#interleukin-6

[jppres]

The role of plasma angiotensin-converting enzyme and interleukin-6 levels on the prognosis of non-dialysis chronic kidney disease patients

Image: Max Pixel Article published in J. Pharm. Pharmacogn. Res., vol. 11, no. 1, pp. 55-62, January-February 2023. DOI: https://doi.org/10.56499/jppres22.1518_11.1.55 Hendri Susilo1,2**, Mochammad Thaha3,4, Budi Susetyo Pikir1,2, Mochamad Yusuf Alsagaff1,2, Satriyo Dwi Suryantoro3,4, Ifan Ali Wafa5, Nando Reza Pratama5, David Setyo Budi5, Bayu Satria Wiratama6, Citrawati Dyah Kencono…

[bpod-bpod]

Culture of Disorder

Human neural progenitor cells generated from induced pluripotent stem cells – cells from reprogrammed mature cells – for modelling effects of pro-inflammatory molecule IL-6 released in maternal immune activation, a potential contributor to neurodevelopmental disorders in the offspring

Read the published research paper here

Image from work by Kseniia Sarieva and colleagues

Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in and cover image of Disease Models & Mechanisms, November 2023

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[mitalipingale]

https://bundas24.com/read-blog/112096_interleukin-6-il-6-inhibitors-market-size-analysis-and-forecast-2031.html

The Interleukin-6 (IL-6) Inhibitors Market in 2023 is US$ 33.3 billion, and is expected to reach US$ 77.41 billion by 2031 at a CAGR of 11.12%.

[tchaikovskym]

data analysis is so draining but man i have correlations!!

[covid-safer-hotties]

Reference preserved in our archive

Abstract Background: COVID-19 emerged in December 2019 and rapidly became a global pandemic. It has since been associated with the progression of various endocrine disorders, including thyroid disease. The long-term effects of this interplay have yet to be explored. This review explores the relationship between COVID-19 and thyroid diseases, emphasizing thyroid gland function and the clinical implications for managing thyroid disorders in infected individuals.

Objectives: This narrative review intends to provide insight into the scope of research that future clinical studies may aim to address regarding the long-term effects of COVID-19 infection on thyroid health.

Methods: Keywords including “thyroid disease”, “COVID-19”, and “long-term” were used to search PubMed and Google Scholar for updated and relevant clinical research.

Results: COVID-19 affects the thyroid gland multifacetedly and includes direct viral invasion, immune-mediated damage, and hypothalamic-pituitary-thyroid axis disruption. Approximately 15% of COVID-19 patients experience thyroid dysfunction, which can present as thyrotoxicosis, hypothyroidism, or non-thyroidal illness syndrome (NTI). Noteworthy findings include inflammatory thyroiditis. Long-term effects, including those observed in children, include persistent hypothyroidism and exacerbated pre-existing thyroid-autoimmune conditions. Management of thyroid disorders in COVID-19 patients requires consideration: anti-thyroid drug (ATD) therapy used to treat hyperthyroidism in COVID-19 patients may need adjustment to prevent immunosuppression. Radioactive iodine (ROI) alternatives and interleukin-6 (IL-6) receptor antagonists could offer potential benefits and should be further explored.

Conclusion: Longitudinal follow-ups post-COVID-19 for patients with new and pre-existing thyroid disorders can improve disease outcomes. In addition, pathophysiological research on thyroid dysfunction in COVID-19 may help develop strategies to prevent and alleviate thyroid gland abnormalities post-COVID-19.

[your-blorbo-is-a-dog]

The Doctor from Darkwood…

⭐️ The Doctor from Darkwood is a Shar Pei.

Traditionally kept as a property guardian, the shar pei was driven to the brink of extinction in the 20th century. The breed was once very popular, but war and political turmoil in China caused it to nearly disappear in the 1970s. When the Guinness Book of World Records released a book naming it the rarest dog in the world, demand increased in America, and breeders began mixing Shar Pei with other dogs such as bull terriers to sell them to unknowing buyers. This gave them softer mouths, and they became known as “meat-mouth” shar peis while the originals are called “bone-mouth” shar peis. The Shar-pei is predisposed to several skin conditions including: allergic skin disease, cutaneous mucinosis, intertrigo, otitis externa, and vasculopathy, as well as Shar Pei fever, a swelling of the hocks due to more prominent anti-inflammatory genes ( interleukin 6 ). As long as he doesn’t try to lock everyone in a church again, am I right? .. too soon?

[mleprae]

Cytokines are so cute, you know those weird numbers you see in medical text? The one you'll likely see around is Interleukin, shortned to IL. The name literally means 'Cell communication', they're chemicals that cells release to speak to one another, depending what interleukin you find in a test, you can deduce what these little guys are planning and doing at the moment

The most common ones are TNF-a (tumor necrosis alpha) and IL-6, both stimulate inflammation in damaged area. Inflammation is just the cells setting up the battlefield, the redness is due to bloodflow in the area bringing more immune cells in, the pain is that sometimes the area increases, pressing onto nerves. It's your body telling you that you need to stop using that part.

IL-6 and TNF-a are the cytokines that the cells use to call one another, kind of a "I need backup here" signal. Some of these cytokines are pyrogenic, which is what we call the ones that go to the brain and tell it to raise body temperature!

You also have interferons (shortned to IFN), those are what cells produce to warn others in a "I'm infected with something, stay away" kind of way, this tells the other cells that they need to protect themselves, it also calls some cells responsible to kill infected cells to do their jobs

[auszeitstille]

Millions missing

Knapp 1 1/2 Jahre sind vergangen, seit dem ersten Verdacht, an ME/CFS erkrankt zu sein. Und dem langsamen Verschwinden, aus meinem eigenen Leben.

Kurze Zeit später fand ich raus, dass überdurchschnittlich viele, eine positive EBV Anamnese haben. Ein Virus, das meiner Meinung nach jahrzehntelang unterschätzt wurde. Dabei setzt diese Erkrankung so viele von uns, völlig außer Gefecht und befördert einige ins Krankenhaus, wie auch mich, damals mit 13 Jahren.

Angegriffene Organe, der gesamte Organismus völlig aus dem Gleichgewicht. Lebenslanges Risiko der Reaktivierung, Chronifizierung und mögliche Ursache, einer am Ende unheilbaren Erkrankung. Aber wer hätte das schon ahnen können? Am allerwenigsten ich selbst.

8 Monate, seit ich geschwächt bei meiner Hausärztin saß und ihr berichtete, dass ich nach einem schweren, aber unklaren Infekt im Sommer 2020, nicht wieder auf die Beine kam; dass ich mich mittlerweile seit Monaten krank fühle. Tägliche Grippesymptome, neurologische und motorische Ausfälle, eine bleierne Erschöpfung und starke Schmerzen.

Sie hat mich nicht ernst genommen. Der Klassiker. Schließlich war ich untergewichtig und steckte wieder tief in der Essstörung.

Für sie war mein Fall völlig klar.

Thema abgeschlossen.

Für mich allerdings nicht.

Ich kämpfte mich wieder raus aus dem Untergewicht, aber nichts hat sich dadurch verändert oder gar verbessert. Denn ich wusste, dass mit meinem Körper etwas nicht stimmt. Ich konnte es spüren.

6 Monate, seit ich mir eingestehen musste, dass mein altes Leben, so wie ich es kannte, nicht mehr existiert.

Der Versuch eine Balance zu finden zwischen Ärzte-Odyssee, Ausschlussdiagnostik und „das bildest du dir doch eh bloß ein“ Gedanken in meinem verdrehten Kopf.

3 Monate, seit ich einen anderen Arzt fand, der sich auskennt und vor allem: der mich ernst nahm.

1 Monat, seit der immunologischen Laboruntersuchung und den erschreckenden Ergebnissen mit erhöhten GPCR Autoantikörper, Interleukin Werten und dem eindeutigen Nachweis, einer Autoimmunreaktion.

3 Wochen, seit der offiziellen ME/CFS Diagnose meines Arztes, der von Anfang an wusste, dass ich zwar eine ganze Palette an psychischen Erkrankungen mitbringe, aber das akute Problem, eindeutig körperlicher Natur ist.

Seit dem. Steht alles still.

Denn mit der Diagnose, kam die Depression. Die nackte Angst, die pure Verzweiflung.

Nie war mein Blogname passender. Aber diesmal, gibt es kein Weg raus. Die auszeitstille, ist nicht mehr nur eine Auszeit. Die Stille wird bleiben, so lange, bis die Politik endlich hinsieht. Wir brauchen Forschung, Akzeptanz, Therapie und bitte bitte bitte irgendwann eine Heilung.

Egal wer das hier liest: bitte sieh hin, werde laut. Erkundige dich über ME/CFS, kläre auf und trage unsere Botschaft in die Welt hinaus. Wir sind sichtbar, wir wollen leben.

[medicomunicare]

Neuromyelitis optica "taken out of Breg": lymphocyte and cytokine signatures will grant the treatment conditions

No autoimmune diseases can currently be cured, only treated, and this is also true for neuromyelitis optica spectrum disorder (NEMOSD). Neuromyelitis optica disorder spectrum is one of them and it causes inflammation of the central nervous system, leading to vision and sensory loss, weakness and bladder dysfunction. The condition, which sometimes flares up in waves, has a treatment consisting of…

[emergencydrug]

Tofacitinib mechanism of action

Tofacitinib is a medication used to treat certain autoimmune diseases, primarily rheumatoid arthritis, psoriatic arthritis, and ulcerative colitis. Its mechanism of action involves targeting specific molecules and pathways in the immune system to reduce inflammation and modulate the immune response. Here's an overview of how tofacitinib works:

Janus Kinase (JAK) Inhibition: Tofacitinib drug belongs to a class of known as Janus Kinase (JAK) inhibitors. JAKs are enzymes that play a crucial role in transmitting signals within immune cells. By inhibiting specific JAK enzymes, tofacitinib interferes with the signaling pathways that lead to inflammation and immune system activation.

Cytokine Inhibition: JAK enzymes are involved in the signaling of various cytokines, which are small proteins that regulate immune responses. Tofacitinib primarily inhibits JAK1 and JAK3, which are associated with signaling by cytokines like interleukin-6 (IL-6), interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-7 (IL-7), interleukin-15 (IL-15), and interferon-gamma (IFN-gamma). By blocking these cytokine signals, tofacitinib helps reduce inflammation and control immune system activity.

Immune System Modulation: Tofacitinib helps modulate the immune response by reducing the activity of certain immune cells, particularly T cells and B cells, which are involved in autoimmune diseases. It can also affect other immune cells like natural killer (NK) cells and dendritic cells.

[vomitdodger]

From the article:

The American Academy of Pediatrics FALSELY states that “Vaccines are not associated with autism.”

Following is a list of abstracts from 212 papers demonstrating the multiple associations between vaccines and autism.

Autism is a largely immune mediated condition, and the purpose of a vaccine is to change the behavior of the immune system. Vaccines and their ingredients can cause the underlying medical conditions that are commonly found in children who have been given an autism diagnosis. These conditions include immune system impairment, autoimmune conditions, neuroinflammation, gastrointestinal damage, neurological regression, mitochondrial dysfunction, oxidative stress, glial cell activation, interleukin-6 secretion dysregulation, damage to the blood–brain barrier, seizures, dendritic cell dysfunction, mercury poisoning, aluminum toxicity, gene activation and alteration, glutathione depletion, impaired methylation, impaired thioredoxin regulation, impairment of the opioid system, cellular apoptosis, endocrine dysfunction, and other disorders.

[sommesick]

Autoimmune Registry adds Long COVID to its List of Diseases

The Autoimmune Registry has determined that biomarkers of immune system activity similar to those seen in many autoimmune and autoinflammatory diseases justify the inclusion of Long COVID on its list of diseases.

High levels of antibodies to the immune-system proteins called type I interferons (IFNs) have been associated with severe COVID-19.   Other studies have shown that severely ill patients tend to have a high concentration of pro-inflammatory cytokines, such as interleukin (IL)-6, compared to those who are moderately ill.

The Autoimmune Registry has decided to include Long COVID in its list of autoimmune diseases to support research into this emerging chronic condition.

[covid-safer-hotties]

Also preserved in our archive

"Just a cold" that increases intercranial abnormalities

By Nikhil Prasad

Medical News: A groundbreaking study conducted at San Marco University Hospital in Catania, Sicily, Italy, has revealed new insights into the potential impacts of SARS-CoV-2 on newborns. Researchers from this hospital and the University of Ferrara carried out an ultrasonographic analysis on newborns exposed to the virus, highlighting a significant incidence of minor intracranial abnormalities compared to unexposed infants. The findings raise important questions about the long-term neurological implications for children born during the COVID-19 pandemic.

The Study at a Glance This Medical News report delves into the research conducted by Bruna Scalia, Marco Andrea Nicola Saporito, and their colleagues, investigating cranial ultrasonography (cUS) findings in infants born to mothers who tested positive for SARS-CoV-2 during pregnancy or at delivery. The team analyzed data from 278 newborns, evenly split between exposed and unexposed cohorts. The study adhered to stringent observational protocols to ensure the reliability of results.

Key Findings Among the 139 newborns exposed to SARS-CoV-2, 23% exhibited intracranial abnormalities on cUS, compared to 16.5% in the unexposed group. Minor abnormalities were most prevalent and included subependymal cysts (SEPCs), choroid plexus cysts (CPCs), frontal horn cysts (FHCs), and lenticulostriate vasculopathy (LV). Major abnormalities, such as cerebellar hemorrhages and arachnoid cysts, were rare but noteworthy.

Interestingly, infants exposed to SARS-CoV-2 during pregnancy had a higher rate of abnormalities (38.4%) than those exposed at birth (19.5%). The second trimester emerged as a particularly critical period, with the majority of abnormalities observed in this subgroup.

Why These Findings Matter The study's results are alarming for public health professionals and expectant mothers. While SARS-CoV-2's immediate risks to newborns have been considered minimal, this research suggests subtle yet significant neurological effects. These abnormalities, although classified as minor, may carry long-term implications for cognitive and behavioral development.

The link between maternal inflammation and fetal development is not new, but the cytokine storm induced by SARS-CoV-2 appears to heighten this risk. The researchers hypothesize that inflammatory markers like interleukin-6 could cross the placenta, affecting the fetal brain and potentially disrupting synaptogenesis.

Methodology Details All newborns in the study underwent cranial ultrasonography within their first week of life. The scans were conducted using standardized equipment by experienced neonatologists. The findings were categorized as normal, minor, or major abnormalities. To exclude confounding factors, the study excluded infants with other infections or genetic disorders.

Demographic factors, such as gestational age and birth weight, were comparable across both groups. However, premature birth and maternal complications, such as gestational diabetes and hypertension, were noted as potential contributors to the observed abnormalities.

Implications for Future Research The findings call for more extensive, longitudinal studies to understand the long-term effects of these abnormalities. Current evidence suggests a potential association between minor abnormalities like SEPCs and neuropsychiatric conditions such as autism and ADHD. Further investigation could clarify whether these cUS findings are precursors to such outcomes.

What Experts Are Saying The study's authors emphasize caution, noting that minor intracranial abnormalities do not necessarily predict adverse outcomes. However, they recommend routine cranial ultrasonography for newborns exposed to SARS-CoV-2 as a precautionary measure. "The cost-effectiveness and non-invasive nature of cUS make it a valuable tool in monitoring these infants," said lead researcher Bruna Scalia.

Limitations and Strengths of the Study One limitation of the study was its relatively small sample size, particularly for subgroups like prenatally exposed infants. Additionally, the lack of serological testing for unexposed mothers could have introduced undetected cases into the control group. However, the study's rigorous methodology and use of a well-matched control group lend credibility to its conclusions.

Study Conclusions The research underscores a statistically significant increase in minor intracranial abnormalities among SARS-CoV-2-exposed newborns. These findings are particularly pronounced in infants exposed during the second trimester of pregnancy. While the abnormalities observed in the study were predominantly minor, their potential impact on long-term neurological outcomes cannot be overlooked. The researchers advocate for the following:

-Routine cUS Screening: Cranial ultrasonography should be performed on all newborns exposed to SARS-CoV-2 to identify abnormalities early.

-Long-Term Follow-Up: Exposed infants should be enrolled in neurodevelopmental follow-up programs to monitor their progress and intervene if necessary.

-Expanded Research: Larger, multicenter studies are needed to confirm these findings and explore the mechanisms behind SARS-CoV-2's impact on fetal brain development.

By highlighting these abnormalities, the study adds a critical layer to our understanding of COVID-19's broader implications, particularly for future generations.

The study findings were published in the peer-reviewed Italian Journal of Pediatrics. link.springer.com/article/10.1186/s13052-024-01826-3

[nursingwriter]

Symptoms of Periodontitis Smoking and periodontitis Diabetes and periodontitis Diagnosis of periodontitis Types of probes Probing force and probe diameter Histopathological alteration in the periodontal tissues Bleeding on probing (BOP) refers to bleeding of the gums induced by gentle manipulation of the tissue at the depth of the gingival sulcus or at the interface between the gingival and a tooth. This is frequently accomplished by the use of a periodontal probe. BOP is a sign of inflammation of the gums and is indicative of some sort of destruction and erosion to the lining of the sulcus. Periodontal disease is a set of inflammatory diseases usually affecting the tissues that surround and support the teeth otherwise called periodontium. This disease involves progressive loss of the alveolar bone around the teeth, and without treatment it can lead to loosening and possible eventual loss of teeth. Periodontitis is caused by microorganisms adhering and growing on the tooth surface, along with an overly aggressive immune response against this microorganism. The diagnosis is through inspecting the soft gum tissues around the teeth with a probe and x-ray films and visual analysis to determine the amount of bone loss around the teeth (Lang & Tonetti, 1996). The cause of gingivitis is poor oral hygiene leading to the accumulation of mycotic and bacterial matrix at the gum line, called dental plaque. Other causes are poor nutrition and underlying medical problem such as diabetes. Finger nick tests have been approved to identify and screen patients for possible contributory causes of gum disease such as diabetes. In a number of patients, gingivitis worsens into to periodontitis. This comes about as a result of destruction of the gingival fibers; the gum tissues separate from the tooth and deepened sulcus. Sub-gingival microorganisms colonize the periodontal pockets causing advanced inflammation in the gum tissues and progressive bone loss. Another strong risk factor that could predispose one periodontitis is one's genetic susceptibility. Several conditions and diseases, such as diabetes, Down syndrome and other diseases affecting one's resistance to infection increase susceptibility to periodontitis. Another factor making periodontitis a difficult disease to study is that human host response can also affect the alveolar bone resorption. Host response to the bacteria is mainly determined by genetics, however, immune development may play a role in susceptibility (Heins & Karpinia, 1998). 1.1 Symptoms of Periodotitis Periodontitis has very few symptoms in early stages and in many individuals it goes undetected till it has significantly progressed and that is when they seek treatment. Symptoms include redness or bleeding of gums while brushing teeth or biting into hard food, gum swelling that recurs, halitosis and a persistent metallic taste in the mouth. Also gingival recession, causing apparent lengthening of teeth, deep pockets between the teeth and the gums and loose teeth, in the later stages. However, gingival inflammation and bone destruction are painless; hence, most patients assume that painless bleeding after teeth cleaning is insignificant, although this may be a symptom of progressing periodontitis. Periodontitis is associated to increased inflammation in the body indicated by raised levels of C-reactive protein and Interleukin-6 which increases the risk of stroke myocardial infarction and atherosclerosis. It also associated to those over 60 years of age to impairments in delayed memory and calculation abilities. (Heins & Karpinia,1998). 1.2 Smoking and periodontitis. Cigarette smoking has been highly associated with impaired healing of surgical wounds and related to periodontitis. (Silverstein et al., 2000). The harmful effects of cigarette smoking on the periodontal status have also been well-documented. The adverse effect of smoking in implants has been described in a study of the outcome of 2,194 implants placed in 540 subjects. The study showed that a considerably higher percentage of implant failures occurred in smokers than in non-smokers. Smokers had total implant failure rate of 11.3%, and only 4.8% of the implants failure rate in non-smokers (Chaves et al., 1993). However, limited information exists with consideration of the consistently natural occurring plaque and bleeding on probing in the oral cavity under normal oral hygiene measures. The study was to explain the distribution of tooth surfaces covered by supragingival plaque and gingival units bleeding on probing in a steady state environment of no dental interference. Also relative consistency of plaque and bleeding was studied. 65 volunteers, 14 women and 51 men ranging from the age of 19 to 30 years, participated. 33 volunteers were heavy smokers and 32 non-smokers. Clinical examinations discovered mild, plaque-induced gingivitis without clear destructive periodontitis. Within a 6-month period, occurrence and amount of plaque, calculus and gingival bleeding was site-specifically examined four times. Well-defined, symmetric and regular patterns of plaque and calculus distribution in the oral cavity were observed, which were rather the same in smokers and non-smokers. It is worth noting that smokers had uniformly more plaque in all regions of the oral cavity as compared to non-smokers. In contrast, there was no obvious pattern of bleeding on probing. Stability of observations was considerably less than for plaque scores and it was particularly true for smokers, where the relationship between bleeding scores was smaller than in non-smokers. A large part of the difference in gingival bleeding may be due to presently unknown factors other than plaque and calculus with extensive consequences for preventive program (Lang et al., 2001). 1.3 Diabetes and periodontitis Another risk factor for periodontitis is uncontrolled diabetes. So far, facts related to disease-free implant survival in diabetics is still preliminary. A one-year report of implant survival in Type II diabetics showed a 7.3% failure rate. This shows that osseointegration can be obtained in the most diabetic patients. However, the standard of a long-term prognosis of implants placed in these subjects is presently unknown. 1.4 Diagnosis of periodontitis Periodontal probing is commonly used criteria for diagnosis of gingival inflammation. Periodontal Screening and Recording (PSR), a painless procedure used to measure and determine the severity of periodontitis, where the dentist uses a mirror and a periodontal probe to measure pocket depth. The probe is held along the length of the tooth with the tip placed in the pocket. The tip of the probe will then touch the point where the connective tissue attaches to the tooth. The dentist will 'walk' the probe to six specific points on each tooth, three on the buccal and 3 on the lingual side. The dentist measures the depth of the probe at each point. Pocket depth greater than 3mm indicates disease presence. These measurements help establish the condition of the connective tissues and amount of gingival overgrowth or recession. Tooth mobility is determined by pushing each tooth between two instrument handles and observing any movement. Mobility is a strong indicator of bone support or loss of the same. X-rays are taken to show any loss of bone structure supporting the teeth. 18 x-rays make up the full mouth series necessary for diagnosis (Nguyen, 2008). A periodontal probe is an instrument used in the dental armamentarium .It's usually long, thin and blunted at the end. Its main use is to measure pocket depths around a tooth to determine the state of health of the periodontum. There are markings inscribed onto the head of the instrument for accuracy and readability. Proper use of the periodontal probe is required to maintain accuracy. The tip of the instrument is positioned with light pressure of 10-20g into the gingival sulcus. It is essential to keep the periodontal probe parallel to the contours of the root of the tooth and to put in the probe down to the base of the pocket. This results in obscuring a part of the periodontal probe's tip. The first marking visible over the pocket indicates the size of the pocket depth. It has been establish that the average, healthy pocket depth is around 3mm without bleeding upon probing. Depths more than 3mm can be linked with "attachment loss" of the tooth to the adjacent alveolar bone, which is a feature in periodontitis. Pocket depths more than 3mm can also be an indication of gingival hyperplasia. 1.5 Types of probes. There are different types of periodontal probes, and each has its own mode of indicating measurements on the tip of the device. They include, Michigan O. probe with markings at 3mm, 6mm and 8mm, Williams probe with circumferential lines at 1mm, 2mm, 3mm, 5mm, 7mm, 8mm, 9mm, and 10mm and PCP12 probe with Marquis markings has alternating shades every 3mm. Unlike other types of probes, Naber's probe is curved and used for measuring into the furcation area between the roots of a tooth. Periodontal probe can also be used for measurement and tooth preparations during restorative procedures, gingival recession, attached gingiva, and oral lesions or pathologies (James et al., 2001). 1.6 Probing force and probe diameter The relationship between bleeding on probing, probing force and probe diameter is usually determined by the pressure exerted on the gingival tissues and resistance from the healthy or inflamed tissue. This pressure is directly proportional to the force on the probe and inversely proportional to the probe tip diameter. Large probing diameters reduce probe progress into inflamed connective tissue hence this effect of change in probe diameter reduces the pressure in a greater manner than an increase of similar change in probe force. According to the research conducted by Silverstein et al., (2000), the pressure used to place the probe tip at the base of the periodontal sulcus is approximately 50 N/cm2 and at the base of the junction epithelium is 200 N/cm2. A tip diameter of 0.6 mm is needed to reach the base of the sulcus. Clinical inflammation does not reflect the severity of histological inflammation, and the recordings may not illustrate probing depth. Therefore, probing depth does not identify anatomical locations at the base of the sulcus. Probe tips must have a diameter of 0.6 mm and a 0.20 gram force (50 N/cm2) to gain a pressure which demonstrates estimated probing depth. This pressure is useful for the measurement of the reduction of clinical probing depth, which includes the formation of a long junctional epithelium as a result of treatment. but, different forces or diameter tips are essential for the measurement of healthy or inflamed histological periodontal probing depths. A research was done to establish whether probing force had an influence on the amount of clinical attachment-gain assessed after treatment by scaling and root planing. A probing device was constructed which permitted concurrent monitoring of probing force and probe penetration and which standardized the insertion pathway for recurring measurements. In 10 periodontal patients, 2 deep pockets were selected then measured before and after periodontal treatment by scaling and root-planing. Depth-force plots were compared by superimposition. Depth values were determined at 5 different force levels (0.25, 0.50, 0.75, 1.00 and 1.25 N) on every plot and changes of clinical attachment levels were calculated. A major relationship was seen between probing force and attachment level. The values obtained with 0.25 N. were extensively different from the values obtained with higher forces (p 5mm patients, respectively. The groups was again divided into 25 -- 50 and >50 years age subgroups. The result showed a significant decrease in the appearance of Tumors Necrosis Factor Receptor-Associated Death Domain (TRADD). This was observed in 25 -- 50 years of periodontal disease group compared to the periodontal healthy group. BCL2-associated X protein expression in the periodontal disease group was considerably decreased in 25 -- 50 years age group but increased in the >50 years age group compared to periodontal healthy age groups. Periodontal disease patients of both 25 -- 50 years and >50 years age increased in the expression of Cytochrome C. And Caspase-3 compared to the respective periodontal healthy groups. The periodontal disease patients showed a stronger correlation with age in the expression of Tumors Necrosis Factor Receptor-Associated Death Domain and BCL2-associated X protein compared to the periodontal healthy groups. (Archives of Oral Biology) Non-surgical periodontal therapy results in a great decrease of pocket probing depths and bleeding on probing, and attachment gain. When combined with periodontal maintenance a long-term stability of periodontal conditions, which shows a decreased incidence of extra attachment loss and reduction in bleeding on probing is possible and has been evidenced even in residual pockets with probing depths of greater than 7 mm. This data shows that significant changes in the immune/inflammatory response take place after treatment. Though, it is not clear, whether the clinical signs following periodontal therapy are related with an expression profile of inflammatory and immunological genes that is well-matched with periodontal health (Thomas et al., 2008). Read the full article