The influence of socioeconomic deprivation on multimorbidity at different ages: a cross-sectional study

Background

Multimorbidity occurs at a younger age in individuals in areas of high socioeconomic deprivation but little is known about the ‘typology’ of multimorbidity in different age groups and its association with socioeconomic status.

Aim

To characterise multimorbidity type and most common conditions in a large nationally representative primary care dataset in terms of age and deprivation.

Design and setting

Cross-sectional analysis of 1 272 685 adults in Scotland.

Method

Multimorbidity type of participants (physical-only, mental-only, mixed physical, and mental) and most common conditions were analysed according to age and deprivation.

Results

Multimorbidity increased with age, ranging from 8.1% in those aged 25–34 to 76.1% for those aged ≥75 years. Physical-only (56% of all multimorbidity) was the most common type of multimorbidity in those aged ≥55 years, and did not vary substantially with deprivation. Mental-only was uncommon (4% of all multimorbidity), whereas mixed physical and mental (40% of all multimorbidity) was the most common type of multimorbidity in those aged <55 years and was two- to threefold more common in the most deprived compared with the least deprived in most age groups. Ten conditions (seven physical and three mental) accounted for the top five most common conditions in people with multimorbidity in all age groups. Depression and pain featured in the top five conditions across all age groups. Deprivation was associated with a higher prevalence of depression, drugs misuse, anxiety, dyspepsia, pain, coronary heart disease, and diabetes in multimorbid patients at different ages.

Conclusion

Mixed physical and mental multimorbidity is common across the life-span and is exacerbated by deprivation from early adulthood onwards.     

Preventing root caries development under oral biofilm challenge in an artificial mouth

Objectives: To study the preventive effects of chlorhexidine against root caries under oral biofilm in an artificial mouth. Study Design: Sixteen human tooth-root disks were inoculated with a salivary sample that was produced by mixing the unstimulated saliva of three adults who had no untreated caries. The disks were incubated in an artificial mouth fed with a 5% sucrose solution three times daily for one week. Eight disks received a twice daily rinse of 0.12% chlorhexidine (test group). The other eight disks were rinsed in distilled water (control). The biofilm was then studied with three techniques: colony forming unit (CFU) counting, scanning electron microscopy (SEM) and confocal laser scanning microscopy (CLSM). The changes in the chemical structure of the root surface were studied using Fourier transform infra-Red spectroscopy. Type-I collagen and proteoglycans on the root surface were quantified using immunocytochemical staining. Results: The log CFU for the test and control groups were 4.21 and 8.27, respectively (p<0.001). The CFU count of Streptococci and Lactobacilli were negligible. Both the SEM and the CLSM showed suppressed bacteria growth in the test group. The log [amide-I: HPO42-] of the test and control groups were 1.11 and 1.93, respectively (p=0.02). The mean counts of sound type-I collagen in the test and control groups were 16.8/?m2 and 13.0/?m2, respectively (p<0.001), whereas the mean counts of intact proteoglycans were 5.6/?m2 and 3.5/?m2, respectively (P<0.001). Conclusions: Chlorhexidine suppressed the growth of selected cariogenic bacteria in oral biofilm on the root surface and thus protected tooth-root from cariogenic challenge. Key words:Chlorhexidine, biofilm, caries risk, root, caries, artificial mouth, demineralization, streptococci, lactobacilli, proteoglycans, collagen I.     

The Osteoinductive Activity of Bone Morphogenetic Protein (BMP) Purified by Repeated Extracts of Bovine Bone

Native bone morphogenetic proteins (BMPs) extracted from bone have been used clinically to stimulate bone regeneration and repair. However, preparation of purified BMP is a laborious process. This study investigated the yield, activity and cost effectiveness of repeatedly extracting the same bone matrix to produce purified BMP.

While repeated extraction was able to increase the yield 62% the activity of the partially purified BMP in later extracts decreased both in vitro and in vivo. This decline in activity appears to be due to an increase in non-BMP contaminants, such as collagen, in the extracts. When the first three extracts were combined and processed together activity was equivalent to that of the first extract. A simple analysis based on the cost of reagents used and the time required for purification indicates that separate processing of the extracts is inefficient while combining the first and second extracts and processing them together would result in a small cost saving.

Based on this study we would recommend that the demineralized bone matrix be extracted no more than twice and that the extracts be combined for further processing.     

The immune response of allophenic mice to the synthetic polymer L-glutamic acid, L-lysine, L-phenylalanine. II. Lack of gene complementation in two nonresponder strains

The genetic control of the immune response of inbred strains of mice to certain antigens has been demonstrated to be governed by a set of Ir genes linked to the major histocompatibility complex (H-2) of mice (1,2). Until recently, the control was thought to be governed by single, dominant genes, located within the I region of the H-2 complex. Merryman et al. (3) originally demonstrated that the immune response to the synthetic terpolymer L-glutamic acid, L-lysine, L-phenylaline (GL) is under dominant, H-2-linked Ir gene control (4-7). This was shown both by crossing two nonresponder parental strains to produce responder offspring in the F(1) generation, and by the analysis of appropriate recombinant stains of mice. The two complementing genes have been mapped in the IA and IC regions of the H-2 complex, and have been termed β and α, respectively (5,6). Thus, any strain of mouse may contain neither, one, or both genes. Only mice containing both genes are capable of responding to GL. It has been shown using F(1) hybrid and recombinant strains of mice, that the α- and β-genes can complement each other in either the cis (on the same chromosome) or in the trans (on different chromosomes) position (8). In this paper we report the results of studies aimed at answering the question of whether or not the α- and β- genes can complement each other when they are present in different lymphoid cells. To this end we have constructed allophenic mice composed of two nonresponder strains (A and C57BL/6), which show gene complementation in the F(1) generation. Allophenic mice are chimeras containing two cell types coexisting in a “normal” environment. The mice were tested for the specific cellular composition of the two parental cell types and were found to possess a complete range in the relative proportion of the two cell types. This report demonstrates that regardless of the mixture of cell types present in the allophenic mice, none of them were responders to GL. Thus no complementation of the α- and β-genes is seen when the two genes are present in different cells.     

Hepatic inflammation and fibrosis biomarkers are associated with cardiovascular risk factors but not cardiovascular disease in people with type 2 diabetes: the Edinburgh Type 2 Diabetes Study

BackgroundBoth cardiovascular disease and liver disease are particularly common in people with type 2 diabetes and it is possible that the two conditions are inter-related. Non-invasive biomarkers are increasingly used to estimate liver inflammation and fibrosis. In this study the association of these biomarkers with cardiovascular risk factors and disease was explored in a large, representative population of people with type 2 diabetes mellitus.MethodsCytokeratin 18 (CK18, biomarker of hepatic inflammation) and the European Liver Fibrosis panel (ELF, biomarker of hepatic fibrosis) were measured in a random subgroup of 564 adults, aged 60–75 years at recruitment, participating in the Edinburgh Type 2 Diabetes Study (ET2DS). Data on conventional CV risk factors (body-mass index [BMI], waist circumference, blood pressure, total cholesterol, triglycerides, smoking status) and prevalent cardiovascular disease (validated myocardial infarction, angina, stroke and transient ischaemic attack events) were also available.FindingsMedian CK18 was 102 U/L [IQR 76–137, range 29–993] and mean ELF was 8·9 U/L [SD 0·8, range 6·9–11·6]. After adjustment for age and sex, increased CK18 was significantly associated with higher triglyceride levels (r=0·157, p=0·002). Increased ELF score was associated with higher BMI (r=0·202, p<0·001), waist circumference (r=0·139, p=0·008), and diastolic blood pressure (r=–0·045, p=0·025). Despite these associations, neither biomarker was significantly associated with prevalent cardiovascular disease (prevalent cardiovascular disease vs no cardiovascular disease, mean CK18 108·1 U/L [SD 26·2] vs 105·5 [22·6], p=0·473 and mean ELF 8·94 [0·77] vs 8·89 [0·76], p=0·442).InterpretationIn people with type 2 diabetes, non-invasive biomarkers of hepatic inflammation and fibrosis are associated with a number of cardiovascular risk factors but do not appear to associate with pre-existing vascular disease. Further investigation is required to determine whether liver biomarkers predict incident cardiovascular disease in this high risk group.FundingDiabetes UK.     

Impacted third molars and risk of angle fracture

The purpose of this study was to assess the influence of the presence, position, and severity of impaction of the mandibular third molars, on the incidence of mandibular angle fractures. A retrospective cohort study was designed for patients presenting to the Division of Oral and Maxillofacial Surgery, Toronto General Hospital (Toronto, Canada), for treatment of mandibular fractures from January 1995 to June 2000. The independent variables in this study were the presence, position and severity of impaction of third molars. The outcome variable was the incidence of mandibular angle fractures. Hospital charts and panoramic radiographs were used to determine and classify these variables. The demographic data included age, sex, mechanism of injury and number of mandibular fractures. The study sample comprised 413 mandibular fractures in 214 patients. The incidence of angle fractures was found to be significantly higher in the male population and was most commonly seen in the third decade of life. Assault remained the most significant aetiological factor. Patients with third molars had thrice the increased risk of angle fractures when compared to patients without (P<0.001). Impaction of third molars significantly increased the incidence of angle fractures (P<0.001). The severity and angulation of third molar impactions were not significantly associated with angle fractures. This study provides evidence that patients with retained impacted third molars are significantly more susceptible to angle fracture than those without. The risk for angle fracture, however, does not seem to be influenced by the severity of impaction.     

Characterization of hyaluronan and TSG‐6 in skin scarring: differential distribution in keloid scars,normal scars and unscarred skin

Background Hyaluronan (HA) is a major component of the extracellular matrix (ECM) with increased synthesis during tissue repair. Tumour necrosis factor‐stimulated gene‐6 (TSG‐6) is known to catalyze the covalent transfer of heavy chains (HC1 and HC2) from inter‐α‐inhibitor (IαI) onto HA, and resultant HC?HA complexes have been implicated in physiological and pathological processes related to remodelling and inflammation. Objective The aims of this study were to determine the expression of HA, TSG‐6 and the IαI polypeptides in unscarred skin, normal scars and keloid scars. Methods Formalin‐fixed paraffin‐embedded sections of unscarred skin, normal scars and keloid scars were prepared from patient samples collected during scar revision surgery. Haematoxylin and eosin, as well as immunofluorescent staining for HA, TSG‐6 and the three polypeptide chains of IαI (i.e. HC1, HC2 and bikunin) were performed. Results All skin types stained positive for TSG‐6, HC1, HC2 and bikunin, associated with keratinocytes, fibroblasts and skin appendages all in close proximity to HA. Keloid lesions showed altered HA organization patterns compared with unscarred skin and normal scars. TSG‐6 staining was significantly more intense in the epidermis compared with the dermis of all sample types. There was a significant reduction in TSG‐6 levels within keloid lesions compared with the dermis of unscarred skin (P = 0.017). Conclusion TSG‐6 is expressed in unscarred skin, where its close association with HA and IαI could give rise to TSG‐6‐mediated HC?HA formation within this tissue. A reduction in the beneficial effects of TSG‐6, caused by diminished protein levels in keloid lesions, could contribute to this abnormal scarring process.