استئوآرتریت Flashcards
شایع ترین سن بروز استئوارتریت ؟
در خانوما شایع تر یا اقایون؟
بالای ۵۰ سال
زیر ۴۰ سال نادر
بالای ۶۰ خیلی شایع
خانوما
شایع ترین مفاصلی که در استئوارتریت درگیر میشن ؟
affected joints include the hip, knee, and first metatarsal phalangeal joint (MTP) and cervical and lumbosacral spine. In the hands, the distal and proximal interphalangeal joints and the base of the thumb are often affected.
We thus develop OA in joints that were ill designed for human tasks such as pincer grip (OA in the thumb base) and walking upright (OA in knees and hips).
کدوم مفاصل در استئوارتریت درگیر نمیشن؟
Usually spared are the wrist, elbow, and ankle.
Some joints, like the ankles, may be spared because their articular cartilage may be uniquely resistant to loading stresses.
چه تغیراتی در ساختار مفصل در طی استئوارتریت وجود دارد؟
OA can be diagnosed based on structural abnormalities or on the symptoms these abnormalities evoke. According to cadaveric studies, by elderly years, structural changes of OA are nearly universal.
🔺These include cartilage loss (seen as joint space loss on x-rays) and osteophytes. Many persons with x-ray evidence of OA have no joint symptoms, and although the prevalence of structural abnormalities is of interest in understanding disease pathogenesis, what matters more from a clinical perspective is the prevalence of symptomatic OA.
How is symptomatic OA of the knee?
Symptomatic OA of the knee (pain on most days of a recent month plus x-ray evidence of OA in that knee
استئوارتریت چیه و در طی ان چه تغییراتی رخ میدهد؟
OA is joint failure, a disease in which all structures of the joint have undergone pathologic change, often in concert. The pathologic sine qua non of disease is hyaline articular cartilage loss, present in a focal and, initially, nonuniform manner. This is accompanied by increasing thickness and sclerosis of the subchondral bony plate, by outgrowth of osteophytes at the joint margin, by stretching of the articular capsule, by variable degrees of synovitis, and by weakness of muscles bridging the joint. In knees, meniscal degeneration is part of the disease. There are numerous pathways that lead to joint failure, but the initial step is often joint injury in the setting of a failure of protective mechanisms.
ریسک فاکتور های سیستمیک OA?
1-Age is the most potent risk factor for OA. Radiographic evidence of OA is rare in individuals aged <40; however, in some joints, such as the hands, OA occurs in >50% of persons aged >70.
2-Older women are at high risk of OA in all joints, a risk that emerges
as women reach their sixth decade. Although hormone loss with menopause may contribute to this risk, there is little understanding of the unique vulnerability of older women versus men to OA.
چرا با افزایش عمر Joint vulnerability به استئوررتیرت زیاد میشه؟
Aging increases joint vulnerability through several mechanisms. Whereas dynamic loading of joints stimulates cartilage matrix synthesis by chondrocytes in young cartilage, aged cartilage is less responsive to these stimuli. Partly because of this failure to synthesize matrix with loading, cartilage thins with age, and thinner cartilage experiences higher shear stress and is at greater risk of cartilage damage.
Also, joint protectors fail more often with age.
Muscles that bridge the joint become weaker with age and also respond less quickly to oncoming impulses.
Sensory nerve input slows with age, retarding the feedback loop of mechanoreceptors to muscles and tendons related to their tension and position.
Ligaments stretch with age, making them less able to absorb impulses.
These factors work in concert to increase the vulnerability of older joints to OA.
کدام ریسک فاکتور ها از طریق تاثیر لوکال بر محیط اطراف مفصل ان را مستعد ارتوروز میکنن؟
۱-تغییرات اناتومیک : دفورمیتی مادرزادی ، developmental abnormalities,:
With changes in joint anatomy, for example, load across the joint is no longer distributed evenly across the joint surface, but rather shows an increase in focal stress.
در مفصل hip چه ابنورمالیتی های اناتومیکی میتونن مستعد OA کنن؟
In the hip, three uncommon developmental abnormalities occurring in utero or in childhood, congenital dysplasia, Legg-Perthes disease, and slipped capital femoral epiphysis, leave a child with distortions of hip joint anatomy that often lead to OA later in life. Girls are predominantly affected by acetabular dysplasia, a mild form of congenital dislocation, whereas the other abnormalities more often affect boys. Depending on the severity of the anatomic abnormalities, hip OA occurs either in young adulthood (severe abnormalities) or middle age (mild abnormalities). Femoroacetabular impingement can develop during adolescence. It is a clinical syndrome in which anatomic abnormalities of the femoral head and/or the acetabulum result in abnormal contact between the two bones especially during hip flexion and rotation, leading to cartilage and labral damage and hip pain and ultimately in later life to possible hip OA.
علل premature OA در زانو و‌هیپ؟
Tears of ligamentous and fibrocartilaginous structures that protect
the joints, such as the meniscus in the knee and the labrum in the hip, can lead to premature OA. Meniscal tears increase with age and when chronic are often asymptomatic but lead to adjacent cartilage damage and accelerated OA
What is malalignment across the joint ?
چجوری فرد رو مستعد ارتروز میکنن؟
Varus (bowlegged) knees with OA are at exceedingly high risk of cartilage loss in the medial or inner compartment of the knee, whereas valgus (knockkneed) malalignment predisposes to rapid cartilage loss in the lateral compartment. Malalignment causes this effect by increasing stress on a focal area of cartilage, which then breaks down. There is evidence that malalignment in the knee not only causes cartilage loss but leads to underlying bone damage, producing bone marrow lesions seen on magnetic resonance imaging (MRI). Malalignment in the knee often produces such a substantial increase in focal stress within the knee (as evidenced by its destructive effects on subchondral bone) that severely malaligned knees may be destined to progress regardless of the status of other risk factors
ضعیف شدن ماهیچه ۴سر چجوری مستعد ارتروز زانو میکنه؟
Weakness in the quadriceps muscles bridging the knee increases the
risk of the development of painful OA in the knee.
اثر تغیرات density استخوان بر استعداد ابتلا به ارتروز؟
The role of bone in serving as a shock absorber for impact load is not
well understood, but persons with increased bone density are at high risk of OA, suggesting that the resistance of bone to impact during joint use may play a role in disease development.
عواملی که با مکانیسم loading factors سبب مستعد شذن به ارتوروز میشن؟
1-Obesity
2-Repeated Use of Joint and Exercise:
There are two categories of repetitive joint use, occupational use and leisure time physical activities. Workers performing repetitive tasks as part of their occupations for many years are at high risk of developing OA in the joints they use repeatedly.
رابطه و مکانیسم افزایش وزن و ارتروز؟
در کدام مفاصل؟
Three to six times body weight is transmitted across the knee during single-leg stance. Any increase in weight may be multiplied by this factor to reveal the excess force across the knee in overweight persons during walking. Obesity is a well-recognized and potent risk factor for the development of knee OA and, less so, for hip OA.
Obesity precedes the development of disease and is not just a consequence of the inactivity present in those with disease.
🌸 Not only is obesity a risk factor for OA in weight-bearing joints, but obese persons have more severe symptoms from the disease
چاقی به عنوان زیسک فاکتور اتروز در خانوم ها مهم تره یا اقایون؟
It is a stronger risk factor for disease in women than in men,
and in women, the relationship of weight to the risk of disease is linear, so that with each pound increase in weight, there is a commensurate increase in risk.
🚴🏻♀️🤾🏻♀️Weight loss in women lowers the risk of developing symptomatic disease.
چاقی به جز افزایش لودینگ بارچه مکانیسم دیگه ای میتونه باعث ارتوروز شه؟
Obesity’s effect on the development and progression of disease is mediated mostly through the increased loading in weight-bearing joints that occurs in overweight persons.
However, a modest association of obesity with an increased risk of hand OA suggests that systemic products of adipose tissue such as adipokines may affect disease risk also.
استفاده زیاد از مفاصل مث کارگران و کشاورزان با چه مکانیسمی سبب ارتوروز میشه?
One reason why workers may get disease is that during long days at work, their muscles may gradually become exhausted, no longer serving as effective joint protectors. It is widely recommended for people to adopt an exercise-filled
lifestyle, and long-term studies of exercise suggest no consistent association of exercise with OA risk in the majority of persons. However, persons who already have injured joints may put themselves at greater risk by engaging in certain types of exercise. For example, persons who have already sustained major knee injuries are at increased risk of progressive knee OA as a consequence of running. In addition, compared to nonrunners, elite runners (professional runners and those on Olympic teams) have high risks of both knee and hip OA. Lastly, although recreational runners are not at increased risk of knee OA, studies suggest that they have a modest increased risk of disease in the hip.
پاتوفیزیولوژی OA?
از کدوم قسمت مفصل شروع میشه و چجوری پیش میره؟
The pathology of OA provides evidence of the involvement of many joint structures in disease. Cartilage initially shows surface fibrillation and irregularity. As disease progresses, focal erosions develop there, and these eventually extend down to the subjacent bone. With further progression, cartilage erosion down to bone expands to involve a larger proportion of the joint surface, even though OA remains a focal disease with nonuniform loss of cartilage
در پاتولوزی OA وارد شدن اسیب به غضروف، با چه مکانیسمی سبب درگیری بقیه ساختار های مفصل میشه؟
After an injury to cartilage, chondrocytes undergo mitosis and clustering. Although the metabolic activity of these chondrocyte clusters is high, the net effect of this activity is to promote proteoglycan depletion in the matrix surrounding the chondrocytes. This is because the catabolic activity is greater than the synthetic activity.
As disease develops, collagen matrix becomes damaged, the negative charges of proteoglycans get exposed, and cartilage swells from ionic attraction to water molecules.
Chondrocytes at the basal level of cartilage undergo apoptosis. With loss of cartilage comes alteration in subchondral bone.
Stimulated by growth factors and cytokines, osteoclasts and osteoblasts in the subchondral bony plate, just underneath cartilage, become activated. Bone formation produces a thickening and stiffness of the subchondral plate that occurs even before cartilage ulcerates. Trauma to bone during joint loading may be the primary factor driving this bone response, with healing from injury (including microcracks) producing stiffness. Small areas of osteonecrosis usually exist in joints with advanced disease. Bone death may also be caused by bone trauma with shearing of microvasculature, leading to a cutoff of vascular supply to some bone areas.
Additional pathologic changes occur in the capsule, which stretches,
becomes edematous, and can become fibrotic.
چرا غضزوفی که یبار بهش اسیب وارد شده مستعد اسیب های بیشتزه؟
Because in damaged cartilage proteoglycans are no longer forced into close proximity, cartilage does not bounce back after loading as it did when healthy, and cartilage becomes vulnerable to further injury.
هالمارك OA در رادیولوژی؟
At the margin of the joint, near areas of cartilage loss, osteophytes
form.
These start as outgrowths of new cartilage, and with neurovascular invasion from the bone, this cartilage ossifies. Osteophytes are an important radiographic hallmark of OA
سینویوم در OA با حالت سالم چه فرقی داره؟
The synovium produces lubricating fluids that minimize shear stress
during motion. In healthy joints, the synovium consists of a single discontinuous layer filled with fat and containing two types of cells, macrophages and fibroblasts, but in OA, it can sometimes become edematous and inflamed. There is a migration of macrophages from the periphery into the tissue, and cells lining the synovium proliferate. Inflammatory cytokines and alarmins secreted by the synovium activate chondrocytes to produce enzymes which accelerate destruction of matrix.
