic endotheliopathy?

The aim of the present article is to review the role of endothelial damage and dysfunction in the vaso-occlusive episodes associated with sickle cell disease (SCD). This inherited hematological disorder leads to irreversible damage of multiple organs through a wide variety of mechanisms, such as sickling of red cells, oxidative state due to ischemic-reperfusion episodes, inflammation, hypercoagulation state, and platelet activation, among others. In SCD, the endothelium arises as the key entity where most of these processes, which eventually lead to increased morbidly and mortality, interact. This review begins with the already accepted idea that organ-specific vasculopathy precedes clinical manifestation, and briefly explains one of the main triggers of vaso-occlusive episodes, the complex interplay between blood cells and the dysfunctional endothelium. Endothelial protective strategies emerge as a potential tool for the prevention of organ-specific disease in SCD. Actually, this knowledge is currently used for the development of potential pharmacologic interventions to improve the lives of SCD patients.     

Is anti-topoisomerase I a serum marker of pulmonary involvement in systemic sclerosis?

STUDY OBJECTIVE: To determine the value of the level of anti-topoisomerase I (anti-topo I) to evaluate lung involvement defined by abnormal high-resolution computed tomography (HRCT) score and pulmonary function tests (PFTs) in systemic sclerosis (SS). PATIENTS: Forty-eight patients with SS, 20 with lung involvement and 28 with no lung involvement. DESIGN: PFT measurement, HRCT scoring of lung involvement, and anti-topo I assay by enzyme-linked immunosorbent assay. Normal anti-topo I level was defined as < 30. RESULTS: There was a significant association between cutaneous extent and anti-topo I level (6.5% of patients with limited cutaneous scleroderma had abnormal anti-topo I levels vs 70.6% of patients with diffuse cutaneous scleroderma, p = 0.0001). In patients with diffuse cutaneous scleroderma, pulmonary involvement was associated with a higher percentage of abnormal anti-topo I level: 91.7% vs 20% (p = 0.010). In patients with diffuse cutaneous scleroderma, a significant association was found between the class of anti-topoII level and total lung capacity (median, 69 in patients with abnormal anti-topo I level vs 87 in patients with normal anti-topo I level, p = 0.010), between the class of anti-topo I level and HRCT score (median, 12 in patients with abnormal anti-topo I level vs 5 in patients with normal anti-topo I level, p = 0.05). CONCLUSION: Anti-topo I can be considered as a marker of lung involvement in patients with diffuse cutaneous scleroderma.