Measurement and assessment of grief in a large international sample.

BACKGROUND: In 2022, the International Classification of Diseases (ICD-11) and an update of the Diagnostic Statistical Manual of Mental Disorders (DSM 5 TR) were released for implementation worldwide and now include the new Prolonged Grief Disorder (PGD). The newest definition of PGD is based on robust clinical research from the Global North yet until now has not been tested for global applicability. METHODS: The current study assesses the new PGD ICD-11 criteria in a large international sample of 1393 bereaved adults. The majority of the sample was included from the USΑ. Additionally, we conduct a sub-sample analysis to evaluate the psychometric properties, probable caseness of PGD, and differences in network structure across three regions of residency (USA, Greece-Cyprus, Turkey-Iran). RESULTS: The psychometric validity and reliability of the 33-item International Prolonged Grief Disorder Scale (IPGDS) were confirmed across the whole sample and for each regional group. Using the strict diagnostic algorithm, the probable caseness for PGD for the whole sample was 3.6 %. Probable caseness was highest for the Greece-Cyprus group (6.9 %) followed by Turkey-Iran (3.2 %) and the USA (2.8 %). Finally, the network structure of the IPGDS standard items and cultural supplement items (total of 33 items) confirmed the strong connection between central items of PGD, and revealed unique network connections within the regional groups. LIMITATIONS: Future research is encouraged to include larger sample sizes and a more systematic assessment of culture. CONCLUSION: Overall, our findings confirm the global applicability of the new ICD-11 PGD disorder definition as evaluated through the newly developed IPGDS. This scale includes culturally sensitive grief symptoms that may improve clinical precision and decision-making.

Local variations in turnover of periodontal collagen fibers in rats.

BACKGROUND AND OBJECTIVE: The exact cause of orthodontic relapse is still unclear, although it is often suggested to be caused by periodontal collagen fibers. We hypothesize that long-lived collagen fibers in the periodontium cause relapse. The aim was to determine the half-life of periodontal collagen fibers around rat molars. MATERIAL AND METHODS: Thirty weanling rats were repeatedly injected with (3) H-proline, and autoradiography of histological sections was performed at 1, 4, 8, 15, 22, 29, 36, 57, 78 and 113 d after labeling. Grain densities determined in specific areas of the periodontium were used to calculate collagen half-life. RESULTS: The half-life (t(½) ) was found to decrease from the supra-alveolar region to the apical periodontal ligament region. It was longer in the supra-alveolar region (1.39 ± 0.14 wk) compared with the deeper regions (p < 0.05). The t(½) of the upper periodontal ligament region (0.78 ± 0.20 wk) was longer than that of the inter-radicular periodontal ligament region (0.42 ± 0.07 wk, p < 0.05). The t(½) of the apical periodontal ligament region was 0.61 ± 0.15 wk. CONCLUSION: The data indicate that long-lived collagen fibers do not exist in the soft tissues of the periodontium, and are probably not responsible for relapse. The differences in collagen half-life might be caused by local variations in compressive strain induced by normal function.

Mechanobiology of tooth movement.

This review describes the mechanical and biological signalling pathways during orthodontic tooth movement and provides an update of the current literature. A theoretical model is introduced to elucidate the complex cascade of events after the application of an orthodontic force to a tooth. In this model, the events are divided into four stages: matrix strain and fluid flow, cell strain, cell activation and differentiation, and remodelling. Each stage is explained in detail and discussed using recent literature.

Relaxin stimulates MMP-2 and alpha-smooth muscle actin expression by human periodontal ligament cells.

The main cells in the periodontal ligament (PDL) are the fibroblasts, which play an important role in periodontal remodelling. Matrix metalloproteinases (MMPs) are largely responsible for the degradation of extracellular matrix proteins in the PDL. Previous studies have indicated that MMP production can be stimulated by the hormone relaxin. This hormone facilitates delivery by softening the connective tissues of the reproductive tract, and it prepares the mammary gland for lactation. Periodontal remodelling takes place during orthodontic tooth movement, which might be enhanced by relaxin. Therefore, we investigated the effects of relaxin on gelatinase expression of human PDL cells. Cultures of human PDL cells were incubated with relaxin. Gelatinase (MMP-2 and -9) expression, alpha-smooth muscle actin expression (alpha-SMA), total MMP activity and DNA content were measured. Both proMMP-2 and active MMP-2 was identified in the cultures. There was a clear trend showing a dose-dependent increase of MMP-2 production, which was significant at 250 ng/ml. Total MMP activity was not affected. A stimulation of alpha-SMA expression was found at 50 ng/ml. The results indicate that relaxin activates human PDL cells by the stimulation of MMP-2 and alpha-smooth muscle actin.

CMT-3 inhibits orthodontic tooth displacement in the rat.

OBJECTIVE: Orthodontic tooth movement requires extensive remodeling of the periodontal ligament (PDL) and the alveolar bone. Osteoclasts resorb bone, allowing teeth to migrate in the direction of the force. Matrix metalloproteinases (MMPs) are able to degrade the extracellular matrix of the periodontal tissues. Chemically modified tetracyclines (CMTs) can inhibit MMPs, but lack antimicrobial activity. We hypothesize that CMT-3 will decrease the rate of orthodontic tooth movement in the rat. DESIGN: Eighteen Wistar rats received a standardized orthodontic appliance at one side of the maxilla. During 14 days, three groups of six rats received a daily dose of 0, 6 or 30mg/kg CMT-3, and tooth displacement was measured. Thereafter, osteoclasts were counted on histological sections using an ED-1 staining. Multi- and mononuclear ED-1-positive cells in the PDL were also counted. In addition, sections were stained for MMP-9. RESULTS: CMT-3 significantly inhibited tooth movement (p=0.03) and also decreased the number of osteoclasts at the compression sides in the 30mg/kg group (p<0.05). Significantly more mono- than multinuclear ED-1-positive cells were present in the PDL, but no significant differences were found between the dosage groups. Osteoclasts in the 30mg/kg group seemed to contain less MMP-9 than in the control. CONCLUSIONS: CMT-3 inhibits tooth movement in the rat, probably by reducing the number of osteoclasts at the compression side. This might be due to induction of apoptosis in activated osteoclasts or reduced osteoclast migration. Reduced MMP activity by CMT-3 might also directly inhibit degradation of the organic bone matrix.