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Osteoarthritis

Osteoarthritis (OA) of the Medial Side of the Knee.


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Osteoarthritis (OA)

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammadmain Rezazadehsaatlou [2]; Robert G. Schwartz, M.D. [2], Piedmont Physical Medicine and Rehabilitation, P.A., [3] Irfan Dotani

Synonyms and keywords: OA; Ostearthritis; Ostarthritis; Osteoarthrosis; Arthritis; Degenerative arthritis; Degenerative joint disease; DJD; Arthrosis; Hypertrophic osteoarthritis; Facets disease, Facets syndrome; Osteoarthrosis deformans; Malum senile, Morbus senilis; Wear-and-tear arthritis.

Overview
Osteoarthritis of the Medial Side of the Knee.

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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Historical Perspective
Osteoarthritis historical perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Mohammadmain Rezazadehsaatlou [2], Irfan Dotani [3]

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 experiences pain with weight bearing. This word is derived from the Greek word “osteo“, meaning “of the bone”, “arthro“, meaning “joint”, and “itis“, meaning inflammation. Inflammation, however, is not a common finding in this regard. OA possesses a great degree of variability in disease onset, progression, and severity. 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. In the 1950s, the links 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 Dr. Charnley and Dr. McKee [1] [2] [3].

Historical Perspective

According to the available pieces of evidence, osteoarthritis (OA) has been called by different terminologies: arthrosis deformans, osteoarthrosis-osteoarthritis, degenerative joint disease, Morbus (malum) coxae seniles[4]. Loss of cartilage associated with bone features (such as osteophytes and subchondral bone sclerosis) is common among all types of OA[5]. As mentioned before, this illness has been called by many names over the years, but none of them are entirely satisfactory for this condition. Despite the fact that the word “Osteoarthritis” is a misnomer because it implies a definite existence of an inflammatory process, it has been used for many decades in the English language and will probably continue to do so because of its well-known appeal compared to other more accurate terms of degenerative joint disease[4]. Osteoarthritis is considered a non-inflammatory disease of movable joints characterized by the possible formation of new bone at the articular surface and subchondral bone involvement with the abrasion and deterioration of involved articular cartilages [6][7].

The historical view of osteoarthritis from antiquity to the present year has a conventional perspective which can be found among paleopathological findings of skeletal discoveries. With no doubt, osteoarthritis can be called as a disease with the best paleopathology documents. For example, in a 200 million-year-old Dimetrodon Permian reptile recovered in Texas, USA there was an interesting piece of evidence of a compound fracture in its spine which was infected with pus formation. Moreover, the first polyarthritis in history was found on the posterity in the Mesozoic Platecarpus found in Kansas. All joints on the left hallux of this reptile had deformations, potentially caused by osteoarthritis. According to the microscopic evaluations of its bones, there was the common feature of increased vascular spaces with overgrowth of its articular margins which can be found in osteoarthritis pathology. Consequently, osteoarthritis can be called the oldest known disease on earth. On the other hand, osteoarthritis was found in the fossil of a Neanderthal man from La Chapelle-aux-Saints. In another piece of evidence, chronic osteoarthritis found in ancient Egypt with a history of older than 3000 years. Also, severe osteoarthritis of the hip in a Romano-Briton with a “lipped” acetabulum and deformation on the femoral head was also found in this regard. Among ancient Egyptian, Early Eskimo, Iron Age British, and American Indian populations, there is a strong correlation of evidence with the vertebral lipping limited to the lumbar region [8] .

Available visual arts in addition to historical pieces of evidence can be an important tool for paleopathological study in this regard. While searching for specific evidence for OA in history, some important data was found. Because painters are known to be good observers, they can transfer what they had seen from their society through their arts to us. From their drawings, they can help us find things that we cannot get from available skeletons. Here, we can find some impressive arts indicative of osteoarthritis during the ancient histories[9][10][11][12][13][14]:

I: In a Greek script from the late 14th century (kept in National Library, Paris), there is a Byzantine physician visiting a patient having a straight rigid spine with his hand stuck in a bent position (suggestive of spinal stenosis). We can conclude that the patient suffered from diffuse idiopathic spinal hyperostosis (DISH; Forestier disease).

I: In a Greek script from the late 14th century (kept in National Library, Paris), there is a Byzantine physician visiting a patient having a straight rigid spine with his hand stuck in a bent position (suggestive of spinal stenosis). We can conclude that the patient suffered from diffuse idiopathic spinal hyperostosis (DISH; Forestier disease)

.

II: In a great art by Jan Van Eyck (St. Bavo Cathedral, Ghent) about the St. John Baptist of the Adoration of the Lamb, we can see a typical Heberden node on his left thumb.

II: In a great art by Jan Van Eyck (St. Bavo Cathedral, Ghent) about the St. John Baptist of the Adoration of the Lamb, we can see a typical Heberden node on his left thumb.

III: Similar to the above-mentioned art, in another painting by different artist (Frans Hals) about the Portrait of Sara Andriesdr Hessix (Lisbon, Portugal), we can see a typical Heberden node on her both hands.

III: Similar to above-mentioned art, in another painting by a different artist (Frans Hals) about the Portrait of Sara Andriesdr Hessix (Lisbon, Portugal), we can see a typical Heberden node on her both hands.

IV: In a painting by George de la Tour ’s about the St. Hieronymus (as penitent), with a little care we can found Hallux valgus on his foot.

IV: In a painting by George de la Tour’s about the St. Hieronymus (as penitent), with a little care we can found Hallux valgus on his foot.

V: In another artwork by Diego Velasquez (1632) about the Jester “Don John of Austria”, the gesture of this indicative for genu valgum.

V: In another artwork by Diego Velasquez (1632) about the Jester “Don John of Austria”, the gesture of this indicative for genu valgum.

According to the ancient era, osteoarthritis is a common finding in Egyptian mummies and also in ancient skeletons found in England. There are strong pieces of evidence in ancient skeletons with osteoarthritis in their shoulders. Moreover, some degenerative changes in the lumbar spine were found. Historical evidence revealed that arthritis was considered to be clinical presentations of gout and there are some physical signs described by Hippocrates (460–375 BC), in this regard. There is a big question that despite the significant pieces of evidence of osteoarthritis in ancient skeletons, physicians did not recognize osteoarthritis until the 18th century. However, according to the book named, “The Biology of Degenerative Joint Disease”, by Sokoloff in 1969, there are a number of pathological descriptions indicative of osteoarthritis.

In 1793, Sandiford of Leiden described osteoarthrosis of the hip.

In 1802, William Heberden in his book named “Commentaries on the History and Cure of Diseases” has described a disease which had no connection with gout. He also described the small nodes which later we know those nodes with his name.

In 1805, John Haygarth described polyarticular disease influencing the distal interphalangeal and other joints, resembling almost perfectly OA as seen in our present modern society.

In 1824, Bell, similar to Sandifort in 1793, had described osteoarthrosis of the hip.

In 1829, Benjamin C Brodie revealed a non-inflammatory erosion of articular cartilage peculiar to the elderly.

In 1831, Robert Adams distinguished osteoarthritis from polyarticular rheumatoid arthritis considering its localized character (also he even tried to use “partial” rheumatic arthritis name for osteoarthritis). This big step in differentiating OA from rheumatic arthritis had a huge acceptance in many parts of European scientist.

In 1835, J V Cruveilhier and Cruveilhier’s mentor Laennec (inventor of the stethoscope) were used the term “unsure” for defects in the articular cartilage of involved joints.

In 1835, Robert Smith named the degenerative joint disease as: “sui generis” and after that, he came with the description of “malum coxae senilis” related to the osteoarthritis of the hip.

In 1857, Schöman made monographs affirming Adams’ great work (in 1831) and published them were published 1857.

In 1859, Alfred Baring Garrod separated the osteoarthritis and rheumatic arthritis and he was the first one proposed the name rheumatic arthritis.

In 1869, Charcot and Virchow, known as the fathers of cellular pathology, used the term “arthritis deformans” for both osteoarthritis and rheumatic arthritis.

In 1889, John Kent Spender was the first one introduced the term osteoarthritis.

In 1890, AE Garrod was granted the current title of “osteoarthritis“.

In 1895, (Soon after the introduction of X-rays as a great step in medicine by Wilhelm Konrad Röntgen), Joel E. Goldthwait were able to differentiate two main forms of arthritis: a) the “atrophic” type, which was found as polyarticular, in young population, and b) the “hypertrophic” type, non-polyarticular form occurred in fewer joints in young population. Then, hypertrophic arthritis and Atrophic arthritis were considered as osteoarthritis and rheumatic arthritis, respectively.

In 1908, Hoffa and Wollenberg Confirmed the work done by Joel E. Goldthwait.

In 1909, Nichols and Richardson Confirmed the work done by Joel E. Goldthwait.

In 1907, Albutt and Rolleston in a book named Albutt and Rolleston’s System of Medicine describes both osteoarthritis and rheumatic arthritis separately with their own different special pathological specifications.

In 1910, Sir William Osler in his book “The Principles and Practise of Medicine” clearly worked on these two diseases and tried to differentiate them based on the clinical features and pathology.

In 1952, Kellgren and Moore connected the Heberden noduli to osteoarthritis, considering it as a primary generalized OA in order to differentiate it primary generalized OA from secondary OA.

In the 1950s and 1960s, Kellgren and Lawrence introduced a radiographic scoring system in grading OA.

In 1953, Collins described the possible association of age with the prognosis of trauma in pathological evaluations.

In 1970, Dick et al worked on the radionuclide studies evidence of synovial inflammation.

In 1982, Goldenberg et al worked on the histological evidence of synovial inflammation.

In 1989, Hans Valkenburg’s team worked on the descriptive epidemiology of osteoarthritis.

In 1997, Spector et al worked on the biochemical evidence of synovial inflammation.

In 2001, Sokoloff highlighted malum coxae senilis, hip osteoarthritis.

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.
  4. 4.0 4.1 Inoue K, Hukuda S, Fardellon P, Yang ZQ, Nakai M, Katayama K, Ushiyama T, Saruhashi Y, Huang J, Mayeda A, Catteddu I, Obry C (January 2001). “Prevalence of large-joint osteoarthritis in Asian and Caucasian skeletal populations”. Rheumatology (Oxford). 40 (1): 70–3. PMID 11157144.
  5. Kwiecinski J, Rothschild BM (June 2016). “No rheumatoid arthritis in ancient Egypt: a reappraisal”. Rheumatol. Int. 36 (6): 891–5. doi:10.1007/s00296-015-3405-z. PMID 26650735.
  6. Sharma L (January 2016). “Osteoarthritis year in review 2015: clinical”. Osteoarthr. Cartil. 24 (1): 36–48. doi:10.1016/j.joca.2015.07.026. PMC 4693145. PMID 26707991.
  7. Glyn-Jones S, Palmer AJ, Agricola R, Price AJ, Vincent TL, Weinans H, Carr AJ (July 2015). “Osteoarthritis”. Lancet. 386 (9991): 376–87. doi:10.1016/S0140-6736(14)60802-3. PMID 25748615.
  8. Wallace IJ, Worthington S, Felson DT, Jurmain RD, Wren KT, Maijanen H, Woods RJ, Lieberman DE (August 2017). “Knee osteoarthritis has doubled in prevalence since the mid-20th century”. Proc. Natl. Acad. Sci. U.S.A. 114 (35): 9332–9336. doi:10.1073/pnas.1703856114. PMC 5584421. PMID 28808025.
  9. Yucesoy B, Charles LE, Baker B, Burchfiel CM (January 2015). “Occupational and genetic risk factors for osteoarthritis: a review”. Work. 50 (2): 261–73. doi:10.3233/WOR-131739. PMC 4562436. PMID 24004806.
  10. Dequeker J, Luyten FP (January 2008). “The history of osteoarthritis-osteoarthrosis”. Ann. Rheum. Dis. 67 (1): 5–10. doi:10.1136/ard.2007.079764. PMID 18077542.
  11. Cibere J, Sayre EC, Guermazi A, Nicolaou S, Kopec JA, Esdaile JM, Thorne A, Singer J, Wong H (June 2011). “Natural history of cartilage damage and osteoarthritis progression on magnetic resonance imaging in a population-based cohort with knee pain”. Osteoarthr. Cartil. 19 (6): 683–8. doi:10.1016/j.joca.2011.02.008. PMID 21329760.
  12. Buchanan WW, Kean WF, Kean R (2003). “History and current status of osteoarthritis in the population”. Inflammopharmacology. 11 (4): 301–16. doi:10.1163/156856003322699483. PMID 15035784.
  13. Leyland KM, Hart DJ, Javaid MK, Judge A, Kiran A, Soni A, Goulston LM, Cooper C, Spector TD, Arden NK (July 2012). “The natural history of radiographic knee osteoarthritis: a fourteen-year population-based cohort study”. Arthritis Rheum. 64 (7): 2243–51. doi:10.1002/art.34415. PMID 22422507.
  14. Franklin J, Ingvarsson T, Englund M, Ingimarsson O, Robertsson O, Lohmander LS (May 2011). “Natural history of radiographic hip osteoarthritis: A retrospective cohort study with 11-28 years of followup”. Arthritis Care Res (Hoboken). 63 (5): 689–95. doi:10.1002/acr.20412. PMID 21557524.

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Classification
Osteoarthritis classification

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

Overview

Since OA can affect any joint in human body. there several different classification system based on the involved joint and its location.

Classification

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[1][2]:

  • Pain consisted of 5 items:

-Staying in bed, sitting or lying, standing, walking, and using stairs.

  • Stiffness consisted of 2 items:

-After waking up in morning and 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, heavy household duties, light household duties, putting on/taking off socks, lying in bed, rising from bed, getting in and/or getting out of bath, getting on/off toilet.

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 then it was accepted by WHO in 1961[3]

Classification for Subsets of Osteoarthritis
I: Idiopathic
A: Localized
1: Hands: Heberden’s and Bouchard’s nodes (nodal), erosive interphalangeal arthritis (nonnodal), carpometacarpal 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: hemochromatosis, ochronosis, Gaucher’s disease, hemoglobinopathy, Ehlers-Danlos

c. Calcium Deposition Disease 1. Calcium pyrophosphate deposition disease

2. Apatite arthropathy

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’s joints)

3. Miscellaneous: frostbite, Kashin-Beck disease, Caisson’s disease

Knee

[4][5] [6]

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
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
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

Hip

[7][8][9]

Kellgren-Lawrence system
Grade Description
0 No  joint space narrowing (JSN) or reactive changes
I Doubtful JSN, possible osteophytic lipping
II Definite osteophytes, possible JSN
III Moderate osteophytes, definite JSN, some sclerosis, possible bone-end deformity
IV Large osteophytes, marked JSN, severe sclerosis, definite bone ends deformity
Tönnis classification
Grade Description
0 No osteoarthritis signs
I (Mild) Increased sclerosis, the slight narrowing of the joint space, slight loss of head sphericity or lipping at the joint margins
II (Moderate) Small cysts, moderate narrowing of the joint space, moderate loss of head sphericity
III (Severe) Large cysts, severe narrowing or obliteration of the joint space, severe deformity of the head

Shoulder

[10]

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

[11][12][13][14]

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
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
Lane grading of lumbar disc degeneration
Grade Joint space narrowing Osteophytes anterior and posterior Sclerosis
0 None None None
I Definite (mild) narrowing Small Present
II Moderate Moderate
III Severe (complete loss of joint space) Large
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
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)
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

[15][16]

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 

[17][18][19]

 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
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
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
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 abducts or adducts, supinated midfoot, plantarflexed first ray, etc
IV Types 1–3 plus subtalar, calcaneocuboid, or talonavicular arthritis

References

  1. Menkes CJ (February 1991). “Radiographic criteria for classification of osteoarthritis”. J Rheumatol Suppl. 27: 13–5. PMID 2027113.
  2. Glyn-Jones S, Palmer AJ, Agricola R, Price AJ, Vincent TL, Weinans H, Carr AJ (July 2015). “Osteoarthritis”. Lancet. 386 (9991): 376–87. doi:10.1016/S0140-6736(14)60802-3. PMID 25748615.
  3. Altman RD (February 1995). “The classification of osteoarthritis”. J Rheumatol Suppl. 43: 42–3. PMID 7752134.
  4. Wright RW (July 2014). “Osteoarthritis Classification Scales: Interobserver Reliability and Arthroscopic Correlation”. J Bone Joint Surg Am. 96 (14): 1145–1151. doi:10.2106/JBJS.M.00929. PMC 4083772. PMID 25031368.
  5. Dell’Isola A, Steultjens M (2018). “Classification of patients with knee osteoarthritis in clinical phenotypes: Data from the osteoarthritis initiative”. PLoS ONE. 13 (1): e0191045. doi:10.1371/journal.pone.0191045. PMC 5766143. PMID 29329325.
  6. Luyten FP, Bierma-Zeinstra S, Dell’Accio F, Kraus VB, Nakata K, Sekiya I, Arden NK, Lohmander LS (February 2018). “Toward classification criteria for early osteoarthritis of the knee”. Semin. Arthritis Rheum. 47 (4): 457–463. doi:10.1016/j.semarthrit.2017.08.006. PMID 28917712.
  7. Falez F, Casella F, Papalia M (March 2015). “Current concepts, classification, and results in short stem hip arthroplasty”. Orthopedics. 38 (3 Suppl): S6–13. doi:10.3928/01477447-20150215-50. PMID 25826635.
  8. Lee S, Nardo L, Kumar D, Wyatt CR, Souza RB, Lynch J, McCulloch CE, Majumdar S, Lane NE, Link TM (June 2015). “Scoring hip osteoarthritis with MRI (SHOMRI): A whole joint osteoarthritis evaluation system”. J Magn Reson Imaging. 41 (6): 1549–57. doi:10.1002/jmri.24722. PMC 4336224. PMID 25139720.
  9. Steinhoff H, Lieutenant K, Schlitter J (1989). “Residual motion of hemoglobin-bound spin labels as a probe for protein dynamics”. Z. Naturforsch., C, J. Biosci. 44 (3–4): 280–8. PMID 2545217.
  10. Walch G, Boulahia A, Boileau P, Kempf JF (1998). “Primary glenohumeral osteoarthritis: clinical and radiographic classification. The Aequalis Group”. Acta Orthop Belg. 64 Suppl 2: 46–52. PMID 9922529.
  11. Lakshmanan P, Jones A, Howes J, Lyons K (February 2005). “CT evaluation of the pattern of odontoid fractures in the elderly–relationship to upper cervical spine osteoarthritis”. Eur Spine J. 14 (1): 78–83. doi:10.1007/s00586-004-0743-z. PMC 3476682. PMID 15723251.
  12. Kanai H, Igarashi M, Yamamoto S (February 2002). “Vertebral body fracture of the lumbar spine in elderly women: more severe in osteoarthritis of the knee than in femoral neck fracture”. Orthopedics. 25 (2): 163–7. PMID 11866149.
  13. Junker S, Krumbholz G, Frommer KW, Rehart S, Steinmeyer J, Rickert M, Schett G, Müller-Ladner U, Neumann E (January 2016). “Differentiation of osteophyte types in osteoarthritis – proposal of a histological classification”. Joint Bone Spine. 83 (1): 63–7. doi:10.1016/j.jbspin.2015.04.008. PMID 26076655.
  14. Rutges JP, Duit RA, Kummer JA, Bekkers JE, Oner FC, Castelein RM, Dhert WJ, Creemers LB (December 2013). “A validated new histological classification for intervertebral disc degeneration”. Osteoarthr. Cartil. 21 (12): 2039–47. doi:10.1016/j.joca.2013.10.001. PMID 24120397.
  15. Wang XD, Zhang JN, Gan YH, Zhou YH (May 2015). “Current understanding of pathogenesis and treatment of TMJ osteoarthritis”. J. Dent. Res. 94 (5): 666–73. doi:10.1177/0022034515574770. PMID 25744069.
  16. Su N, Liu Y, Yang X, Luo Z, Shi Z (October 2014). “Correlation between bony changes measured with cone beam computed tomography and clinical dysfunction index in patients with temporomandibular joint osteoarthritis”. J Craniomaxillofac Surg. 42 (7): 1402–7. doi:10.1016/j.jcms.2014.04.001. PMID 24864071.
  17. Nüesch C, Valderrabano V, Huber C, von Tscharner V, Pagenstert G (July 2012). “Gait patterns of asymmetric ankle osteoarthritis patients”. Clin Biomech (Bristol, Avon). 27 (6): 613–8. doi:10.1016/j.clinbiomech.2011.12.016. PMID 22261013.
  18. Claessen FM, Meijer DT, van den Bekerom MP, Gevers Deynoot BD, Mallee WH, Doornberg JN, van Dijk CN (April 2016). “Reliability of classification for post-traumatic ankle osteoarthritis”. Knee Surg Sports Traumatol Arthrosc. 24 (4): 1332–7. doi:10.1007/s00167-015-3871-6. PMC 4823329. PMID 26611896.
  19. Barg A, Pagenstert GI, Hügle T, Gloyer M, Wiewiorski M, Henninger HB, Valderrabano V (September 2013). “Ankle osteoarthritis: etiology, diagnostics, and classification”. Foot Ankle Clin. 18 (3): 411–26. doi:10.1016/j.fcl.2013.06.001. PMID 24008208.
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Pathophysiology
What is going on in involved joint?!

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohammadmain Rezazadehsaatlou [2], Irfan Dotani [3]

Overview

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.

Pathophysiology

Different pathogenic mechanisms have been proposed to be responsible for the occurrence of OA. Heredity, obesity, hypoxia, synovitis–capsulitissubchondral bone overload, joint instability (mechanical integrity disturbances) are the most important underlying causes in this regard. In the current pathogenesis of osteoarthritis (OA), all joint tissues including cartilage, bone, synovium, ligamentous capsular structures, and surrounding muscle are involved. OA is characterized by structural changes such as active bone remodeling, synovial inflammation, and articular cartilage degradation leading to the loss of joint function and angular deformity or malalignment. Also, a variety of biomarkers in synovial fluid have helped to create more clear insight into the biological response of joints to injury. However, no biomarker has been declared to be reliable for monitoring the development, progression, and response to therapy of OA. Its been reported that certain factors can increase the risk of the OA development such as hereditary elements, trauma and mechanical stress, joint injury, age, obesity, physical activity, bone mineral density (BMD), and congenital anomalies. During the last years, signaling pathways have drawn a lot of attention and proven that these pathways play important roles in inflammation and in the remodeling of the subchondral bone, synovium, enzyme activation, and extracellular matrix degradation in articular cartilage [1] [2] [3][4].

Subchondral Bone

OA leads to the sub-chondral bone remodeling. This event is often along with the sub-chondral cysts formation as a result of focal resorption. OA can alter chondrocyte metabolism in bony cells. Osteoarthritis, influencing whole joint systems, includes both articular cartilage and underlying bone structures. One of the most common findings in OA is the subchondral bone plate thickening. The diseased bone becomes brittle and sclerotic, and the frequent turnovers affect bone quality. There is still controversy about whether the subchondral bone change happens simultaneously with the changes in articular cartilage or not. Articular overgrowths such as subchondral bone lead to microtrauma, hardening, remodeling, and displacement of the osteochondral line. Consequently, the energy-dissipation capacity and elasticity of the articular cartilage decrease. Macroscopic changes of the subchondral bone especially in load-bearing areas are increased osteogenetic reactions, increased stiffness, increased density, and excessive formation of bone and cartilage (called osteochondrophytes). OA is also capable of influencing the non–weight-bearing joints, such as hands, spine, shoulders, and temporomandibular joints. The osteochondrophytes usually can be found in intra-articular, marginal, extraarticular, insertional, or enthesiophytes. The osteochondrophytes frequently involves the joint space, and with synovial metaplastic fragments or flaps of cartilage, they lead to the articular ‘joint mice’ formation. On the other hand, the bone remodeling caused by microfractures within the superficial bone trabeculae with the formation of subchondral bone cysts (known as erosive alterations). Bony changes such as sclerosis of the subchondral bone plate, alterations in trabecular structure, osteophytes and bone marrow lesions are associated with the initiation and progression of OA. It’s been reported that the subchondral bone changes prior to the articular cartilage changes. Meanwhile, it’s been found that the molecular pathways (for example, cytokines such as IL-1, TNF-α, fibrinolytic system including plasminogen, tissue plasminogen activators, urokinase plasminogen activators, and plasmin) have in subchondral play important roles in the disbalance between the physiological connection of bone deposition and remodeling and resorption potential. Higher osteoblastic activity results in an exaggerated reparative response. In contrast, an increased osteoclastic degradative activity results in a predominantly erosive bony condition[5][6][7][8][9][10][11].

Articular Cartilage

The articular cartilage damage is one of the most important pathological causes of OA. It is not clear whether this pathological event originates from the cartilage or subchondral bone, loss and/or damage to articular cartilage or both of them are responsible for the development and progression of OA. Human articular cartilage system, acting as a shock absorber, consists of a hydrated extracellular matrix (as the functional elements of the tissue) with few numbers of chondrocytes within. 70–80% of cartilage consists of water and collagens and proteoglycans are the major organic components. Collagen type II builds a network of fibers containing molecules within. Collagen type XI helps collagen type II in fibril network formation and also limiting the fiber diameter. Collagen type IX make crosslinks the whole collagen network. Heparan sulfate proteoglycans such as perlecan, have important roles (such as interactions with heparin-binding growth factors like fibroblast growth factors, heparin binding forms of vascular endothelial growth factor (VEGF), and bone morphogenetic proteins (BMP)) in chondrogenesis. Higher demolition of heparan sulfate proteoglycans by glycosidases and matrix metalloproteinases are known to responsible for OA. Calcification and ossification in articular cartilage during OA and aging occurs due to the differentiation of chondrocytes. During the degenerative changes in involved joints, calcification happens simultaneously with to increasing alkaline phosphates and pyrophosphate levels.  Since the Articular cartilage has no internal vascular or lymphatic supply system so it is dependent on near tissues including subchondral bone and synovial membrane in receiving nutrients elements and excretion of products of made by articular matrix turnover and chondrocyte metabolism [12][13][1][9][14][15][16].

Synovial Membrane

The main task of Synovial Membrane is repairing any defects found in joint. The cellular compartment of the synovial membrane of the SM is a major source of synovial fluid. These components are responsible for management of chondrocyte activities and maintaining the integrity of articular cartilage surfaces (using lubricin and hyaluronic acid molecules) in diarthrodial joints. After a joint injury, the concentration of this molecular system changes. During the progression of OA, this synovial membrane changes into the main origin of proinflammatory and catabolic products such as metalloproteinases and aggrecanases. Thus, any damage to the synovial membrane can result in reducing of cartilage-protecting factors, and also an increase in production of articular matrix degradation factors. A normal synovial membrane has full control on the transmitted molecules in and out of the joint space. During some conditions such as trauma, inflammation, and OA this permeability of synovial membrane disrupts leading to reduced concentrations of lubricin and hyaluronic acid[17][18][19][20].
A model of Toll-like Receptor (a) and complement activation (b) in the joint leading to synovitis and potentiation of cartilage erosion in OA
.

Joint Instability

Joint instability occurs due to the ligament laxity enhancement, poor muscles conditions, or ligament tearing or strain in a ligament or abnormal muscles status. Joint instability increases the incidence of OA. Joint instability could be found as a result of synovitis produces excessive amounts of synovial fluid[21][22].

Hypoxia

Neovascularization in synovial membrane, subchondral bone, and cartilage is a common finding in OA. Neovascularization in the injured area increases the nutrients delivery of to the stressed articular cartilage and subchondral and also could cause the synovitis development in bone. Hypoxia as a common pathophysiological element of OA and rheumatoid arthritis because during OA, cartilage thinning and cartilage erosion, ECM composition changes, and the cartilage fissures development are the most common findings in involved joint. These structural alteration influence the oxygen gradient near the articular cartilage. In OA and rheumatoid arthritis, the two important angiogenic peptides including vascular endothelial growth factor and platelet-derived cellular endothelial growth factor. The increases due to the excessive expression of nuclear hypoxia-inducible factors. These angiogenic peptides increase local neovascularization and increase vascular permeability, consequently causing inflammation, cartilage damage, edema, and protein vascular leak that worsen the joint involvement [23][24].

References

  1. 1.0 1.1 Vincent KR, Conrad BP, Fregly BJ, Vincent HK (May 2012). “The pathophysiology of osteoarthritis: a mechanical perspective on the knee joint”. PM R. 4 (5 Suppl): S3–9. doi:10.1016/j.pmrj.2012.01.020. PMC 3635670. PMID 22632700.
  2. Wise BL, Niu J, Yang M, Lane NE, Harvey W, Felson DT, Hietpas J, Nevitt M, Sharma L, Torner J, Lewis CE, Zhang Y (June 2012). “Patterns of compartment involvement in tibiofemoral osteoarthritis in men and women and in whites and African Americans”. Arthritis Care Res (Hoboken). 64 (6): 847–52. doi:10.1002/acr.21606. PMC 3340516. PMID 22238208.
  3. Andriacchi TP, Koo S, Scanlan SF (February 2009). “Gait mechanics influence healthy cartilage morphology and osteoarthritis of the knee”. J Bone Joint Surg Am. 91 Suppl 1: 95–101. doi:10.2106/JBJS.H.01408. PMC 2663350. PMID 19182033.
  4. Haq I, Murphy E, Dacre J (July 2003). “Osteoarthritis”. Postgrad Med J. 79 (933): 377–83. PMC 1742743. PMID 12897215.
  5. Stone L (November 2008). “Aches, pains and osteoarthritis”. Aust Fam Physician. 37 (11): 912–7. PMID 19037464.
  6. Dieppe PA, Lohmander LS (2005). “Pathogenesis and management of pain in osteoarthritis”. Lancet. 365 (9463): 965–73. doi:10.1016/S0140-6736(05)71086-2. PMID 15766999.
  7. Witt KL, Vilensky JA (April 2014). “The anatomy of osteoarthritic joint pain”. Clin Anat. 27 (3): 451–4. doi:10.1002/ca.22120. PMID 22730047.
  8. Hassan H, Walsh DA (January 2014). “Central pain processing in osteoarthritis: implications for treatment”. Pain Manag. 4 (1): 45–56. doi:10.2217/pmt.13.64. PMID 24641343.
  9. 9.0 9.1 Dimitroulas T, Duarte RV, Behura A, Kitas GD, Raphael JH (October 2014). “Neuropathic pain in osteoarthritis: a review of pathophysiological mechanisms and implications for treatment”. Semin. Arthritis Rheum. 44 (2): 145–54. doi:10.1016/j.semarthrit.2014.05.011. PMID 24928208.
  10. Salaffi F, Ciapetti A, Carotti M (June 2014). “The sources of pain in osteoarthritis: a pathophysiological review”. Reumatismo. 66 (1): 57–71. PMID 24938198.
  11. Mobasheri A, Rayman MP, Gualillo O, Sellam J, van der Kraan P, Fearon U (May 2017). “The role of metabolism in the pathogenesis of osteoarthritis”. Nat Rev Rheumatol. 13 (5): 302–311. doi:10.1038/nrrheum.2017.50. PMID 28381830.
  12. Carter DR, Beaupré GS, Wong M, Smith RL, Andriacchi TP, Schurman DJ (October 2004). “The mechanobiology of articular cartilage development and degeneration”. Clin. Orthop. Relat. Res. (427 Suppl): S69–77. PMID 15480079.
  13. Krasnokutsky S, Attur M, Palmer G, Samuels J, Abramson SB (2008). “Current concepts in the pathogenesis of osteoarthritis”. Osteoarthr. Cartil. 16 Suppl 3: S1–3. doi:10.1016/j.joca.2008.06.025. PMID 18723377.
  14. Martel-Pelletier J (2004). “Pathophysiology of osteoarthritis”. Osteoarthr. Cartil. 12 Suppl A: S31–3. PMID 14698638.
  15. Houard X, Goldring MB, Berenbaum F (November 2013). “Homeostatic mechanisms in articular cartilage and role of inflammation in osteoarthritis”. Curr Rheumatol Rep. 15 (11): 375. doi:10.1007/s11926-013-0375-6. PMC 3989071. PMID 24072604.
  16. Scotece M, Mobasheri A (November 2015). “Leptin in osteoarthritis: Focus on articular cartilage and chondrocytes”. Life Sci. 140: 75–8. doi:10.1016/j.lfs.2015.05.025. PMID 26094910.
  17. Henrotin Y, Pesesse L, Sanchez C (2009). “Subchondral bone in osteoarthritis physiopathology: state-of-the art and perspectives”. Biomed Mater Eng. 19 (4–5): 311–6. doi:10.3233/BME-2009-0596. PMID 20042798.
  18. Mortellaro CM (September 2003). “Pathophysiology of osteoarthritis”. Vet. Res. Commun. 27 Suppl 1: 75–8. PMID 14535372.
  19. Martel-Pelletier J (November 1998). “Pathophysiology of osteoarthritis”. Osteoarthr. Cartil. 6 (6): 374–6. doi:10.1053/joca.1998.0140. PMID 10343769.
  20. Onuora S (October 2014). “Osteoarthritis: a role for CXCR2 signalling in cartilage homeostasis”. Nat Rev Rheumatol. 10 (10): 576. doi:10.1038/nrrheum.2014.148. PMID 25179389.
  21. Goldring SR, Goldring MB (2006). “Clinical aspects, pathology and pathophysiology of osteoarthritis”. J Musculoskelet Neuronal Interact. 6 (4): 376–8. PMID 17185832.
  22. Funck-Brentano T, Cohen-Solal M (July 2015). “Subchondral bone and osteoarthritis”. Curr Opin Rheumatol. 27 (4): 420–6. doi:10.1097/BOR.0000000000000181. PMID 26002035.
  23. Maldonado M, Nam J (2013). “The role of changes in extracellular matrix of cartilage in the presence of inflammation on the pathology of osteoarthritis”. Biomed Res Int. 2013: 284873. doi:10.1155/2013/284873. PMC 3771246. PMID 24069595.
  24. Poole AR (October 1999). “An introduction to the pathophysiology of osteoarthritis”. Front. Biosci. 4: D662–70. PMID 10525481.

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Causes
Osteoarthritis causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohammadmain Rezazadehsaatlou [2] Robert G. Badgett, M.D. [2] Luke Rusowicz-Orazem, B.S.; , Irfan Dotani [4]

Overview

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[1][2].

Causes

Causes by Organ System

Cardiovascular No underlying causes
Chemical/Poisoning No underlying causes
Dental No underlying causes
Dermatologic Paget disease
Drug Side Effect No underlying causes
Ear Nose Throat No underlying causes
Endocrine Acromegaly, Hemochromatosis, hyperparathyroidism, Pituitary cancer, Pituitary tumors, Reduced sex hormones
Environmental No underlying causes
Gastroenterologic Hemochromatosis, Wilson disease
Genetic Adam12, Alkaptonuria  , Asymmetric leg length, Bmp, Clip, Col11a2, Ehlers-danlos syndrome, Erg, Familial chondrocalcinosis, Frzb, Gdf5, Il10, Larsen syndrome  , Mcf2l, Mmp3, Multiple epiphyseal dysplasia  , Nail-patella syndrome  , Osteochondritis dissecans  , Spondyloepiphyseal dysplasia tarda  , Tgfb1, Thalassemia, Wilson disease
Hematologic Diabetes, Hemochromatosis, Thalassemia
Iatrogenic Meniscectomy, Surgery
Infectious Disease Syringomyelia, Tabes dorsalis, Viral hepatitis
Musculoskeletal/Orthopedic Aseptic necrosis of bone, Asymmetric leg length, Avascular necrosis, Chondrocalcinosis 1  , Chondrocalcinosis 2, Developmental dysplasia of the hip, Ehlers-danlos syndrome, Familial chondrocalcinosis, Fracture of bone, Joint injury, Meniscectomy, Multiple epiphyseal dysplasia  , Muscle dysfunction, Osteochondritis dissecans  , Syringomyelia, Tabes dorsalis
Neurologic No underlying causes
Nutritional/Metabolic Diabetes, Obesity
Obstetric/Gynecologic No underlying causes
Oncologic Pituitary cancer, Pituitary tumors
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal/Electrolyte No underlying causes
Rheumatology/Immunology/Allergy Allergies, Aseptic necrosis of bone, Avascular necrosis, Chondrocalcinosis 1  , Chondrocalcinosis 2, Crystal deposition, Gout, Lupus, Rheumatoid arthritis, Satoyoshi syndrome
Sexual No underlying causes
Trauma Developmental dysplasia of the hip, Fracture of bone, Joint injury, Physical trauma, Trauma
Urologic Alkaptonuria 
Miscellaneous Aging

===Causes in Alphabetical Order=== [3][4][5]

References

  1. Bennet D (March 1993). “Arthritis–its classification, pathogenesis and clinical relevance”. Tijdschr Diergeneeskd. 118 Suppl 1: 19S–23S. PMID 8480308.
  2. Man GS, Mologhianu G (March 2014). “Osteoarthritis pathogenesis – a complex process that involves the entire joint”. J Med Life. 7 (1): 37–41. PMC 3956093. PMID 24653755.
  3. Renberg WC (September 2005). “Pathophysiology and management of arthritis”. Vet. Clin. North Am. Small Anim. Pract. 35 (5): 1073–91, v. doi:10.1016/j.cvsm.2005.05.005. PMID 16129133.
  4. Harari J (July 1997). “Clinical evaluation of the osteoarthritic patient”. Vet. Clin. North Am. Small Anim. Pract. 27 (4): 725–34. PMID 9243778.
  5. Rychel JK (February 2010). “Diagnosis and treatment of osteoarthritis”. Top Companion Anim Med. 25 (1): 20–5. doi:10.1053/j.tcam.2009.10.005. PMID 20188335.

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Differentiating Osteoarthritis from other Diseases
Osteoarthritis differential diagnosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohammadmain Rezazadehsaatlou [2], Irfan Dotani [3]

Overview

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

Differentiating Osteoarthritis from other Diseases

Diseases which can have similar symptoms are [1][2][3][4]:

Diagnoses of arthritis are largely clinical, but laboratory tests such as ANA, erythrocyte sedimentation rate, C-reactive protein can help differentiate osteoarthritis from an inflammatory cause of arthritis.

Disease Differentiating signs and symptoms Diagnostic findings
Fibromyalgia
  • All lab tests are normal
Rheumatoid arthritis
  • Markers of systemic inflammation (ESR, CRP) are typically elevated.
SLE
Chronic fatigue syndrome Fatigue plus 4 of the following symptoms:
  • Diagnosis of exclusions
  • Symptoms must present for more than 6 months
Spondyloarthritis
Polymyalgia rheumatica
Osteoarthritis
  • Localized joint pain
  • Restricted to affect joints
  • Older at onset
  • X-ray of the involved joints demonstrate degenerative changes
Hypothyroidism
  • TSH is elevated and free T4 is low.
Myopathaies (polymyositis and dermatomyositis)
Neuropathy

References

  1. Pereira D, Ramos E, Branco J (2015). “Osteoarthritis”. Acta Med Port. 28 (1): 99–106. PMID 25817486.
  2. Sakalauskienė G, Jauniškienė D (2010). “Osteoarthritis: etiology, epidemiology, impact on the individual and society and the main principles of management”. Medicina (Kaunas). 46 (11): 790–7. PMID 21467838.
  3. Glyn-Jones S, Palmer AJ, Agricola R, Price AJ, Vincent TL, Weinans H, Carr AJ (July 2015). “Osteoarthritis”. Lancet. 386 (9991): 376–87. doi:10.1016/S0140-6736(14)60802-3. PMID 25748615.
  4. Chu CR, Millis MB, Olson SA (August 2014). “Osteoarthritis: From Palliation to Prevention: AOA Critical Issues”. J Bone Joint Surg Am. 96 (15): e130. doi:10.2106/JBJS.M.01209. PMC 4116563. PMID 25100783.

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Epidemiology and Demographics
Osteoarthritis epidemiology and demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Mohammadmain Rezazadehsaatlou [2], Irfan Dotani [3]

Overview

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 [1] [2].

Epidemiology

Prevalence

The obtained OA prevalence had significant differences due to the various definitions of OA. Some use only the radiographic criteria for OA while others prefer the clinical criteria in their study protocols. A combination of radiographic and clinical criteria would be the best method for OA prevalence, but unfortunately, the combination of these two criteria would be more costly than using each criterion alone. The available data about the incidence and prevalence of osteoarthritis are different. For example, OA mostly assessed by radiography which there should be a marked damage to be detectable in radiography. Near 6% of adults with the age of 30 years suffer from repeated knee pain and in their radiographic evaluation reveal osteoarthritis. As previously mentioned in risk factors for OA are age, sex, nutritional deficiencies, occupational involvements, trauma, genetic, and race. It was predicted that more than 26 million people in the USA have OA. The OA in hand, hip, and knee have positive correlations with age and as mentioned before OA is more common women than men, particularly after the age of 50 ( due to the menopause and hormonal changes)[3][4][5].

Hand OA

The incidence rate of OA reported by the Fallon Community Health Plan in Massachusetts (U.S.A) was the frequency of knee OA, hand OA, and hip OA were  240/100 000 person-years, 100/100 000 person-years, and 88/100 000 person-years, respectively (Figure1).

Figure1: Incidence of clinical osteoarthritis of the hand, knee, and hip among participants in the Fallon Health Plan, USA.  Oliveria SA et al. Arthritis Rheum. 1995; 38:1134-1141. © 1995, American College of Rheumatology.

The prevalence of hand OA is in the range of 27% 80%. 75% of women with the age of 60 – 70 years had distal interphalangeal (DIP) OA.  The US National Health and Nutrition Examination Survey (NHANES III) reported the prevalence of hand OA in 8% of the population. In a cohort study, the prevalence of symptomatic OA was twice as high in women than men (26.2%vs 13.2%, respective). Meanwhile, another study, conducted in Iran, reported the prevalence of hand OA among patients with the age of 40-50 years and >70 years 2.2%, and 22.5%, respectively [6][7].

Knee OA

Knee OA is less common than hand OA, although, knee OA occurs commonly in women (female-to-male ratio: 1.5:1-4:1). Epidemiology of knee OA in the USA is similar to European population. In a study by Framingham, the frequencies of Knee OA among patients with the age of 25-34 years and older than 75 years are 1% and 50%, respectively. Similar to Hand OA, the symptomatic knee OA in men and women older than 20 years old nearly doubles and triples, respectively (Figure 2). In contrast to a similar study conducted in China, the bilateral knee OA was reported to be around twice higher than Framingham Study in the USA. Accordingly, the prevalence of knee OA in Iranian rural area was 19.3%.

The symptomatic knee OA in men and women older than 20 years old in the Framingham Osteoarthritis Study. Abbreviations: BMI, body mass index; OA, osteoarthritis. Reproduced with permission from reference: Nguyen US et al. Ann Intern Med. 2011;155:725-732. © 2011, American College of Physicians .

Hip OA

Comparing to the OA in hand or knee, the Hip OA has less common occurrence. The prevalence of hip OA in women older than 65 years old in the USA was reported between 1.0% to 6.2%. The prevalence of hip OA in the African and Asian population was 2.8 and 1.4 Percents, respectively[8][9][10].

Incidence

In a study performed by the Fallon Community Health Plan a well-known health maintenance organization in north-east of United States of America, the incidence rate of hip OA, hand OA, and knee OA were 88 per 100 000 person-years, 100 per 100 000 person-years, and 240 per 100 000 person-years, respectively. In another study, the incidence rate of knee OA and hip OA conducted in Rochester, Minnesota were reported 163.8 per 100 000 person-years and 47.3 per 100 000 person-years, respectively[11][12].

References

  1. 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.
  2. Lawrence RC, Felson DT, Helmick CG, Arnold LM, Choi H, Deyo RA, Gabriel S, Hirsch R, Hochberg MC, Hunder GG, Jordan JM, Katz JN, Kremers HM, Wolfe F (January 2008). “Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II”. Arthritis Rheum. 58 (1): 26–35. doi:10.1002/art.23176. PMC 3266664. PMID 18163497.
  3. Cleveland RJ, Callahan LF (2017). “Can Osteoarthritis Predict Mortality?”. N C Med J. 78 (5): 322–325. doi:10.18043/ncm.78.5.322. PMID 28963268.
  4. Palazzo C, Nguyen C, Lefevre-Colau MM, Rannou F, Poiraudeau S (June 2016). “Risk factors and burden of osteoarthritis”. Ann Phys Rehabil Med. 59 (3): 134–8. doi:10.1016/j.rehab.2016.01.006. PMID 26904959.
  5. Thomas AC, Hubbard-Turner T, Wikstrom EA, Palmieri-Smith RM (June 2017). “Epidemiology of Posttraumatic Osteoarthritis”. J Athl Train. 52 (6): 491–496. doi:10.4085/1062-6050-51.5.08. PMC 5488839. PMID 27145096.
  6. Leung GJ, Rainsford KD, Kean WF (March 2014). “Osteoarthritis of the hand I: aetiology and pathogenesis, risk factors, investigation and diagnosis”. J. Pharm. Pharmacol. 66 (3): 339–46. doi:10.1111/jphp.12196. PMID 24329488.
  7. Fontana L, Neel S, Claise JM, Ughetto S, Catilina P (April 2007). “Osteoarthritis of the thumb carpometacarpal joint in women and occupational risk factors: a case-control study”. J Hand Surg Am. 32 (4): 459–65. doi:10.1016/j.jhsa.2007.01.014. PMID 17398355.
  8. Issa SN, Sharma L (February 2006). “Epidemiology of osteoarthritis: an update”. Curr Rheumatol Rep. 8 (1): 7–15. PMID 16515759.
  9. Sharma L, Kapoor D, Issa S (March 2006). “Epidemiology of osteoarthritis: an update”. Curr Opin Rheumatol. 18 (2): 147–56. doi:10.1097/01.bor.0000209426.84775.f8. PMID 16462520.
  10. Vina ER, Kwoh CK (March 2018). “Epidemiology of osteoarthritis: literature update”. Curr Opin Rheumatol. 30 (2): 160–167. doi:10.1097/BOR.0000000000000479. PMID 29227353.
  11. Felson DT (January 2004). “An update on the pathogenesis and epidemiology of osteoarthritis”. Radiol. Clin. North Am. 42 (1): 1–9, v. doi:10.1016/S0033-8389(03)00161-1. PMID 15049520.
  12. Guan SQ, Teng F, Zhang ZY (June 2017). “[The development of the epidemiology in osteoarthritis]”. Zhonghua Nei Ke Za Zhi (in Chinese). 56 (6): 450–452. PMID 28592048.

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Risk Factors
Osteoarthritis risk factors

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

Overview

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

Risk Factors

I: Systemic risk factors for Osteoarthritis

Gender

Knee, hip, and hand osteoarthritis are higher in women than men. It has also been reported that the frequency of osteoarthritis in women and men are 68% and 58% respectively. And it has been reported that women have a greater level of pain and disability.

Race

There are significant differences in the prevalence and the joint involvement patterns of OA between different racial and ethnic groups. The African American women had similar OA of Hip similar to white women. Its been reported that the knee OA in the USA is more common in Blacks than whites. Prevalence of hip OA in among whites in Africa and the Caribbean was higher than blacks. In another study, comparing the prevalence of knee OA between Chinese and whites in the USA, despite the higher rate of obesity among whites, knee OA was higher among Chinese women. The frequencies of hand OA and hip OA in Chinese population is 50% and 10% of the normal population. It can be concluded that the lower risk of hip and hand OA can be due to the genetic factors while the higher prevalence of knee OA can be linked to their squatting and other daily and occupational physical activities, which causes excessive pressure on their knee.

Age

Age plays an important role in the development of osteoarthritis. The correlation between age and the occurrence of OA is complex. Higher age through oxidative damage, thinning of cartilage, muscle weakening, reduces the basic cellular mechanisms that maintain tissue homeostasis which leads to an insufficient response to stress or joint injury, demolition of joint tissue destruction. Higher age leads to decrease in the tensile property of cartilage in articular cartilage in the accumulation of glycation consequently it can cause mechanical failure

Genetics

It’s been showed that genetic factors play important roles in development and even the prognosis of osteoarthritis. genetic factors are leads to osteoarthritis in nearly 70% of cases. Moreover, specific genes such as chromosomes 2, 3, 4, 6, 7, 11, 16, the X. It’s been reported that there is a strong correlation between the chromosome 2q13–32 and particular types of OA. For example, chromosomes 4, 6, 7, and 16 (susceptible locus: 4q35, 6p12.3–q13, 7q34-7q36.3, 7p15-7p21, 7q22, and 16p12.3-p12.1, respectively) are linked for hip and hand OA. The previously mentioned locus of chromosome 4 and 7 are also linked to knee OA.

Hormones

The osteoarthritis of knee, hip, and hand significantly increases around the time of menopause. Because of this, it’s been hypothesized that hormonal factors might be involved in the occurrence of OA. Up to this time, there is no report regarding the confirmation regarding the possible correlation between sex hormones and hand, knee, or hip OA in women. Osteocalcin, as a marker of bone turnover, decreases in women after their menopause which consequently women after menopause are more susceptible to knee arthritis.

Diet

Dietary related agents have an important roll in OA. Lower vitamin D, vitamin C, and selenium intakes have been associated with an increased risk of progression of knee OA in the older population. Also, using unrefined carbohydrates and junk foods in daily diet increase the chance of chronic diseases. Meanwhile, chondrocytes is an important and powerful origin of reactive oxygen species (ROC). Chondrocytes can damage cartilage collagen and synovial fluid hyaluronate. Meanwhile, micronutrients antioxidants, by providing defense against tissue injuries, are helpful to protect against osteoarthritis.

Smoking

Smoking is proven to be correlated with an increased risk of cartilage loss and knee pain in OA.

II: Local risk factors for Osteoarthritis

Physical activity

Doing repetitive and excessive joint loading which is common in specific heavy physical activities such as long-distance runners, karate, kung fu, and gymnastic could increase the risk of knee injury and developing OA in involved joints.

Trauma and injury to Joint

The traumatic injuries are known to have a strong association with the development of OA. Acute injuries such as bone fractures and dislocations, meniscal tearing and cruciate tearing, direct damage to local tissues, normal biomechanics disruption, increase the risk of OA development. Articular cartilage bears pressures from daily physical activities. Joints injuries and trauma the cartilage can influence their flexibility, eliminate cellular system and consequently decrease the subchondral loading capability.

Obesity

Higher body mass index (BMI) is a well-known predictor for risk factors of OA. It’s been reported that the correlation between obesity and knee OA is greater than with hip OA. Also, OA is associated with the metabolic syndrome, cardiovascular risk factors such as hypertension and hypercholesterolemia. Although the association between diabetes and OA is contradictory, it has been hypothesized that higher glucose concentrations product ROS and glycation leading to the cartilage degeneration and degradation. Since high BMI and obesity are considered as the major risk factor for OA, it’s been found that weight loss improves patient outcomes.

A meta-analysis of weight reduction and knee osteoarthritis concluded that weight loss of 5 percent from baseline was sufficient to reduce disability. Additionally, pain and disability were reduced if patients lost more than 6 kg (13.2 lb). Aerobic exercise is important for weight loss but can be challenging in persons with osteoarthritis of weight-bearing joints. Swimming, elliptical training, cycling, and upper body exercise may help in such cases.

Occupation

Occupation facing heavy loads and having stress activities such as workers whose jobs require repeated pincer grip and prolonged squatting and kneeling are consequently associated hand OA and knee OA, respectively [1].

Congenital abnormalities

The mechanical alignment of the knee plays an important roll in distributing the pressure through the articular surfaces. In a normal knee, 60-70% of the pressure is transferred through the medial compartment. Any structural problems like valgus or varus influences pressure distribution in joint and this misalignment play an important role in the development and progression of OA.

References

  1. Yucesoy B, Charles LE, Baker B, Burchfiel CM (January 2015). “Occupational and genetic risk factors for osteoarthritis: a review”. Work. 50 (2): 261–73. doi:10.3233/WOR-131739. PMC 4562436. PMID 24004806.

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Screening
Osteoarthritis screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Mohammadmain Rezazadehsaatlou[2], Irfan Dotani [3]

Overview

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

Screening

Accurate data about the prevalence of OA can be useful for the health care system to have appropriate plans for management of OA patients. Nowadays, the OA screening in general population depends on the self-reported symptoms recorded during the clinical evaluation. An approved screening algorithm OA with sufficient sensitivities and specificities is necessary for OA management. Due to the lack of a reliable screening test for OA, the assessments of the prevalence of OA in a general population is difficult. Meanwhile, some scientist have worked on the screening questionnaires for identifying the knee or hip OA. Using only a questionnaire to identify OA cases without the physical examinations and radiographs would be non-verifiable[1][2][2].

References

  1. Manek NJ, Lane NE (March 2000). “Osteoarthritis: current concepts in diagnosis and management”. Am Fam Physician. 61 (6): 1795–804. PMID 10750883.
  2. 2.0 2.1 Roux CH, Saraux A, Mazieres B, Pouchot J, Morvan J, Fautrel B, Testa J, Fardellone P, Rat AC, Coste J, Guillemin F, Euller-Ziegler L (October 2008). “Screening for hip and knee osteoarthritis in the general population: predictive value of a questionnaire and prevalence estimates”. Ann. Rheum. Dis. 67 (10): 1406–11. doi:10.1136/ard.2007.075952. PMID 18077540.

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Natural History, Complications and Prognosis
Osteoarthritis natural history, complications and prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammadmain Rezazadehsaatlou[2], Irfan Dotani [3].

Overview

The orthopedic surgeons are frequently asked by their patients regarding the final outcome and the prognosis of their diseased joint/joints caused by OA.

Natural History

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 [1][2][3][4][5] :

Hip OA

Its been reported that the patients with unilateral idiopathic hip OA are most likely to develop OA in the contralateral hip. In a 10 years expectancy, the frequencies of OA development and undergoing the total hip total hip replacement (THR) among the contralateral hips considered as normal are 35-45% and 5-20%, respectively. Therefore, due to the importance of this topic and lack of confidential information in this regard, a long-term longitudinal study is needed in order to answer this big question that how often and how long does takes for symptomatic joint injury and the requirement of surgical involvement in this regard. Meanwhile, the incidence and prevalence rates of THR in hip OA were 2.5% and 17%, respectively.

Knee OA

Based on the radiological evaluation of knee OA, the incidence rate of knee OA was 2-4% annually and this incidence rate was higher among women. Though most importantly, its been reported that the incidence rate of OA in radiography evaluations was twice higher than symptomatic OA which highlights the role of radiography in this regard. In a cohort study, the OA progression in a 3-year evaluation reported to be 15.5%.

Hand OA

The hand as the most common and important peripheral site of osteoarthritis (OA), because the hand involvement in OA could affect patients life through disability. Meanwhile, the base of the thumb, and distal interphalangeal joints (DIPs), proximal interphalangeal joints (PIPs) of fingers are the most common site for hand OA. The prevalence of hand OA among men and women older than 65 years is 64-78% and 71 to 99%, respectively.

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.

Unfortunately, despite high prevalence and influence of OA on human life, there are only a limited studies working on the complications caused by OA. Possible complications of osteoarthritis include[6][7][8][9]:

  • Gout.

Gout is known as an inflammatory form of arthritis caused by high amount of urate leading to sodium urate crystals formation around the involved joints. Gout may affect the cartilage system and trigger the crystal formation, especially in cases with higher serum levels of urate. In the foot, osteoarthritis in the big toe is a common site for involvement it could be considered as a common site of the occurrence of gout.

Osteoarthritis can also lead to calcium pyrophosphate crystals formation in diseased cartilage. This is process named calcification or chondrocalcinosis. Chondrocalcinosis can be developed in any joint, with/without the existence of osteoarthritis. In a patient with osteoarthritis, chondrocalcinosis is common in the knee.

  • Long-term (chronic) pain.
  • Rapid and the complete breakdown of cartilage resulting in loose tissue material in the joint (chondrolysis).
  • Joint deformities (hard or bony nodules that form where two bones come together, often giving the joint a knobby or knotted appearance)
  • Bone death (osteonecrosis).
  • Stress fractures (hairline crack in the bone that develops gradually in response to repeated injury or stress).
  • Muscle weakness (often occurs when a joint becomes too painful to use, especially with knee osteoarthritis).
  • Bleeding within the joint.
  • Infection in the joint.
  • Deterioration or rupture of the tendons and ligaments around the joint, leading to loss of stability.
  • Pinched nerve (in osteoarthritis of the spine).
  • Depression.
  • Anxiety.
  • Sleep disruption.
  • Weight gain.
  • Difficulty performing daily activities and Reduced productivity.
  • Loss of independent living.
  • Impaired balance.
  • Increased risk of falling.

Prognosis

  • Most osteoarthritis cases do stabilize[10].
  • Some osteoarthritis cases progress[11].
  • A small number of osteoarthritis patients improve spontaneously[11].

References

  1. Anania A, Abdel MP, Lee YY, Lyman S, González Della Valle A (October 2013). “The natural history of a newly developed flexion contracture following primary total knee arthroplasty”. Int Orthop. 37 (10): 1917–23. doi:10.1007/s00264-013-1993-3. PMC 3779550. PMID 23835560.
  2. Amstutz HC, Le Duff MJ (August 2016). “The Natural History of Osteoarthritis: What Happens to the Other Hip?”. Clin. Orthop. Relat. Res. 474 (8): 1802–9. doi:10.1007/s11999-016-4888-y. PMC 4925421. PMID 27172820.
  3. Wyles CC, Heidenreich MJ, Jeng J, Larson DR, Trousdale RT, Sierra RJ (February 2017). “The John Charnley Award: Redefining the Natural History of Osteoarthritis in Patients With Hip Dysplasia and Impingement”. Clin. Orthop. Relat. Res. 475 (2): 336–350. doi:10.1007/s11999-016-4815-2. PMC 5213917. PMID 27071391.
  4. Clarson LE, Nicholl BI, Bishop A, Daniel R, Mallen CD (April 2016). “Discussing prognosis with patients with osteoarthritis: a cross-sectional survey in general practice”. Clin. Rheumatol. 35 (4): 1011–7. doi:10.1007/s10067-015-3094-8. PMC 4819557. PMID 26474771.
  5. Bloch B, Srinivasan S, Mangwani J (2015). “Current Concepts in the Management of Ankle Osteoarthritis: A Systematic Review”. J Foot Ankle Surg. 54 (5): 932–9. doi:10.1053/j.jfas.2014.12.042. PMID 26028603.
  6. Hawker GA, Croxford R, Bierman AS, Harvey P, Ravi B, Kendzerska T, Stanaitis I, King LK, Lipscombe L (January 2017). “Osteoarthritis-related difficulty walking and risk for diabetes complications”. Osteoarthr. Cartil. 25 (1): 67–75. doi:10.1016/j.joca.2016.08.003. PMID 27539890.
  7. NEUWIRTH E (September 1954). “Neurologic complications of osteoarthritis of the cervical spine”. N Y State J Med. 54 (18): 2583–90. PMID 13194134.
  8. Dekker J, van Dijk GM, Veenhof C (September 2009). “Risk factors for functional decline in osteoarthritis of the hip or knee”. Curr Opin Rheumatol. 21 (5): 520–4. doi:10.1097/BOR.0b013e32832e6eaa. PMID 19550331.
  9. Heidari B (2011). “Knee osteoarthritis prevalence, risk factors, pathogenesis and features: Part I”. Caspian J Intern Med. 2 (2): 205–12. PMC 3766936. PMID 24024017.
  10. Hochberg MC (September 1996). “Prognosis of osteoarthritis”. Ann. Rheum. Dis. 55 (9): 685–8. PMC 1010279. PMID 8882152.
  11. 11.0 11.1 Anandacoomarasamy A, March L (February 2010). “Current evidence for osteoarthritis treatments”. Ther Adv Musculoskelet Dis. 2 (1): 17–28. doi:10.1177/1759720X09359889. PMC 3383468. PMID 22870434.

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Diagnosis

Diagnosis

Diagnostic Criteria | History and Symptoms | Physical Examination | Laboratory Findings | X Ray | CT | MRI | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies | Stem cell

Case Studies

Case Studies

Case #1
Related Chapters
External links

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