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Fusce tincidunt augue in velit tincidunt sed tempor felis porta. J Diabetes Investig. Characteristics of pulse-waveform and laser-Doppler indices in frozen-shoulder patients. Bio Signal Pro Contr. Pietrzak M. Adhesive capsulitis: an age related symptom of metabolic syndrome and chronic low-grade inflammation? Med Hypotheses. Efficacy and cost-effectiveness of physiotherapy following glenohumeral joint distension for adhesive capsulitis: a randomized trial.
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Epidemiology and new developments in the diagnosis of prosthetic joint infection. Int J Artif Organs. Propionibacterium acnes biofilm is present in intervertebral discs of patients undergoing microdiscectomy. Clinical impact of positive propionibacterium acnes cultures in orthopedic surgery. Orthop Traumatol Surg Res. Transient bacteremia induced by toothbrushing: a comparison of the sonicare toothbrush with a conventional toothbrush. Pediatr Dent.
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Comparison of treatments for frozen shoulder: a systematic review and meta-analysis. Surgical and non-surgical treatment of frozen shoulder. Survey on surgeons treatment preferences. Muscl Ligam Tendons J. The effect of anterior versus posterior glide joint mobilization on external rotation range of motion in patients with shoulder adhesive capsulitis.
Adhesive capsulitis of the shoulder: review of pathophysiology and current clinical treatments. Intraarticular injection of relaxin-2 alleviates shoulder arthrofibrosis. Treatment of adhesive capsulitis of the shoulder. J Am AcadOrthop Surg. Adhesive capsulitis: a treatment approach. Clin Orthop Relat Res. Frozen shoulder: the effectiveness of conservative and surgical interventions—systematic review. Br J Sports Med. Comparisons of non-surgical interventions for frozen shoulder: a systematic review and network meta-analysis.
Egger G. Peer reviewed: in search of a germ theory equivalent for chronic disease. Prev Chronic Dis. De Punder K, Pruimboom L. The dietary intake of wheat and other cereal grains and their role in inflammation. LPS-induced low-grade inflammation increases hypothalamic jnk expression and causes central insulin resistance irrespective of body weight changes. Int J of Mol Sci. Metabolic endotoxemia and diabetes mellitus: a systematic review.
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Infect Immun. Influence of lactoferrin on propionibacterium acnes-induced inflammation in vitro and in vivo. Dermatologic Ther. A randomized, double-blind, placebo-controlled trial to determine the efficacy and safety of lactoferrin with vitamin E and zinc as an oral therapy for mild to moderate acne vulgaris.
Int J Dermatol. A systematic review of lactoferrin use in dermatology. Crit Rev Food Sci Nutr. Kim M, Kim H. The roles of glutamine in the intestine and its implication in intestinal diseases. Int J Mol Sci. Glutamine and whey protein improve intestinal permeability and morphology in patients with Crohn's disease: a randomized controlled trial. Dig Dis Sci. Recent developments in prebiotics to selectively impact beneficial microbes and promote intestinal health. Curr Opin Biotechnol. Prebiotics: why definitions matter.
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Reversing established sepsis with antagonists of endogenous high-mobility group box 1. A literature review. More tea for septic patients? Anti-septicaemic effect of polysaccharide from panax ginseng by macrophage activation. J Infect. Caging a beast in the inflammation arena: use of Chinese medicinal herbs to inhibit a late mediator of lethal sepsis, HMGB1.
Allopregnanolone levels and reactivity to mental stress in premenstrual dysphoric disorder. Progesterone metabolite allopregnanolone in women with premenstrual syndrome. Allopregnanolone in women with premenstrual syndrome. Horm Metab Res. Allopregnanolone concentrations and premenstrual syndrome. Eur J Endocrinol. Fluoxetine in the treatment of premenstrual dysphoria. N Engl J Med. Citalopram increases pregnanolone sensitivity in patients with premenstrual syndrome: an open trial.
Selective serotonin reuptake inhibitors directly alter activity of neurosteroidogenic enzymes. Shanmugan S, Epperson CN. Estrogen-serotonin interactions: implications for affective regulation. Effect of estrogen-serotonin interactions on mood and cognition. Behav Cogn Neurosci Rev. Gonadal hormones modulate 5-hydroxytryptamine2A receptors: emphasis on the rat frontal cortex. Estrogen control of central neurotransmission: effect on mood, mental state, and memory.
Cell Mol Neurobiol. Effects of tamoxifen on serotonin transporter and 5-hydroxytryptamine 2A receptor binding sites and mRNA levels in the brain of ovariectomized rats with or without acute estradiol replacement. Brain Res Mol Brain Res. Widespread increases of cortical serotonin type 2A receptor availability after hormone therapy in euthymic postmenopausal women.
Fertil Steril. Rapid response to fluoxetine in women with premenstrual dysphoric disorder. Depress Anxiety. Effects of metergoline on symptoms in women with premenstrual dysphoric disorder. Dynamic plasticity: the role of glucocorticoids, brain-derived neurotrophic factor and other trophic factors.
Sex and stress hormone influences on the expression and activity of brain-derived neurotrophic factor. Subchronic treatment with fluoxetine and ketanserin increases hippocampal brain-derived neurotrophic factor,? Br J Pharmacol. Changes of serum concentrations of brain-derived neurotrophic factor BDNF during treatment with venlafaxine and mirtazapine: role of medication and response to treatment.
Elevated gray matter volume of the emotional cerebellum in women with premenstrual dysphoric disorder. J Affect Disord. Gray matter abnormalities in patients with premenstrual dysphoric disorder: an optimized voxel-based morphometry. Toward a functional neuroanatomy of premenstrual dysphoric disorder. Menstrual cycle effects on amygdala reactivity to emotional stimulation in premenstrual dysphoric disorder. Horm Behav. Cortical gamma-aminobutyric acid levels across the menstrual cycle in healthy women and those with premenstrual dysphoric disorder: a proton magnetic resonance spectroscopy study.
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Frozen shoulder is a common epidemiological affliction. Data acquired from people who suffer from this type of damage in other joints such as the hip, wrist and ankle also exist; although these syndromes are less common. Treatment for frozen shoulder is primarily physical physiotherapy, manual therapysecondary medical corticosteroid injections and finally surgical but with limited success. The difficulty in treating this type of condition successfully lies in the lack of knowledge about the risk factors involved and the pathophysiology underlying this mysterious syndrome.
This review gives an overview of the current scientific position of frozen shoulder in terms of evolutionary factors, etiology, the different mechanisms of action involved, current treatment options and other possible interventions based on recent discoveries of pathophysiological mechanisms.
Sometimes the shoulder joint becomes stiff, inextensible, and painful in a mysterious way, which is how frozen shoulder FS presents itself. Its etiology can be both primary or secondary to other conditions.
It is a difficult condition to define and diagnose precisely, as well as to treat effectively. Some known risk factors for its development are diabetes, Dupuytren's syndrome, thyroid disease especially hypothyroidismnephrolithiasis, cancer, Parkinson's disease, shoulder injury, smoking, heart and neck surgery or chronic regional pain syndrome 5.
FS can be very disabling, and, against the current opinion of many health professionals, FS does not resolve spontaneously in a large number of patients 7. Understanding the shared pathways between FS and the aforementioned comorbidities opens the possibility to develop new interventions based on common pathophysiological mechanisms such as insulin resistance and low-grade inflammation LGI. Most people who develop FS do so between 40 and 60 years of age 10being unusual in patients over 70 with the exception of secondary traumatic FS The incidence among women is 1.
This group of patients has greater associated disability, along with a greater reduction in their range of mobility The accumulated level of glycated hemoglobin A1c HbA1c is a determining factor, hence those patients with poorer blood glycemia control accumulate an increased risk for the development of FS Interestingly, a hypothesis to explain FS is proposed by the authors of the aforementioned study which states that the pathology could be more related to an asymmetric control of the brain rather than to some traumatic factor.
The prognosis of FS is highly variable. In contradiction to the common assumption that FS completely resolves over time, a meta-analysis found this to be scientifically invalid and that if left untreated, FS may persist for the more than 3 years or even never resolve 7. Mechanisms that may be key to the development of FS, such as the accumulation of advanced glycation end products AGE in the shoulder 16 associated with insulin resistance with compensatory hyperinsulinemia 17chronic hypoxia 18chronic LGI 19and endotoxemia, also exist.
FS is characterized by the spontaneous onset of symptoms such as pain, stiffness and progressive loss of mobility It presents in some cases, but not all, as a fibrotic state with capsular and ligament involvement and an inflammatory-based contracture that restricts the rotational interval of the affected shoulder.
Although agreement on the development of FS is not unified, it seems that it is proliferative, fibroblastic and inflammatory in nature These pathological mechanisms appear to be responsible for the activation of fibroblast and deregulation in collagen synthesis in people suffering from FS.
S is a biomarker for the presence of neuronal tissue and the increased presence of this nerve tissue could give a partial explanation for the pain associated with FS The evaluation of cadavers and the use of open arthroscopic surgery have shown synovial hyperplasia with increased vascularization during the initial period It ends with an incipient fibrosis located mainly in the rotator cuff interval formed by the tendons of the subscapular, biceps and supraspinatus muscles, and coracohumeral and superior glenohumeral ligamentstogether with the base of the coracoid process 26 and in the subscapular recess The thickening of the coracohumeral ligament, which is the roof of the rotator cuff interval, is indicated as one of the specific manifestations of FS and the main limiting factor for external rotation, although given its relationship with the subscapular and supraspinatus tendons it also contributes to restricting internal rotation In more advanced stages of FS, the thickening and contraction of the glenohumeral capsule culminates in limiting the range of movement in all directions Recently, two studies in a subgroup of patients diagnosed with FS have shown that there is no significant capsule restriction 29 All patients showed a significant increase in their passive range of motion ROMespecially in abduction while under general anesthesia conditions, compared to their ROM while awake.
In a more recent study 30the above research group confirmed the results of their study carried out in with five more patients suffering from FS and presenting with significant loss of shoulder range of motion in abduction and external rotation. Hollman L et al. This finding supports the hypotheses of the existence of a fear-based brain induced movement limitation, although more research is needed to determine the number of patients suffering from this type of FS.
The cited data help to better understand the development of FS and show that progression has been made in regard to the knowledge of the possible risk factors and the underlying pathophysiological mechanisms causing FS. Although this advance is clear, FS is still not completely understood and epidemiological data show the need for further investigation 4.
The purpose of the review is to increase knowledge about less known risk factors and pathophysiological mechanisms which lead to the development of FS and also to propose new interventions based on those factors and mechanisms. Bipedalism liberated the hands which made it easier for humans to throw projectiles. The human shoulder evolved by optimizing the storage and generation of elastic energy, especially in the maximum range of external rotational movement, which facilitated the launching of projectiles at high speed From an evolutionary perspective, manual work and the use of the upper limbs, especially among women, used to be much higher than today Today's lifestyle has dramatically decreased the use of the upper limbs, in contrast to its evolutionary design, most likely leading to atrophy of parts of the complex ligament capsule of the shoulder The non-use of a body part can result in neuroanatomical reorganization in different parts of the brain, such as occurs with phantom pain 33 or in the production of pain or neglect syndrome of that same part The fear of pain or the fact that little used tissue can be more easily damaged can produce a fear-based brain reaction and generate a muscle defense response that could lead to FS 30 The shoulder, the joint in the body with the greatest range of motion, would have its movement further limited by this possible muscle protection response Lack of movement may be responsible for chronic hypoxia in a joint that already has low partial oxygen pressure pO2 36providing a suitable environment for the establishment of an inflammatory process mediated by the activation of transcription factors such as hypoxia- inducible factor 1 HIF-1nuclear factor Kappa B NF-kB as well as the activation of several vascular and endothelial growth factors VEGF and MMP 1, 3 and 13 36 which are associated with inflammation, angiogenesis and tissue destruction A sedentary lifestyle is a risk factor which does not depend on the physical activity performed; it is also associated with an increase in inflammatory activity and the development of insulin resistance Similarly, oxidative stress associated with the presence of inflammatory cytokines affecting different parts of the shoulder ligament capsule complex may lead to an increased accumulation of free radicals, advanced glycation end products and, probably, subclinical alterations in both the connective tissue and the extracellular matrix A neglect syndrome may also be significant evidence of having had hemiplegia and could be the explanation for the risk of presenting FS after a stroke In short, it seems that the underuse of the full range of motion in modern sedentary humans could cause a predisposition for the development of FS.
Other more recent risk factors would then exacerbate the actual syndrome called FS. Inflammatory lipoproteins such as low-density lipoproteins LDL and non-high density lipoproteins non-HDLassociated with vascular inflammation and immune reactions have been identified as independent risk factors for FS 23 Vascular endothelial cell activation is accompanied by an increased expression of intercellular adhesion molecule-1 ICAM-1which has been shown to present elevated levels in the joint capsule and synovial fluid of FS patients compared to controls.
Furthermore, the maintenance of chronic LGI has been shown to produce phenotypic alterations in fibroblasts and therefore lead to FS This persistent fibroblast activation may play a role in the pathology of frozen shoulder and could explain the cellular mechanisms behind capsular fibrosis and persistent inflammation In this context, the role of alarmins, endogenous molecules that are released into the extracellular milieu after infection or tissue injury and that signal cell and tissue damage, may play a key role, and could explain the cellular mechanisms behind capsular fibrosis and nerve growth.
Alarmins high mobility group box 1 HMGB1IL, SA8, and SA9 have been shown to be elevated in the shoulder capsule of patients with frozen shoulder when compared to controls, as well as to be associated with significantly increased neoinnervation linked to patient-reported pain HMGB1 has been shown to be induced by damage-associated molecular patterns DAMPscytokines, and certain states of cellular stress, is considered crucial to the onset and perpetuation of FS. The release of HMGB1 upon stress perpetuates the inflammatory tissue response seen in patients.
The significant pain associated with frozen shoulder is linked to an increased peripheral nerve ingrowth The involvement of IL has been shown to be part of the key pathologic features of angiogenesis and capsular tissue fibrosis since elevated nuclear expression of IL in FS stromal cells has been found. It appears that in FS the S proteins are upregulated in macrophages and are therefore likely to be involved in macrophage differentiation and recruitment, which supports the concept that FS has a strong inflammatory and immunological origin Under such circumstances, the extracellular matrix ECM that the fibroblasts produce is altered and an imbalance in ECM turnover appears, as well as an altered ratio between MMPs and tissue inhibitor of metalloproteases TIMPswhich has been shown to be almost ten times lower in FS patients vs.
Recently, another possible cause for the development of FS has been described: an infectious one, related to several bacteria that usually inhabit human skin. The most often identified is Propionibacterium acnes P. Although several studies have found P. However, the infectious cause likely remains valid, based on data from a study of 10 people with FS when they were compared to 10 patients with shoulder instability.
The authors found multiple alarmins HMGB1, IL, SA8, and SA9 in the joint capsule of the FS patient group in amounts consistent with an infection, while in the control group they found no significant increase of infection related markers Its late growth in favorable environments is often misinterpreted as contamination The systemic infectious potential of P.
Its access to the interior of the body occurs through the mouth and teeth, mainly during dental procedures and more importantly, on a daily basis during tooth brushing Recent studies show how an oral dysbiosis contains microbial communities that can mediate inflammatory pathologies both locally and remotely Another bacterial infiltration route in non-operated people has been identified, namely the migration of bacteria in a dormant stage into various cells including epithelials, erythrocytes and adipocytes The infiltration of these bacteria into certain tissues depends on the level of oxygen present.
Currently, a clinical trial with 40 patients diagnosed with FS is underway comparing the effect of using an antibiotic with the application of prednisone Clinical Trials. In our opinion, based on the data, the risk of endotoxemia as a mechanism of action linked to FS should not be dismissed. Even though there is not a well-defined model for the medical management of FS, there is a wide spectrum of local treatments available, both surgical and non-surgical Frequently, the therapeutic management of FS varies considerably among specialists based on personal experience instead of published evidence It should be noted that none of the current therapeutic options are universally accepted as the most effective in restoring symptoms in patients with FS Common nonsurgical treatments include medication, physical therapy, exercise, manipulation under anesthesia, steroid injection or nerve blockers which can provide temporary relief of symptoms Most drug treatments target COX-1, COX-2 and glucocorticoid receptors with a marginal effect on inflammation and no impact on the accumulation of fibrotic collagenous tissue Surgical methods include open or arthroscopic capsular release and hydrodilation, which improve the shoulder range of motion and alleviate pain but leave other complications Persistent pain and limited motion despite 3 to 6 months of conservative treatment should be taken into account in the choice of surgical treatment The treatment of frozen shoulder evolves according to the stage of the syndrome 66 Thus, during the freezing phase duration 10—36 weeks pain is the most prominent symptom, and steroid injections are the first choice of treatment In the frozen phase 4—12 months restriction of joint movement prevails; in this case, mobilization techniques and joint distension are usually selected despite the limited evidence found Finally, in the thawing phase 12—42 months there is a reduction of pain and a progressive improvement of joint mobility.
A recent systematic review and meta-analysis shows how intra-articular corticosteroid infiltrations are the prevalent intervention in the non-surgical management of FS, especially for pain control and joint function. The combination of corticosteroid infiltrations and physiotherapy may offer some improvement in the pain and freezing phase, with physiotherapy and manual mobilization offering the most benefit in the adhesive phase of the injury In Figure 1 we propose an outline of the pathophysiology of FS, both at the diagnostic and therapeutic levels.
In green, the process related with the development of traumatic FS, for instance by repeated throwing in sports such as baseball or handball. In yellow, we indicate the interventions aimed at the risk factors and mechanisms of action responsible for this mysterious pathology.
In white, we highlight the pathologies associated with a greater risk of developing FS. The mechanisms of action discussed in this review provide a reasonable explanation for these associations.
We must make clear that Dupuytren's syndrome is not the cause of frozen shoulder, but a comorbid pathology connected to the same pathophysiology behind both FS and Dupuytren, including insulin resistance, LGI and low-grade infection The interventions mentioned in Figure 1 aim to offer a solution with the least number of side effects. Figure 1. Current and proposed pathways leading to the Frozen Shoulder Syndrome; from the photo to the film.
Frozen shoulder can be primary idiopathic or secondary traumatic. Baseball and handball players often suffer complete ruptures of the rotator cuff muscles leading to surgical operations and long-term immobilization.
The inability to resolve the inflammatory process promotes the establishment of a chronic LGI process in an environment of chronic hypoxia.
Black Twitter Icon. Les corticoïdes peuvent être utilisés chez la femme enceinte quels que soient leurs voies d'administration, leurs posologies et le terme de. J Dent Res. Systemic steroids cause wounds to heal with incomplete granulation tissue and Use of topical corticosteroids on chronic leg ulcers. Acheter Solupred En Ligne Generique Prednisolone 5, 10, 20 40 mg Pas Cher. @achetersolupredenlig - Reader. 0 Followers 0 Following. Ces anti-inflammatoires non stéroïdiens les plus vendus en France peuvent favoriser des complications infectieuses graves à l'origine. Prebiotics not only provide a source of energy for our bacteria, but also have some health benefits, such as providing both acute and chronic inflammatory relief Caggiano P, Jehkonen M. Figure 1. Foot Ankle Online J. In patients with regional pain syndrome, Jung et al. In contradiction to the common assumption that FS completely resolves over time, a meta-analysis found this to be scientifically invalid and that if left untreated, FS may persist for the more than 3 years or even never resolve 7.The following information was first published in Current Psychiatry , published September , Vol. Check out the article on Current Psychiatry or listen to Dr. Raffi discuss treatment of menstrual—related mood and anxiety disorders.
In an age when psychiatry strives to identify the biologic causes of disease, studying endocrine-related mood disorders is particularly intriguing. DSM-5 defines premenstrual dysphoric disorder PMDD as a depressive disorder, with a month prevalence ranging from 1. PMDD is a disorder of consistent yet intermittent change in mental health and functionality.
This article summarizes what is known about the etiology of PMDD. Further understanding of this disorder may lead to more efficacious treatments. Ruling out premenstrual exacerbation PME. In many women who have a primary mood or anxiety disorder, the late luteal phase is a vulnerable time. At this stage, a diagnosis of PMDD should be provisional at best.
Often, PME is treated by treating the underlying condition. Therefore, a full diagnostic psychiatric interview is important to first rule out other underlying psychiatric disorders. Patients can use one of many PMDD daily symptom charts available online. Alternatively, they can use a cycle-tracking mobile phone application to correlate their symptoms with their cycle and share this information with their providers. Estrogen receptor alpha ESR1 gene. They speculated that because ESR1 is important for arousal, if dysfunctional, this gene could be implicated in somatic as well as affective and cognitive deficits in PMDD patients.
In another study, investigators reported a relationship between PMDD and heritable personality traits, as well as a link between these traits and ESR1 polymorphic variants. Studies on serotonin gene polymorphism and serotonin transporter genotype. Although a study of serotonin gene polymorphism did not find an association between serotonin1A gene polymorphism and PMDD, it did show that the presence of at least 1 C allele was associated with a 2.
In times of acute stress, increased ALLO is known to provide relief. Estrogen, serotonin, and BDNF. Estrogen affects multiple neurotransmitter systems that regulate mood, cognition, sleep, and eating. Estrogen—serotonin interactions are thought to be involved in hormone-related mood disorders such as perimenopausal depression and PMDD. Research in menopausal women also has provided some support for this interaction.
Positron emission tomography studies in humans have found increased cortical serotonin binding modulated by levels of estrogen, similar to those previously seen in rat studies.
For some PMDD patients, SSRIs work within hours to days, as opposed to days or weeks for patients with depression or anxiety, which suggests a separate or co-occurring mechanism of action is in place. BDNF is critical for neurogenesis and is expressed in brain regions involved in learning and memory and also affects regulation. However, studies on this topic have been few and inconsistent. The influence of estrogen and progesterone on mood is also highly dependent on this axis.
Significant stress and trauma exposure have been associated with PMDD. For example, the startle response hypervigilance has been shown to be different in women with PMDD. The possible role of inflammation in PMDD deserves further investigation. The link between a history of stress, trauma, and PMDD raises the question of biologic resiliency and illness in these patients, as it connects to the HPA and HPG axis and production of inflammatory stress hormones and steroid hormones and their metabolites.
PMDD can be conceptualized as variable sensitivity to hormonal response to stress, 58 thus contextualizing biochemical and psychological resiliency.
Perhaps this type of immediate relief is akin to substance use disorders and symptoms of withdrawal. It could be that reinstatement of a certain amount of gonadal steroids in the follicular phase of the cycle diminishes a withdrawal-like response to these steroids.
A systematic approach to the diagnosis of PMDD is essential and should include ruling out premenstrual exacerbation of another underlying or comorbid mood or anxiety disorder.
The etiology of PMDD is complex. PMDD may be a disorder of withdrawal caused by a transient decline in neurosteroids. The Etiology of Premenstral Dysphoric Disorder: 5 interwoven pieces. By Edwin R. Freeman, MD In an age when psychiatry strives to identify the biologic causes of disease, studying endocrine-related mood disorders is particularly intriguing. Bottom Line A systematic approach to the diagnosis of PMDD is essential and should include ruling out premenstrual exacerbation of another underlying or comorbid mood or anxiety disorder.
J Psychiatr Res. Premenstrual dysphoric disorder: evidence for a new category for DSM Am J Psychiatry. Diagnostic and statistical manual of mental disorders, 5th ed. Firstborn adolescent daughters and mothers with and without premenstrual syndrome: a comparison.
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