diagnosed with knee OA (8 females and 4 males) attending physiotherapy sessions at Osteoarthritis (OA) sendi lutut adalah penyakit sendi kronik yang kerap menjadi kesan pencegahan sekunder berbanding mengubati. OSTEOARTHRITIS FAKULTAS KEDOKTERAN UNPATTI Nama Kelompok Devana M Maelissa Eli Ezer Simangunsong Fadilah M Agun. Osteoartritis (OA) adalah gangguan sendi yang bersifat kronis disertai kerusakan tulang rawan sendi berupa disintegrasi dan perlunakan.
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The process of degeneration of the osteoarthritsi has commonly been classified as OA disc space narrowing together ksteoarthritis vertebral osteophyte formation ; however, anatomically, the facet joint is the only synovial joint in the spine that has a similar pathological degenerative process to appendicular joints. The complex relationship between spine radiographs and LBP has many clinical and research challenges. Specific conservative treatments for spine degeneration have not been established; there has, however, been recent interest in use of exercise therapy, because of some moderate benefits in treating chronic LBP.
An understanding of the relationship between spine degeneration and LBP may be improved with further population-based research in the areas of genetics, biomarkers, and pain pathways.
Osteoarthritis OA is the most common form of arthritis, affecting an estimated 27 million adults in the US [ 1 ]. The prevalence of OA has increased over the past two decades, and increases in life expectancy and obesity, both risk factors for OA, have led to concerns over the public health consequences of OA [ 1 ].
Arthritis in general is also a leading cause of disability and a significant cause of reduced quality of life [ 23 ]. Commonly thought of as a disease of the peripheral joints i.
Utilization of health care services resulting from LBP is high, and total social cost is estimated to be greater than billion dollars per year in the United States [ 8 ]. Aside from prevalence and cost, the effect of LBP on the osteowrthritis is substantial.
Approximately million workdays per year are lost as a result of LBP [ 9 ], making it the most common reason for time off from work [ 1011 ].
Because of its high prevalence and effect on health services, the spinal anatomical origins of LBP are of great interest to researchers and clinicians. To address prevention and treatment, understanding the etiology of LBP is important, because it may differ within the large majority of patients in whom we describe the etiology as mechanical or non-specific origin.
Although many imaging techniques can be used to diagnose and quantify OA, plain film radiographs are a commonly utilized technique because they are relatively inexpensive and easily administered [ 14 ]. Specific clinical reasons for use of plain film radiographs for individuals seeking care for LBP include addressing danger signals, for example malignancy, fracture, or dixgnosis, improving patient satisfaction, and improving understanding of the origin of LBP.
In the absence of radicular symptoms, current guidelines suggest plain film radiography is a reasonable initial imaging option for LBP [ 15 ].
Use of plain films of the spine is common, irrespective of the stage or chronicity of LBP. Carey and colleagues[ 18 ], in adlaah stratified probability sample of North Carolina residents, found that The clinical decisions correlating radiographic findings and LBP are complex and poorly understood. The association between radiographic spine degeneration and LBP has been debated since the s [ 19 ]. Osteoarthritsi purpose of this review is to summarize this current evidence while describing the challenges of inconsistent spine OA definitions and to report recent conservative treatment approaches osteoarfhritis LBP.
This review concludes by highlighting recommendations for future spine OA and LBP research to address these two commonly related conditions with substantial public health importance. All of these spinal structures have adequate nerve supply capable of generating LBP.
The vertebral facet joints zygapophyseal joints are synovial joints with the typical features of hyaline cartilage over subchondral bone, a synovial membrane, and a joint capsule [ 21 ]. Facet joint OA is a multifactorial process, and it has been thought that the presence of intervertebral disc degeneration leads to a greater load and motion at the facet joint, resulting in degenerative changes similar to those seen in other synovial joints [ 20 ].
However, the presence of facet joint OA has been found to be present even in the absence of intervertebral disc degeneration [ 22 ]. Situated between two vertebral bodies, the intervertebral disc is made up of two main regions: The collagen content of the intervertebral disc consists of both type I and II collagen, with the nucleus containing only type II whereas the annulus contains both types I and II [ 24 ].
Changes to the disc collagen content can occur naturally with aging, a process commonly referred to as intervertebral disc degeneration. These aging-related changes include a decrease in aggrecan, water, and collagen content [ 25 ], resulting bnding DSN on plain film radiographs. A vertebral osteophyte is a bony outgrowth that arises from the periosteum at the junction of bone and cartilage [ 26 ].
Osteophyte formation in the vertebral column has been shown to be a general indicator of age [ 27 ].
Osteophytes, however, may form without overt cartilage damage, implying they may form in an otherwise healthy joint [ 28 ]. However, the presence of disc space narrowing is highly associated with osteophyte formation [ 29 ]. The process of degeneration in the spine is thought to be initiated by disc degeneration; this disc degeneration is hypothesized to result in segmental instability that increases the load on the facet joints and leads to cartilage alterations [ 21 ].
This process has been clinically debated with little research support.
Spondylosis Center – Spinal Osteoarthritis – Symptoms Exercises Treatments
Using computed tomography CTthey report that, for most individuals, there is ordered progression of spine degeneration beginning with the intervertebral disc. They also remark that increasing age, body mass index BMIand female sex may be related to isolated facet joint degeneration in some individuals [ 30 ].
Osteoarthritis is the clinical outcome of a disease process that results in structural and functional failure of synovial joints.
This process has been characterized by damage to articular cartilage, subchondral bone alteration, a synovial inflammatory response, and an overgrowth of bone and cartilage [ 31 ]. In the spine, both the presence of intervertebral disc degeneration and osteophyte formation at the same vertebral level has been used to define lumbar spine OA, otherwise known as spondylosis [ 32 ]. Intervertebral disc degeneration and osteophyte formation may not share the same pathophysiological process of degeneration or have the anatomical synovial structures necessary to collectively meet the definition of OA.
This has led to challenges and discussion of spine degeneration research because there is no consensus on whether this combination of features DSN and OST in the spine constitutes OA or a separate phenomenon [ 33 ]. As such, a clinically relevant definition that combines spine features to accurately represent spine OA is still unknown [ 34 ] and may not be necessary.
The facet joint, however, is a synovial joint with a process of degeneration that may be associated with OA in appendicular joints [ 6 ]. Findings such as these suggest the pathophysiological course of degeneration in the spine differs, depending on the radiographic feature, from that of hip, knee, and hand OA. Our recent work is the only study to quantify the prevalence of radiographic FOA in a community-based population, revealing the prevalence affecting at least one lumbar level to be The prevalence of these radiographic features has been found to differ by gender and race.
Most recent studies agree that OST is more prevalent [ 343537 ] and severe [ 3537 ] in men whereas prevalence of DSN is greater in women [ 343537 ]. Our recent work is the first to describe these features across a sample of African Americans AA and Caucasians [ 35 ].
The reason for this may be related to racial differences in occupational exposure, BMI, physical activity demands, or anatomical differences. As such, there is still much to be learned about the reasons for these race and gender differences and radiographic changes in the lumbar spine. By far, most epidemiological studies addressing the association between LBP and spine degeneration have been cross-sectional. Most of these cross-sectional studies have been practice-based, using select or small samples that have limited generalizability.
Recently, a series of population-based cross-sectional studies have specifically set out to determine the association between lumbar spine radiographic features and LBP Table 1. Cross-sectional designs with the outcome of LBP have been criticized for their lack of uniformity in LBP questions [ 38 ].
Despite the varying definitions of LBP, and different grading and coding schemes and settings across recent studies, a modest association between DSN and LBP has been consistently found. An topic that is particularly understudied is the association between spine radiographic features and physical function.
In this same cohort, Scheele et al. Our findings with regard to physical function are similar to those of de Schepper et al. Findings from the Johnston County Osteoarthritis Project unpublished. The vague diagnostic classifications and multidimensional, recurrent nature of LBP create challenges for longitudinal designs aimed osteoarhritis determining the temporal relationship between radiographic osteoarthriitis features and LBP. These challenges are compounded by the remaining questions related to the etiologic process of spine degeneration.
Spine degeneration is a process that occurs slowly in some individuals and more rapidly in others [ 25 ]. The age at which the process of spine degeneration begins is largely unknown and may depend on the individual spine.
These different factors make studying the temporal relationship between spine degeneration and LBP difficult. Two previous longitudinal studies, consisting of women only, have found few predictive risk factors for either DSN or OST [ 3341 ].
Notable predictors of DSN progression bandign these studies have been the presence of baseline DSN [ 41 ] and the presence of baseline hip or knee OA [ 33 ]. The presence of baseline DSN was not found to be a risk factor for future back pain [ 42 ]. There is little consistency between studies of risk factors for future spine degeneration or LBP; some studies suggest baseline degeneration as a significant risk factor for future LBP whereas others do not.
Ideally, such knowledge of risk factors could be used to develop primary prevention techniques for these outcomes; however, this topic is largely understudied, although we already have sufficient information to make clinical recommendations adapah the treatment of LBP.
Given the effect of LBP on the US healthcare system, workplace, and individual quality of life, there is great need to better understand bandimg and etiologic factors of LBP. Most research has focused on treating symptoms and functional impairment of LBP rather than on understanding the mechanisms underlying the anatomic and functional diagnossi we currently call spine degeneration and their relationship to symptoms and functional impairment.
Currently, our understanding of the treatment for LBP is, stated simply, that some activity is better than no activity [ 4344 ].
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Exercise therapy is an activity which has long been a xiagnosis option for LBP, with Cochrane and other reviews indicating some effectiveness for treating chronic low back pain [ 45 ]. Specifically, treatment of LBP with yoga has attracted substantial interest in recent years [ 46 — 48 ].
The functional outcomes found in the yoga and stretching group remained statistically superior to those for the self-care group after a follow-up of 26 weeks. These findings suggest it is the physical rather than psychological aspect of yoga that has moderate benefits for chronic LBP.
This trial did not specifically target patients with intervertebral disc degeneration and excluded patients with severe intervertebral disc degeneration, because some patients with severe disc degeneration may not tolerate exercise therapy [ 48 ]. The use of conservative treatment to prevent spine degeneration or conservative treatment for spine degeneration as a primary technique for treating LBP has not yet been reported in the literature.
Reasons for this may be the small number of longitudinal studies, inconsistencies in predictors, and weak risk factors. Furthermore, there are few secondary prevention intervention techniques specifically aimed at treating symptomatic spine degeneration.
Injection therapy has been a popular treatment technique targeting spine features for LBP, and Karppinen et al. Facet joint adalan therapy to treat LBP has increased dramatic in recent years. However, there is little evidence to support the use of this therapy, with recent practice guidelines recommending against the use of facet joint steroid injections [ 50 ]. What future research areas are ahead for understanding of spine degeneration and LBP? The topic of spine degeneration seems to follow the research trends of OA in the knee and hip.
A recent review of the literature indicates several serum and urine biomarkers dixgnosis be useful in understanding the etiology of knee and hip OA [ 51 ]. Minimum work has been performed on this topic, but a few small studies of select samples have found associations between DSN and C-terminal cross-linked telopeptide CTX-IIa biomarker of type II collagen degradation [ 5354 ]. Therefore, it is possible that elevated COMP levels reflect the ongoing process of degeneration in the intervertebral disc, as evidenced by DSN, and results in associated symptoms that have been reported for this degenerative process.
Another topic of increasing interest is understanding the possible involvement of genetics in spine degeneration and LBP. Disc degeneration may be partially explained by genetic factors [ osteoagthritis ] and several review articles have already summarized these genetic factors extensively [ 56 — 60 ]. A relationship between LBP and intervertebral disc degeneration has been established, and several studies have identified genetic risk factors for lumbar disc degeneration [ ostroarthritis ].
However, most of these studies are cross-sectional with small sample sizes, and longitudinal, population-based studies are needed to confirm these findings.
OSTEOARTHRITIS by ezer simangunsong on Prezi
Understanding the involvement of pain pathways in OA is beginning to become clearer as studies are discovering more about central pain sensitization in knee OA [ 61diagnoosis ]. This is also true for other conditions with musculoskeletal components, for example fibromyalgia [ 64bsnding ].
Use of the pressure—pain threshold to improve our understanding of central and peripheral pain sensitization is not new to the study of LBP [ 6667 ]. However, its use with radiographic findings of the lumbar spine has not been studied at the population level and may improve our understanding of nervous system pathways in this complex relationship adalaah spine degeneration and LBP.
The radiographic features of spine degeneration are common and are associated with LBP and reduced physical function.