Osteoarthritis overview: Difference between revisions

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__NOTOC__
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{{Osteoarthritis}}
{{Osteoarthritis}}
{{CMG}}; {{AE}}[[User:DrMars|Mohammadmain Rezazadehsaatlou]]'''''<nowiki/>''''', [[User:Irfan Dotani|Irfan Dotani]]
{{CMG}}; {{AE}} [[User:Ayesha A. Khan|Ayesha A. Khan, MD]][mailto:Ayesha.khan@stvincentcharity.com] [[User:DrMars|Mohammadmain Rezazadehsaatlou]]'''''<nowiki/>''''', [[User:Irfan Dotani|Irfan Dotani]]


=='''Overview'''==
=='''Overview'''==
'''Osteoarthritis / Osteoarthrosis''' (OA, also known as [[degenerative joint disease]], [[degenerative arthritis]], arthrosis or in more colloquial terms "wear and tear") is the most common form of arthritis, caused by wearing of the [[cartilage]] that covers and cushions joint spaces. As the cartilage wears away, the patient may experience pain described as "weight-bearing" whenever walking and standing. Due to the movement limitations caused by pain, regional muscles may experience [[atrophy]]. [[Ligament|Ligaments]] may become laxer as well due to this. OA is derived from the Greek word "''osteo''", meaning "of the bone", "''arthro''", meaning "joint", and "''itis''", meaning [[inflammation]], although inflammation is not a common finding in this regard. [[Osteoarthritis|OA]] possesses a great degree of variability in disease onset, progression, and severity. [[Osteoarthritis|OA]] is characterized by a variety of structural and functional impairments occurring in an involved joint. Destruction, degeneration, articular cartilage loss, and even the soft tissue involvement are the main pathological process of this disease. It can be diagnosed through radiographic evaluations. Moreover, clinical sign and symptoms are helpful in the final diagnosis of this disease. OA can be defined radiologically, clinically, or pathologically, with radiographic OA being considered as the reference standard.[[Osteoarthritis overview#cite note-5|[5]]] The symptoms that are consistently associated with OA are joint pain, stiffness, swelling, and limitation of joint function. Few individuals who present these symptoms may not demonstrate radiographic OA. However, others confirmed to have OA using radiographic techniques may not present with clinical manifestations of the disease.[[Osteoarthritis overview#cite note-5|[5]]] These unique characteristics have made it difficult to identify the underlying mechanisms contributing to the disease as well as the treatments for reducing the incidence and severity of the disease. In addition, the stimuli that may initiate the processes associated with OA are multifactorial and include occupational and non-occupational (e.g., genetics, obesity, age, etc.) factors. [[Osteoarthritis|OA]] affects nearly 43 million patients in [[United States]] and almost 15% of the world population, accounting for 25% of visits to [[Primary care physician|primary care physicians]], and half of all [[NSAID]] (Non-Steroidal Anti-Inflammatory Drugs) [[Medical prescription|prescriptions]]. It is estimated that 80% of the population will have [[Radiograph|radiographic]] evidence of OA by age 65, although only 60% of those will be [[symptomatic]].[[Osteoarthritis overview#cite note-1|[1]]] There is no recent discovery of a cure for OA, as cartilage has not been induced to regenerate. However, if OA is caused by cartilage damage (for example as a result of an injury) Autologous Chondrocyte Implantation may be a possible treatment. Other treatments are with NSAIDs, local injections of [[glucocorticoid]] or [[hyaluronan]], and in severe cases, with [[joint replacement]] surgery. Many physicians have also reported good pain relief by treating ligaments (which is responsible for a bone to bone connection) with [[Prolotherapy]]. Clinical trials employing [[Tissue engineering|tissue-engineering]] methods have demonstrated regeneration of cartilage in damaged knees, including those that have progressed to osteoarthritis.[[Osteoarthritis overview#cite note-2|[2]]] Furthermore, in January 2007, Johns Hopkins University was offering to license a technology of this kind, listing several clinical competitors in its market analysis. Osteoarthritis is capable of influencing any joint in the human body; meanwhile, the most commonly affected joints are the knee and hip joints given that the degree of weight bearing required of these joints is immense. Other joints, such as the [[distal interphalangeal joints]] of the fingers and shoulder joints are also commonly affected as well. The economic burden of OA for United States economy is more than $60 billion per year; which has more economic pressure than [[rheumatoid arthritis]]. This cost can be considered into two subgroups: the medical related costs and the lost expediency of patients at work.
'''Osteoarthritis / Osteoarthrosis''' (OA, also known as [[degenerative joint disease]], [[degenerative arthritis]], arthrosis or in more colloquial terms "wear and tear") is the most common form of arthritis, caused by wearing of the [[cartilage]] that covers and cushions joint spaces. As the cartilage wears away, the patient may experience pain described as "weight-bearing" whenever walking and standing. Due to the movement limitations caused by pain, regional muscles may experience [[atrophy]]. [[Ligament|Ligaments]] may become laxer as well due to this. OA is derived from the Greek word "''osteo''", meaning "of the bone", "''arthro''", meaning "joint", and "''itis''", meaning [[inflammation]], although inflammation is not a common finding in this regard. [[Osteoarthritis|OA]] possesses a great degree of variability in disease onset, progression, and severity. [[Osteoarthritis|OA]] is characterized by a variety of structural and functional impairments occurring in an involved joint. Destruction, degeneration, articular cartilage loss, and even the soft tissue involvement are the main pathological process of this disease. It can be diagnosed through radiographic evaluations. Moreover, clinical sign and symptoms are helpful in the final diagnosis of this disease. OA can be defined radiologically, clinically, or pathologically, with radiographic OA being considered as the reference standard. The symptoms that are consistently associated with OA are joint pain, stiffness, swelling, and limitation of joint function. Few individuals who present these symptoms may not demonstrate radiographic OA. However, others confirmed to have OA using radiographic techniques may not present with clinical manifestations of the disease. These unique characteristics have made it difficult to identify the underlying mechanisms contributing to the disease as well as the treatments for reducing the incidence and severity of the disease. In addition, the stimuli that may initiate the processes associated with OA are multifactorial and include occupational and non-occupational (e.g., genetics, obesity, age, etc.) factors. [[Osteoarthritis|OA]] affects nearly 43 million patients in [[United States]] and almost 15% of the world population, accounting for 25% of visits to [[Primary care physician|primary care physicians]], and half of all [[NSAID]] (Non-Steroidal Anti-Inflammatory Drugs) [[Medical prescription|prescriptions]]. It is estimated that 80% of the population will have [[Radiograph|radiographic]] evidence of OA by age 65, although only 60% of those will be There is no recent discovery of a cure for OA, as cartilage has not been induced to regenerate. However, if OA is caused by cartilage damage (for example as a result of an injury) Autologous Chondrocyte Implantation may be a possible treatment. Other treatments are with NSAIDs, local injections of [[glucocorticoid]] or [[hyaluronan]], and in severe cases, with [[joint replacement]] surgery. Many physicians have also reported good pain relief by treating ligaments (which is responsible for a bone to bone connection) with [[Prolotherapy]]. Clinical trials employing [[Tissue engineering|tissue-engineering]] methods have demonstrated regeneration of cartilage in damaged knees, including those that have progressed to osteoarthritis. Furthermore, in January 2007, Johns Hopkins University was offering to license a technology of this kind, listing several clinical competitors in its market analysis. Osteoarthritis is capable of influencing any joint in the human body; meanwhile, the most commonly affected joints are the knee and hip joints given that the degree of weight bearing required of these joints is immense. Other joints, such as the [[distal interphalangeal joints]] of the fingers and shoulder joints are also commonly affected as well. The economic burden of OA for United States economy is more than $60 billion per year; which has more economic pressure than [[rheumatoid arthritis]]. This cost can be considered into two subgroups: the medical related costs and the lost expediency of patients at work <ref name="pmid25586654">{{cite journal |vauthors=Peter WF, Dekker J, Tilbury C, Tordoir RL, Verdegaal SH, Onstenk R, Bénard MR, Vehmeijer SB, Fiocco M, Vermeulen HM, van der Linden-van der Zwaag HM, Nelissen RG, Vliet Vlieland TP |title=The association between comorbidities and pain, physical function and quality of life following hip and knee arthroplasty |journal=Rheumatol. Int. |volume=35 |issue=7 |pages=1233–41 |date=July 2015 |pmid=25586654 |pmc=4436688 |doi=10.1007/s00296-015-3211-7 |url=}}</ref>


=='''Historical Perspective'''==
=='''Historical Perspective'''==


The earliest descriptions of [[Osteoarthritis|OA]] were provided by Heberden and Haygarth in the 19th century. [[Osteoarthritis overview#cite note-3|[3]]] [[Osteoarthritis overview#cite note-4|[4]]] In the 1930s and 1940s, Dr. Stecher showed that there were two forms of OA: idiopathic and post-traumatic. [[Osteoarthritis overview#cite note-5|[5]]] In the 1950s, the connection between Heberden’s nodes and large joint OA were revealed by Kellgren and Moore. In this regard, the first x-ray grading system for OA was developed by Jonas Kellgren and John Lawrence in the 1950s. Surgical management of OA was developed in the 1960s by Drs. Charnley and McKee.
The earliest descriptions of [[Osteoarthritis|OA]] were provided by Heberden and Haygarth in the 19th century. In the 1930s and 1940s, Dr. Stecher showed that there were two forms of OA: idiopathic and post-traumatic. [[Osteoarthritis overview#cite note-5|[5]]] In the 1950s, the connection between Heberden’s nodes and large joint OA were revealed by Kellgren and Moore. In this regard, the first x-ray grading system for OA was developed by Jonas Kellgren and John Lawrence in the 1950s. Surgical management of OA was developed in the 1960s by Drs. Charnley and McKee <ref name="pmid22632687">{{cite journal |vauthors=Suri P, Morgenroth DC, Hunter DJ |title=Epidemiology of osteoarthritis and associated comorbidities |journal=PM R |volume=4 |issue=5 Suppl |pages=S10–9 |date=May 2012 |pmid=22632687 |doi=10.1016/j.pmrj.2012.01.007 |url=}}</ref>


=='''Classification'''==
=='''Classification'''==


Osteoarthritis is radiographically classified depending on the degree of joint involvement. The Kellgren-Lawrence is a common method to classify the severity of OA in the knee using five different grades. This classification was proposed by Kellgren et al. in 1957 and was then accepted by WHO in 1961.      
Osteoarthritis is radiographically classified depending on the degree of joint involvement. The Kellgren-Lawrence is a common method to classify the severity of OA in the knee using five different grades. This classification was proposed by Kellgren et al. in 1957 and was then accepted by WHO in 1961 <ref name="pmid25628884">{{cite journal |vauthors=Hardcastle SA, Dieppe P, Gregson CL, Davey Smith G, Tobias JH |title=Osteoarthritis and bone mineral density: are strong bones bad for joints? |journal=Bonekey Rep |volume=4 |issue= |pages=624 |date=2015 |pmid=25628884 |pmc=4303262 |doi=10.1038/bonekey.2014.119 |url=}}</ref>... 
 
  {| class="wikitable sortable"
|+'''Classification for Subsets of Osteoarthritis'''
!'''I: Idiopathic'''
!
!
!
|-
|
|'''A: Localized'''
|
|
|-
|
|
|'''1: Hands:  Heberden’s and Bouchard’s nodes (nodal), erosive interphalangeai arthritis (nonnodal), scaphometacarpal joint, scaphotrapezial'''
|
|-
|
|
|'''2. Feet: hallux valgus. hallux rigidus, contracted toes (hammer/cockup toes), talonavicular'''
|
|-
|
|
|'''3. Knee'''
|'''a. Medial compartment'''
'''b. Lateral compartment'''
 
'''c. Patellofemoral compartment (chondromalacia)'''
|-
|
|
|'''4. Hip'''
|'''a. Eccentric (superior)'''
'''b. Concentric (axial, medial)'''
 
'''c. Diffuse (coxae senilis)'''
|-
|
|
|'''5. Spine (particularly cervical and lumbar)'''
|'''a. Apophyseal'''
'''b. Intervertebral (disc)'''
 
'''c. Spondylosis (osteophytes)'''
 
'''d. Ligamentous (hyperostosis [Forestier’s disease or DISH])'''
|-
|
|
|'''6. Other single sites: shoulder, temporomandibular, sacroiliac, ankle, wrist, acromioclavicular'''
|
|-
|
|'''B. Generalized: includes 3 or more areas listed above (Kellgren-Moore)'''
|'''1. Small (peripheral) and spine'''
'''2. Large (central) and spine'''
 
'''3. Mixed (peripheral and central) and spine'''
|
|-
|'''II. Secondary'''
|
|
|
|-
|
|'''A. Posttraumatic'''
|
|
|-
|
|'''B. Congenital or Developmental Diseases'''
|'''1. Localized'''
|'''a. Hip diseases: Legg-Calve-Perthes, congenital hip dislocation, slipped capital femoral epiphysis, shallow acetabulum'''
'''b. Mechanical and local factors: obesity (7). unequal lower extremity length, extreme valgus/varus deformity, hypermobility syndromes, scoliosis'''
|-
|
|
|'''2. Generalized'''
|'''a. Bone dysplasias: epiphyseal dysplasia, spondyloapophyseal dysplasia'''
'''b. Metabolic diseases: hemachromatosis, ochronosis, Gaucher’s disease, hemoglobinopathy, Ehlers-Danlos'''
|-
|
|'''c. Calcium Deposition Disease'''
|'''1. Calcium pyrophosphate deposition disease'''
'''2. Apatite atthropathy'''
 
'''3. Destructive arthropathy (shoulder, knee)'''
|
|-
|
|'''D. Other Bone and Joint Disorders: avascular necrosis, rheumatoid arthritis, gouty arthritis, septic arthritis, Paget’s disease, osteopetrosis, osteochondritis'''
|
|
|-
|
|'''E. Other Diseases'''
|'''1. Endocrine diseases: diabetes mellitus, acromegaly, hypothyroidism, hyperparathyroidism'''
 
'''2. Neuropathic arthropathy (Charcot joints)'''
 
'''3. Miscellaneous: frostbite, Kashin-Beck disease, Caisson’s disease'''
|
|}
 
'''Western Ontario and McMaster Universities Osteoarthritis Index (''WOMAC'')''' is used to evaluate the pain, stiffness, and physical function among patients with hip or/ and knee osteoarthritis (OA). It consists of 24 different items divided into 3 subtypes:
* Pain consisted of 5 items:
-Staying in bed, sitting or lying, standing, walking, using stairs
* Stiffness consisted of 2 items:
-Waking up in morning, later in the day
* Physical Function consisted of 17 items:
-Using stairs, sitting, rising from sitting, standing, bending, walking, getting in and/or getting out of a car, during shopping, doing heavy household duties, doing light household duties, putting on/taking off socks, lying in bed, rising from bed, getting in and/or getting out of the bathtub, getting on/off the toilet
 
== '''Knee''' ==
{| class="wikitable"
|+International Knee Documentation Committee (IKDC Questionnaire)
!Grade
!Description
|-
|A
|No joint space narrowing (JSN)
|-
|B
|>4 mm joint space; small osteophytes, slight sclerosis, or femoral condyle flattening
|-
|C
|2-4 mm joint space
|-
|D
|<2 mm joint space
|}
{| class="wikitable"
|+Merchant system: a 45° "skyline" view for the Patellofemoral join
!Grade
!Description
|-
|I (mild)
|Patellofemoral joint space > 3mm
|-
|II (moderate)
|Joint space < 3 mm but no bony contact
|-
|III(severe)
|Bony surfaces in contact over less than one-quarter of the joint surface
|-
|IV (very severe)
|Bony contact throughout the entire joint surface
|}
{| class="wikitable mw-collapsible mw-collapsed"
|+Ahlbäck classification of osteoarthritis of the knee joint
!Grade
!Description
|-
|0
|Normal
|-
|1
|Joint space narrowing is <3 mm of the joint space or <50% of the other compartment (with or without subchondral sclerosis)
|-
|2
|Obliteration of joint space
|-
|3
|Bone defect/loss <5 mm
|-
|4
|Bone defect and/or loss 5-10 mm
|}
 
== '''Shoulder''' ==
{| class="wikitable"
|+Samilson-Prieto classification
!Grade
!Description
|-
|I
|Inferior humeral or glenoid exostosis, or both, measuring less than 3 mm in height.
|-
|II
|Inferior humeral or glenoid exostosis, or both, between 3 and 7 mm in height, with slight glenohumeral joint irregularity.
|-
|III
|Inferior humeral or glenoid exostosis, or both, more than 7 mm in height, with narrowing of the glenohumeral joint and sclerosis
|}
 
== '''Vertebral column''' ==
{| class="wikitable"
|+Kellgren grading of cervical disc degeneration
!Grade
!Description
|-
!I
|Minimal anterior osteophytosis
|-
!II
|Definite anterior osteophytosis with possible narrowing of the disc space and some sclerosis of vertebral plates
 
|-
!III
|Moderate narrowing of the disc space with definite sclerosis of vertebral plates and osteophytosis
 
|-
!IV
|Severe narrowing of the disc space with sclerosis of vertebral plates and multiple large osteophytes
|}
{| class="wikitable"
|+Kellgren grading of cervical facet joint degeneration
!Grade
!Description
|-
|1
|Doubtful osteophytes on margins of the articular facets of apophyseal joints
|-
|2
|Definite osteophytes and subchondral sclerosis in apophyseal joints
|-
|3
|Moderate osteophytes, subchondral sclerosis and some irregularity of articular facets
|-
|4
|Many large osteophytes and severe sclerosis and irregularity of the apophyseal joints
|}
{| class="wikitable"
|+Lane grading of lumbar disc degeneration
! colspan="1" rowspan="1" |Grade
! colspan="1" rowspan="1" |Joint space narrowing
! colspan="1" rowspan="1" |Osteophytes anterior and posterior
! colspan="1" rowspan="1" |Sclerosis
|-
| colspan="1" rowspan="1" |0
| colspan="1" rowspan="1" |None
| colspan="1" rowspan="1" |None
| colspan="1" rowspan="1" |None
|-
| colspan="1" rowspan="1" |I
| colspan="1" rowspan="1" |Definite (mild) narrowing
| colspan="1" rowspan="1" |Small
| colspan="1" rowspan="1" |Present
|-
| colspan="1" rowspan="1" |II
| colspan="1" rowspan="1" |Moderate
| colspan="1" rowspan="1" |Moderate
| colspan="1" rowspan="1" |–
|-
| colspan="1" rowspan="1" |III
| colspan="1" rowspan="1" |Severe (complete loss of joint space)
| colspan="1" rowspan="1" |Large
| colspan="1" rowspan="1" |–
|}
{| class="wikitable"
|+Thompson macroscopic grading of lumbar disc degeneration on sagittal sections using MRI
!Grade
!Nucleus
!Anulus
!Endplate
!Vertebral body
|-
!I
|Bulging gel
|Discrete fibrous laminae
|Hyaline, uniform thickness
|Rounded margins
|-
!II
|Peripheral white fibrous tissue
|Mucinous material between laminae
|Irregular thickness
|Pointed margins
|-
!III
|Consolidated fibrous tissue
|Extensive mucinous infiltration; loss of annular-nuclear demarcation
|Focal defects in cartilage
|Small chondrophytes or osteophytes at margins
|-
!IV
|Horizontal clefts parallel to endplate
|Focal disruptions
|Fibrocartilage extending from subchondral bone; irregularity and focal sclerosis in subchondral bone
|Osteophytes smaller than 2 mm
|-
!V
|Clefts extended through nucleus and annulus
|
|Diffuse sclerosis
|Osteophytes greater than 2 mm
|}
 
{| class="wikitable"
|+Pathria grading of lumbar facet joint degeneration
!Grade
!Description
|-
|0
|Normal
|-
|I
|Joint space narrowing (mild degenerative disease)
|-
|II
|Narrowing plus sclerosis or hypertrophy (moderate degenerative disease)
|-
|III
|Severe osteoarthrosis with narrowing, sclerosis, and osteophytes (severe degenerative disease)
|}
 
{| class="wikitable"
|+Weishaupt Grading of lumbar facet joint degeneration using CT and MRI
!Grade
!Description
|-
|0
|Normal facet joint space (2–4 mm width)
|-
|I
|Narrowing of the facet joint space (<2 mm) and/or small osteophytes and/or mild hypertrophy of the articular process
|-
|II
|Narrowing of the facet joint space and/or moderate osteophytes and/or moderate hypertrophy of the articular process and/or mild subarticular bone erosions
|-
|III
|Narrowing of the facet joint space and/or large osteophytes and/or severe hypertrophy of the articular process and/or severe subarticular bone erosions and/or subchondral cysts
|}
 
== '''Temporomandibular joint''' ==
{| class="wikitable"
|+Radiographic features Changes are usually more evident on the condylar side of the TMJ joint
|flattening: common (in one series 27%)
|-
|osteophytes: common (27%)
|-
|erosions: 13%
|-
|sclerosis: less common (9%)
|-
|subchondral cysts
|}
 
== '''Ankle''' ==
{| class="wikitable sortable mw-collapsible mw-collapsed"
|+''' Takakura Classification'''
|'''Grade'''
|'''Description'''
|-
|I
|Early sclerosis and osteophyte formation, no joint space narrowing
|-
|II
|Narrowing of medial joint space (no subchondral bone contact)
|-
|IIIA
|Obliteration of joint space at the medial malleolus, with subchondral bone contact
|-
|IIIB
|Obliteration of joint space over roof of talar dome, with subchondral bone contact
|-
|IV
|Obliteration of joint space with complete bone contact
|}
{| class="wikitable"
|+Giannini '''Classification'''
|'''Grade'''
|'''Description'''
|-
|0
|Normal joint or subchondral sclerosis
|-
|I
|Presence of osteophytes without joint-space narrowing
|-
|II
|Joint-space narrowing with or without osteophytes
|-
|III
|Subtotal or total disappearance or deformation of joint space
|}
{| class="wikitable"
|+Cheng '''Classification'''
|'''Grade'''
|'''Description'''
|-
|0
|No reduction of the joint space
Normal alignment
|-
|I
|Slight reduction of the joint space
Slight formation of deposits at the joint margins
 
Normal alignment
|-
|II
|More pronounced change than mentioned above
Subchondral osseous sclerotic configuration
 
Mild malalignment
|-
|III
|Joint space reduced to about half the height of the uninjured side
Rather pronounced formation of deposits
 
Obvious varus or valgus alignment
|-
|IV
|Joint space has completely or practically disappeared
|}
{| class="wikitable"
|+Canadian Orthopedic Foot and Ankle Society (COFAS) classification
|'''Grade'''
|'''Description'''
|-
|I
|Isolated ankle arthritis
|-
|II
|Ankle arthritis with intra-articular varus or valgus deformity or a tight heel cord, or both
|-
|III
|Ankle arthritis with hindfoot deformity, tibial malunion, midfoot abductus or adductus, supinated midfoot, plantarflexed first ray, etc
|-
|IV
|Types 1–3 plus subtalar, calcaneocuboid, or talonavicular arthritis
|}


==Pathophysiology==
==Pathophysiology==
[[Osteoarthritis]] (OA) is a well-known [[degenerative joint disease]] influencing millions of people worldwide. [[Osteoarthritis]] is a complex disease caused by changes in the tissues' [[homeostasis]] of articular [[cartilages]] and [[subchondral bones]]. The [[cell/extracellular matrix]] (ECM) and their interactions play an important role in the [[pathophysiology]] of articular [[cartilage]] and the occurrence of [[Osteoarthritis]]. Consequently, the main feature of [[OA]] is that after this process is involved, the [[articular]] [[cartilages]] of the involved joint no longer will have a normal acting system because the destruction of the articular [[cartilage]]s can no longer act as [[shock]] absorber. abnormal [[integrin]] expression alters cell/ECM signaling and modifies [[chondrocyte]] synthesis, with the following imbalance of [[destructive]] cytokines over regulatory factors. [[IL-1]], [[TNF-alpha]] and other [[pro-catabolic]] [[cytokines]] activate the enzymatic degradation of [[cartilage]] matrix and are not counterbalanced by adequate synthesis of inhibitors. The main [[enzymes]] involved in [[ECM]] breakdown are [[metalloproteinases]] (MMPs), which are sequentially activated by an amplifying cascade. [[MMP]] activity is partially inhibited by the tissue inhibitors of MMPs (TIMPs), whose synthesis is low compared with MMP production in OA [[cartilage]].


==Causes==
==Causes==
Osteoarthritis (OA) is a result of a variety of disorders that lead to structural and functional failure in involved joints. Osteoarthritis, traditionally, has been considered as a disease specifically related to articular cartilage. Presently, it's been proven that OA influencing the whole joint system consisted of capsule, and synovium, subchondral bone, cartilage, menisci, ligaments, and periarticular muscle.


==Differentiating {{PAGENAME}} from Other Diseases==
==Differentiating {{PAGENAME}} from Other Diseases==
OA must be differentiated from other diseases that cause joint impairment and  other related signs and symptoms such as [[Rheumatoid arthritis]], [[Gout]], Joint [[tuberculosis]].


==Epidemiology and Demographics==
==Epidemiology and Demographics==
OA is one of the most frequent diagnoses and is the leading cause of disability among the adult population in the USA. According to the National Health and Nutrition Examination Survey (NHANES), more than 26 million people in the USA were diagnosed with different forms of OA. The National Health Interview Survey (NHIS) reported that the 46.4 million Americans and 21.6% of Americans adults were diagnosed with arthritis. OA can involve any joint, but knees, hips, hands, are most common sites for this involvement.


==Risk Factors==
==Risk Factors==
Osteoarthritis is a multifactorial disease and the interactions between systemic and local factors play important role in development and prognosis of OA.


==Screening==
==Screening==
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==Natural History, Complications, and Prognosis==
==Natural History, Complications, and Prognosis==
===Natural History===
===Natural History===
The orthopedic surgeons are frequently asked by their patients regarding the final outcome and the prognosis of their diseased joint/joints caused by OA. Information about the natural history of OA is very important for upcoming determinations and planning for patients management. A small number of studies are available studied the role of the radiographic findings, joint congruence, or even the daily life activity on the OA progression.


===Complications===
===Complications===
OA is a leading cause of morbidity having significant effects on patients life and the health care system and even it could cause heavy economic burden. According to the American Academy of Orthopedic Surgeons report movement limitation are found in 80% of adults diagnosed with osteoarthritis. Meanwhile, 25% of these patients facing difficulties in their of daily living activities. 11% of them need personal care assistance and 14% required help with their routine needs.


===Prognosis===
===Prognosis===
Most osteoarthritis cases do stabilize. Some osteoarthritis cases progress. A small number of osteoarthritis patients improve spontaneously.


==Diagnosis==
==Diagnosis==
===Diagnostic Criteria===
===Diagnostic Criteria===
There is no specific signs and symptoms of osteoarthritis (OA) diagnosis. Although, osteoarthritis may be diagnosed based on several elements such as patients age, past medical history, and available symptoms. Osteoarthritis of the major joints is diagnosed using a combination of patients past medical history, physical examination, and variety of lab tests including imaging studies such as X-ray.


===History and Symptoms===
===History and Symptoms===
Patients' past medical history is the most useful tool for the osteoarthritis diagnosis.


===Physical Examination===
===Physical Examination===
A physical examination following the medical history is necessary for medical doctors to reach an exact diagnosis. In OA, loss or limited range of motion in specific joints, swelling, tenderness, and bony growths in the surrounding area are the most important keys in physical examination of OA cases.


===Laboratory Findings===
===Laboratory Findings===
If the OA diagnosis is in doubt, laboratory tests are used to help doctors get a confirmation regarding a suspected diagnosis of osteoarthritis.


===Imaging Findings===
===Imaging Findings===
X-Ray and CT-Scan are the most common tools used in this regard.


===Other Diagnostic Studies===
===Other Diagnostic Studies===
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==Treatment==
==Treatment==
===Medical Therapy===
===Medical Therapy===
Nonpharmacologic therapy is consisted of physical therapy and specific type of physical exercises, bracing and splinting. Physical therapy results in short-term pain reduction, and improvement in physical function in the diseased joint to preserve its the ability for daily tasks like walking, dressing, and even bathing. Having moderate activity strengthens the muscles around the diseased joint and this reduces stress and increases the stability of the joint system. On the other hand, resting is another important healing factor in OA. Bracing and splinting as other methods help to support painful or unstable joints. Using a cane can help decrease the weight pressure in diseased hip or knee, but it should be used on the contralateral side of the affected joint.


===Surgery===
===Surgery===
Surgical interventions in OA cases should be considered when the symptoms have no response to the first line treatments because osteoarthritis symptoms can be successfully managed through [[Osteoarthritis medical therapy|non-surgical]] care. For some, however, if they are experiencing severe joint damage, extreme pain, or very restricted mobility, surgery may be a viable option in this regard. The main indication criteria for surgery in OA is pain and disabilities despite the medical treatments. The most common and effective surgical intervention are arthroscopic surgery, osteotomy, and arthroplasty (total joint replacement). Considering the potential benefits of surgery like pain relief, improved movement, increased patients status, and actual disease prognosis, it should be remembered that any surgical interventions have risks. Meanwhile, overweight patients or patients with co-morbidities have higher risk of operation. The current joint prostheses have an expected functional usage for almost 15 to 20 years.


===Prevention===
===Prevention===
Primary prevention for OA include :
* [[Weight loss]]
* Physical activity
* Injury prevention
* Control infectious disease
* Avoidance of [[trauma]] on the joint
* Omega-3 fatty acid


==References==
==References==

Latest revision as of 16:25, 13 May 2020

Osteoarthritis of the Medial Side of the Knee.
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Osteoarthritis Microchapters

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Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Osteoarthritis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

X Ray

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ayesha A. Khan, MD[2] Mohammadmain Rezazadehsaatlou, Irfan Dotani

Overview

Osteoarthritis / Osteoarthrosis (OA, also known as degenerative joint disease, degenerative arthritis, arthrosis or in more colloquial terms "wear and tear") is the most common form of arthritis, caused by wearing of the cartilage that covers and cushions joint spaces. As the cartilage wears away, the patient may experience pain described as "weight-bearing" whenever walking and standing. Due to the movement limitations caused by pain, regional muscles may experience atrophy. Ligaments may become laxer as well due to this. OA is derived from the Greek word "osteo", meaning "of the bone", "arthro", meaning "joint", and "itis", meaning inflammation, although inflammation is not a common finding in this regard. OA possesses a great degree of variability in disease onset, progression, and severity. OA is characterized by a variety of structural and functional impairments occurring in an involved joint. Destruction, degeneration, articular cartilage loss, and even the soft tissue involvement are the main pathological process of this disease. It can be diagnosed through radiographic evaluations. Moreover, clinical sign and symptoms are helpful in the final diagnosis of this disease. OA can be defined radiologically, clinically, or pathologically, with radiographic OA being considered as the reference standard. The symptoms that are consistently associated with OA are joint pain, stiffness, swelling, and limitation of joint function. Few individuals who present these symptoms may not demonstrate radiographic OA. However, others confirmed to have OA using radiographic techniques may not present with clinical manifestations of the disease. These unique characteristics have made it difficult to identify the underlying mechanisms contributing to the disease as well as the treatments for reducing the incidence and severity of the disease. In addition, the stimuli that may initiate the processes associated with OA are multifactorial and include occupational and non-occupational (e.g., genetics, obesity, age, etc.) factors. OA affects nearly 43 million patients in United States and almost 15% of the world population, accounting for 25% of visits to primary care physicians, and half of all NSAID (Non-Steroidal Anti-Inflammatory Drugs) prescriptions. It is estimated that 80% of the population will have radiographic evidence of OA by age 65, although only 60% of those will be There is no recent discovery of a cure for OA, as cartilage has not been induced to regenerate. However, if OA is caused by cartilage damage (for example as a result of an injury) Autologous Chondrocyte Implantation may be a possible treatment. Other treatments are with NSAIDs, local injections of glucocorticoid or hyaluronan, and in severe cases, with joint replacement surgery. Many physicians have also reported good pain relief by treating ligaments (which is responsible for a bone to bone connection) with Prolotherapy. Clinical trials employing tissue-engineering methods have demonstrated regeneration of cartilage in damaged knees, including those that have progressed to osteoarthritis. Furthermore, in January 2007, Johns Hopkins University was offering to license a technology of this kind, listing several clinical competitors in its market analysis. Osteoarthritis is capable of influencing any joint in the human body; meanwhile, the most commonly affected joints are the knee and hip joints given that the degree of weight bearing required of these joints is immense. Other joints, such as the distal interphalangeal joints of the fingers and shoulder joints are also commonly affected as well. The economic burden of OA for United States economy is more than $60 billion per year; which has more economic pressure than rheumatoid arthritis. This cost can be considered into two subgroups: the medical related costs and the lost expediency of patients at work [1]

Historical Perspective

The earliest descriptions of OA were provided by Heberden and Haygarth in the 19th century. In the 1930s and 1940s, Dr. Stecher showed that there were two forms of OA: idiopathic and post-traumatic. [5] In the 1950s, the connection between Heberden’s nodes and large joint OA were revealed by Kellgren and Moore. In this regard, the first x-ray grading system for OA was developed by Jonas Kellgren and John Lawrence in the 1950s. Surgical management of OA was developed in the 1960s by Drs. Charnley and McKee [2]

Classification

Osteoarthritis is radiographically classified depending on the degree of joint involvement. The Kellgren-Lawrence is a common method to classify the severity of OA in the knee using five different grades. This classification was proposed by Kellgren et al. in 1957 and was then accepted by WHO in 1961 [3]... 

Pathophysiology

Osteoarthritis (OA) is a well-known degenerative joint disease influencing millions of people worldwide. Osteoarthritis is a complex disease caused by changes in the tissues' homeostasis of articular cartilages and subchondral bones. The cell/extracellular matrix (ECM) and their interactions play an important role in the pathophysiology of articular cartilage and the occurrence of Osteoarthritis. Consequently, the main feature of OA is that after this process is involved, the articular cartilages of the involved joint no longer will have a normal acting system because the destruction of the articular cartilages can no longer act as shock absorber. abnormal integrin expression alters cell/ECM signaling and modifies chondrocyte synthesis, with the following imbalance of destructive cytokines over regulatory factors. IL-1, TNF-alpha and other pro-catabolic cytokines activate the enzymatic degradation of cartilage matrix and are not counterbalanced by adequate synthesis of inhibitors. The main enzymes involved in ECM breakdown are metalloproteinases (MMPs), which are sequentially activated by an amplifying cascade. MMP activity is partially inhibited by the tissue inhibitors of MMPs (TIMPs), whose synthesis is low compared with MMP production in OA cartilage.

Causes

Osteoarthritis (OA) is a result of a variety of disorders that lead to structural and functional failure in involved joints. Osteoarthritis, traditionally, has been considered as a disease specifically related to articular cartilage. Presently, it's been proven that OA influencing the whole joint system consisted of capsule, and synovium, subchondral bone, cartilage, menisci, ligaments, and periarticular muscle.

Differentiating Osteoarthritis overview from Other Diseases

OA must be differentiated from other diseases that cause joint impairment and other related signs and symptoms such as Rheumatoid arthritis, Gout, Joint tuberculosis.

Epidemiology and Demographics

OA is one of the most frequent diagnoses and is the leading cause of disability among the adult population in the USA. According to the National Health and Nutrition Examination Survey (NHANES), more than 26 million people in the USA were diagnosed with different forms of OA. The National Health Interview Survey (NHIS) reported that the 46.4 million Americans and 21.6% of Americans adults were diagnosed with arthritis. OA can involve any joint, but knees, hips, hands, are most common sites for this involvement.

Risk Factors

Osteoarthritis is a multifactorial disease and the interactions between systemic and local factors play important role in development and prognosis of OA.

Screening

Routine screening for osteoarthritis is not indicated unless the patient is symptomatic.

Natural History, Complications, and Prognosis

Natural History

The orthopedic surgeons are frequently asked by their patients regarding the final outcome and the prognosis of their diseased joint/joints caused by OA. Information about the natural history of OA is very important for upcoming determinations and planning for patients management. A small number of studies are available studied the role of the radiographic findings, joint congruence, or even the daily life activity on the OA progression.

Complications

OA is a leading cause of morbidity having significant effects on patients life and the health care system and even it could cause heavy economic burden. According to the American Academy of Orthopedic Surgeons report movement limitation are found in 80% of adults diagnosed with osteoarthritis. Meanwhile, 25% of these patients facing difficulties in their of daily living activities. 11% of them need personal care assistance and 14% required help with their routine needs.

Prognosis

Most osteoarthritis cases do stabilize. Some osteoarthritis cases progress. A small number of osteoarthritis patients improve spontaneously.

Diagnosis

Diagnostic Criteria

There is no specific signs and symptoms of osteoarthritis (OA) diagnosis. Although, osteoarthritis may be diagnosed based on several elements such as patients age, past medical history, and available symptoms. Osteoarthritis of the major joints is diagnosed using a combination of patients past medical history, physical examination, and variety of lab tests including imaging studies such as X-ray.

History and Symptoms

Patients' past medical history is the most useful tool for the osteoarthritis diagnosis.

Physical Examination

A physical examination following the medical history is necessary for medical doctors to reach an exact diagnosis. In OA, loss or limited range of motion in specific joints, swelling, tenderness, and bony growths in the surrounding area are the most important keys in physical examination of OA cases.

Laboratory Findings

If the OA diagnosis is in doubt, laboratory tests are used to help doctors get a confirmation regarding a suspected diagnosis of osteoarthritis.

Imaging Findings

X-Ray and CT-Scan are the most common tools used in this regard.

Other Diagnostic Studies

Treatment

Medical Therapy

Nonpharmacologic therapy is consisted of physical therapy and specific type of physical exercises, bracing and splinting. Physical therapy results in short-term pain reduction, and improvement in physical function in the diseased joint to preserve its the ability for daily tasks like walking, dressing, and even bathing. Having moderate activity strengthens the muscles around the diseased joint and this reduces stress and increases the stability of the joint system. On the other hand, resting is another important healing factor in OA. Bracing and splinting as other methods help to support painful or unstable joints. Using a cane can help decrease the weight pressure in diseased hip or knee, but it should be used on the contralateral side of the affected joint.

Surgery

Surgical interventions in OA cases should be considered when the symptoms have no response to the first line treatments because osteoarthritis symptoms can be successfully managed through non-surgical care. For some, however, if they are experiencing severe joint damage, extreme pain, or very restricted mobility, surgery may be a viable option in this regard. The main indication criteria for surgery in OA is pain and disabilities despite the medical treatments. The most common and effective surgical intervention are arthroscopic surgery, osteotomy, and arthroplasty (total joint replacement). Considering the potential benefits of surgery like pain relief, improved movement, increased patients status, and actual disease prognosis, it should be remembered that any surgical interventions have risks. Meanwhile, overweight patients or patients with co-morbidities have higher risk of operation. The current joint prostheses have an expected functional usage for almost 15 to 20 years.

Prevention

Primary prevention for OA include :

  • Weight loss
  • Physical activity
  • Injury prevention
  • Control infectious disease
  • Avoidance of trauma on the joint
  • Omega-3 fatty acid

References

  1. Peter WF, Dekker J, Tilbury C, Tordoir RL, Verdegaal SH, Onstenk R, Bénard MR, Vehmeijer SB, Fiocco M, Vermeulen HM, van der Linden-van der Zwaag HM, Nelissen RG, Vliet Vlieland TP (July 2015). "The association between comorbidities and pain, physical function and quality of life following hip and knee arthroplasty". Rheumatol. Int. 35 (7): 1233–41. doi:10.1007/s00296-015-3211-7. PMC 4436688. PMID 25586654.
  2. Suri P, Morgenroth DC, Hunter DJ (May 2012). "Epidemiology of osteoarthritis and associated comorbidities". PM R. 4 (5 Suppl): S10–9. doi:10.1016/j.pmrj.2012.01.007. PMID 22632687.
  3. Hardcastle SA, Dieppe P, Gregson CL, Davey Smith G, Tobias JH (2015). "Osteoarthritis and bone mineral density: are strong bones bad for joints?". Bonekey Rep. 4: 624. doi:10.1038/bonekey.2014.119. PMC 4303262. PMID 25628884.

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