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Osteoarthritis, hip

MedGen UID:
14530
Concept ID:
C0029410
Disease or Syndrome
Synonym: Osteoarthritis of hip
SNOMED CT: Degenerative joint disease of hip (239872002); OA - Osteoarthritis of hip (239872002); Osteoarthritis of hip (239872002)
 
HPO: HP:0008843
Monarch Initiative: MONDO:0006629
OMIM®: 612400

Definition

Osteoarthritis of the hip joint. [from NCI]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVOsteoarthritis, hip

Conditions with this feature

Slipped femoral capital epiphyses
MedGen UID:
57704
Concept ID:
C0149887
Disease or Syndrome
Slipped capital femoral epiphysis is defined as a posterior and inferior slippage of the proximal epiphysis of the femur onto the metaphysis (femoral neck), occurring through the physeal plate during the early adolescent growth spurt.
Namaqualand hip dysplasia
MedGen UID:
609409
Concept ID:
C0432214
Disease or Syndrome
Mild spondyloepiphyseal dysplasia due to COL2A1 mutation with early-onset osteoarthritis is a type 2 collagen-related bone disorder characterized by precocious, generalized osteoarthritis (with onset as early as childhood) and mild, dysplastic spinal changes (flattening of vertebrae, irregular endplates and wedge-shaped deformities) resulting in a mildly short trunk.
Angel-shaped phalango-epiphyseal dysplasia
MedGen UID:
366028
Concept ID:
C1739384
Congenital Abnormality
A form of acromelic dysplasia with the distinctive radiological sign of angel-shaped middle phalanges, a typical metacarpophalangeal pattern profile (mainly affecting first metacarpals and middle phalanges of second, third and fifth digits which all appear short), epiphyseal changes in the hips and in some, abnormal dentition and delayed bone age. A rare disease with less than 20 cases reported in the literature, however, it is likely under diagnosed. Caused by mutations in the growth differentiation factor 5 (GDF5) gene, located on chromosome 20q11.2, encoding CDMP1 (cartilage derived morphogenetic protein). CDMP1 belongs to the TGF beta super family and plays a role in bone growth and joint morphogenesis. Transmitted as an autosomal dominant condition.
Multiple epiphyseal dysplasia type 1
MedGen UID:
325376
Concept ID:
C1838280
Disease or Syndrome
Autosomal dominant multiple epiphyseal dysplasia (MED) presents in early childhood, usually with pain in the hips and/or knees after exercise. Affected children complain of fatigue with long-distance walking. Waddling gait may be present. Adult height is either in the lower range of normal or mildly shortened. The limbs are relatively short in comparison to the trunk. Pain and joint deformity progress, resulting in early-onset osteoarthritis, particularly of the large weight-bearing joints.
Spondyloepiphyseal dysplasia tarda, autosomal recessive
MedGen UID:
338604
Concept ID:
C1849054
Disease or Syndrome
Autosomal recessive form of spondyloepiphyseal dysplasia tarda.
Vitreoretinopathy with phalangeal epiphyseal dysplasia
MedGen UID:
343940
Concept ID:
C1852989
Disease or Syndrome
Spondyloarthropathy, susceptibility to, 1
MedGen UID:
400145
Concept ID:
C1862852
Finding
Ankylosing spondylitis is a form of painful, ongoing joint inflammation (chronic inflammatory arthritis) that primarily affects the spine.  Early symptoms of ankylosing spondylitis typically begin between the ages of 15 and 30. Most commonly, affected individuals first experience chronic back pain and stiffness. This pain worsens with rest or inactivity, and tends to be relieved with physical activity or exercise. \n\nPain in ankylosing spondylitis results from inflammation of the joints between the pelvic bones (the ilia) and the base of the spine (the sacrum). These joints are called sacroiliac joints, and inflammation of these joints is known as sacroiliitis. The inflammation gradually spreads to the joints between the vertebrae, eventually involving the whole spine, causing a condition called spondylitis. Over time, back movement gradually becomes limited as the bones of the spine (vertebrae) fuse together. This progressive bony fusion is called ankylosis. These fused bones are prone to fracture.\n\nAnkylosing spondylitis can involve other joints as well, including the shoulders, hips, and, less often, the knees. As the disease progresses, it can affect the joints between the spine and ribs, restricting movement of the chest and making it difficult to breathe deeply. \n\nAnkylosing spondylitis affects the eyes in more than 30 percent of cases, leading to episodes of eye inflammation called acute iritis. Acute iritis typically affects one eye at a time and causes eye pain and increased sensitivity to light (photophobia). Rarely, ankylosing spondylitis can also cause serious complications involving the heart, lungs, and nervous system. Six to 10 percent of people with ankylosing spondylitis have additional inflammatory disorders such as psoriasis, which affects the skin, or ulcerative colitis or Crohn disease, which both affect the digestive tract.
Aneurysm-osteoarthritis syndrome
MedGen UID:
462437
Concept ID:
C3151087
Disease or Syndrome
Loeys-Dietz syndrome (LDS) is characterized by vascular findings (cerebral, thoracic, and abdominal arterial aneurysms and/or dissections), skeletal manifestations (pectus excavatum or pectus carinatum, scoliosis, joint laxity, arachnodactyly, talipes equinovarus, cervical spine malformation and/or instability), craniofacial features (widely spaced eyes, strabismus, bifid uvula / cleft palate, and craniosynostosis that can involve any sutures), and cutaneous findings (velvety and translucent skin, easy bruising, and dystrophic scars). Individuals with LDS are predisposed to widespread and aggressive arterial aneurysms and pregnancy-related complications including uterine rupture and death. Individuals with LDS can show a strong predisposition for allergic/inflammatory disease including asthma, eczema, and reactions to food or environmental allergens. There is also an increased incidence of gastrointestinal inflammation including eosinophilic esophagitis and gastritis or inflammatory bowel disease. Wide variation in the distribution and severity of clinical features can be seen in individuals with LDS, even among affected individuals within a family who have the same pathogenic variant.
Autosomal dominant osteopetrosis 2
MedGen UID:
465707
Concept ID:
C3179239
Disease or Syndrome
The spectrum of CLCN7-related osteopetrosis includes infantile malignant CLCN7-related autosomal recessive osteopetrosis (ARO), intermediate autosomal osteopetrosis (IAO), and autosomal dominant osteopetrosis type II (ADOII; Albers-Schönberg disease). ARO. Onset is at birth. Findings may include: fractures; reduced growth; sclerosis of the skull base (with or without choanal stenosis or hydrocephalus) resulting in optic nerve compression, facial palsy, and hearing loss; absence of the bone marrow cavity resulting in severe anemia and thrombocytopenia; dental abnormalities, odontomas, and risk for mandibular osteomyelitis; and hypocalcemia with tetanic seizures and secondary hyperparathyroidism. Without treatment maximal life span in ARO is ten years. IAO. Onset is in childhood. Findings may include: fractures after minor trauma, characteristic skeletal radiographic changes found incidentally, mild anemia, and occasional visual impairment secondary to optic nerve compression. Life expectancy in IAO is usually normal. ADOII. Onset is usually late childhood or adolescence. Findings may include: fractures (in any long bone and/or the posterior arch of a vertebra), scoliosis, hip osteoarthritis, and osteomyelitis of the mandible or septic osteitis or osteoarthritis elsewhere. Cranial nerve compression is rare.
Spondyloepiphyseal dysplasia tarda, X-linked
MedGen UID:
762085
Concept ID:
C3541456
Congenital Abnormality
X-linked spondyloepiphyseal dysplasia tarda is a condition that impairs bone growth and occurs almost exclusively in males. The name of the condition indicates that it affects the bones of the spine (spondylo-) and the ends of long bones (epiphyses) in the arms and legs. "Tarda" indicates that signs and symptoms of this condition are not present at birth, but appear later in childhood, typically between ages 6 and 10.\n\nMales with X-linked spondyloepiphyseal dysplasia tarda have skeletal abnormalities and short stature. Affected boys grow steadily until late childhood, when their growth slows. Their adult height ranges from 4 feet 6 inches (137 cm) to 5 feet 4 inches (163 cm). Impaired growth of the spinal bones (vertebrae) primarily causes the short stature. Spinal abnormalities include flattened vertebrae (platyspondyly) with hump-shaped bulges, progressive thinning of the discs between vertebrae, and an abnormal curvature of the spine (scoliosis or kyphosis). These spinal problems also cause back pain in people with this condition. Individuals with X-linked spondyloepiphyseal dysplasia tarda have a short torso and neck, and their arms are disproportionately long compared to their height.\n\nOther skeletal features of X-linked spondyloepiphyseal dysplasia tarda include an abnormality of the hip joint that causes the upper leg bones to turn inward (coxa vara); multiple abnormalities of the epiphyses, including a short upper end of the thigh bone (femoral neck); and a broad, barrel-shaped chest. A painful joint condition called osteoarthritis that typically occurs in older adults often develops in early adulthood in people with X-linked spondyloepiphyseal dysplasia tarda and worsens over time, most often affecting the hips, knees, and shoulders.
Short stature and advanced bone age, with or without early-onset osteoarthritis and/or osteochondritis dissecans
MedGen UID:
777109
Concept ID:
C3665488
Disease or Syndrome
Familial osteochondritis dissecans is a condition that affects the joints and is associated with abnormal cartilage. Cartilage is a tough but flexible tissue that covers the ends of the bones at joints and is also part of the developing skeleton. A characteristic feature of familial osteochondritis dissecans is areas of bone damage (lesions) caused by detachment of cartilage and a piece of the underlying bone from the end of the bone at a joint. People with this condition develop multiple lesions that affect several joints, primarily the knees, elbows, hips, and ankles. The lesions cause stiffness, pain, and swelling in the joint. Often, the affected joint feels like it catches or locks during movement. Other characteristic features of familial osteochondritis dissecans include short stature and development of a joint disorder called osteoarthritis at an early age. Osteoarthritis is characterized by the breakdown of joint cartilage and the underlying bone. It causes pain and stiffness and restricts the movement of joints.\n\nA similar condition called sporadic osteochondritis dissecans is associated with a single lesion in one joint, most often the knee. These cases may be caused by injury to or repetitive use of the joint (often sports-related). Some people with sporadic osteochondritis dissecans develop osteoarthritis in the affected joint, especially if the lesion occurs later in life after the bone has stopped growing. Short stature is not associated with this form of the condition.
Developmental dysplasia of the hip 2
MedGen UID:
811575
Concept ID:
C3715079
Disease or Syndrome
Developmental dysplasia of the hip (DDH) is a debilitating condition characterized by incomplete formation of the acetabulum leading to dislocation of the femur, suboptimal joint function, and accelerated wear of the articular cartilage, resulting in arthritis. Undetected hip dysplasia is the leading cause of osteoarthritis of the hip in young individuals, causing over 40% of cases in that age group (summary by Feldman et al., 2013). For discussion of genetic heterogeneity of developmental dysplasia of the hip, see DDH1 (142700).
Osteoarthritis susceptibility 1
MedGen UID:
854604
Concept ID:
C3887876
Finding
Osteoarthritis is a common disease of the joints that primarily occurs in older adults. This condition is characterized by the breakdown of cartilage, the tough but flexible tissue that covers the ends of the bones at the joints and allows smooth joint movements. One or more parts of the body can be affected, most often the hands, shoulders, spine, knees, or hips.\n\nOsteoarthritis usually develops slowly, causing pain, stiffness, and restricted movement as the condition gets worse. Areas of bone no longer cushioned by cartilage rub against each other and start to break down. Further damage is caused as the body attempts to repair and rebuild these tissues. The immune system, which plays a role in healing injuries, targets these areas, and its response leads to inflammation of the joint tissues. Abnormal growths of bone (osteophytes) and other tissue can also occur, and may be visible as enlarged joints. Enlargement of the joints of the fingers is especially noticeable.\n\nPeople with osteoarthritis typically experience stiffness following periods of inactivity such as upon awakening or rising from a chair; the stiffness usually improves as they move around. In some affected individuals, the condition never causes major problems. In others, severe osteoarthritis can impair mobility and the ability to perform daily tasks, affecting quality of life and increasing the risk of other health conditions such as cardiovascular disease.\n\nOsteoarthritis is most common in middle age or late adulthood, because the cartilage at the joints naturally begins to thin as people age. However, it can occur earlier in life, especially after injuries affecting the joints such as a type of knee injury called an anterior cruciate ligament (ACL) tear. People who are overweight or whose activities are particularly stressful to the joints are also at increased risk of developing osteoarthritis.
Peripheral dysostosis
MedGen UID:
1648357
Concept ID:
C4721502
Disease or Syndrome
A rare primary bone dysplasia with characteristics of cone-shaped epiphyses of the phalanges, hyperextensibility and hyper-flexibility of the fingers and marked delay in ossification of hand bones. Short-limbed short stature, very stubby, short fingers and toes, flat face and nose and a large skull may also be associated. There have been no further descriptions in the literature since 1980.
Loeys-Dietz syndrome 6
MedGen UID:
1794251
Concept ID:
C5562041
Disease or Syndrome
Loeys-Dietz syndrome (LDS) is characterized by vascular findings (cerebral, thoracic, and abdominal arterial aneurysms and/or dissections), skeletal manifestations (pectus excavatum or pectus carinatum, scoliosis, joint laxity, arachnodactyly, talipes equinovarus, cervical spine malformation and/or instability), craniofacial features (widely spaced eyes, strabismus, bifid uvula / cleft palate, and craniosynostosis that can involve any sutures), and cutaneous findings (velvety and translucent skin, easy bruising, and dystrophic scars). Individuals with LDS are predisposed to widespread and aggressive arterial aneurysms and pregnancy-related complications including uterine rupture and death. Individuals with LDS can show a strong predisposition for allergic/inflammatory disease including asthma, eczema, and reactions to food or environmental allergens. There is also an increased incidence of gastrointestinal inflammation including eosinophilic esophagitis and gastritis or inflammatory bowel disease. Wide variation in the distribution and severity of clinical features can be seen in individuals with LDS, even among affected individuals within a family who have the same pathogenic variant.

Professional guidelines

PubMed

van Doormaal MCM, Meerhoff GA, Vliet Vlieland TPM, Peter WF
Musculoskeletal Care 2020 Dec;18(4):575-595. Epub 2020 Jul 9 doi: 10.1002/msc.1492. PMID: 32643252
Skou ST, Roos EM
Clin Exp Rheumatol 2019 Sep-Oct;37 Suppl 120(5):112-117. Epub 2019 Oct 15 PMID: 31621559
Bartels EM, Juhl CB, Christensen R, Hagen KB, Danneskiold-Samsøe B, Dagfinrud H, Lund H
Cochrane Database Syst Rev 2016 Mar 23;3(3):CD005523. doi: 10.1002/14651858.CD005523.pub3. PMID: 27007113Free PMC Article

Curated

UK NICE Guideline NG226, Osteoarthritis in over 16s: diagnosis and management, 2022

Recent clinical studies

Etiology

Rees HW
J Am Acad Orthop Surg 2020 Apr 1;28(7):e288-e291. doi: 10.5435/JAAOS-D-19-00416. PMID: 31800436
Quinn RH, Murray J, Pezold R, Hall Q
J Am Acad Orthop Surg 2018 Oct 15;26(20):e434-e436. doi: 10.5435/JAAOS-D-18-00351. PMID: 30134309
Murphy NJ, Eyles JP, Hunter DJ
Adv Ther 2016 Nov;33(11):1921-1946. Epub 2016 Sep 26 doi: 10.1007/s12325-016-0409-3. PMID: 27671326Free PMC Article
Gala L, Clohisy JC, Beaulé PE
J Bone Joint Surg Am 2016 Jan 6;98(1):63-73. doi: 10.2106/JBJS.O.00109. PMID: 26738905
Bennell K
J Physiother 2013 Sep;59(3):145-57. doi: 10.1016/S1836-9553(13)70179-6. PMID: 23896330

Diagnosis

Hall M, van der Esch M, Hinman RS, Peat G, de Zwart A, Quicke JG, Runhaar J, Knoop J, van der Leeden M, de Rooij M, Meulenbelt I, Vliet Vlieland T, Lems WF, Holden MA, Foster NE, Bennell KL
Osteoarthritis Cartilage 2022 Jan;30(1):32-41. Epub 2021 Sep 29 doi: 10.1016/j.joca.2021.09.010. PMID: 34600121
Hunter DJ, Bierma-Zeinstra S
Lancet 2019 Apr 27;393(10182):1745-1759. doi: 10.1016/S0140-6736(19)30417-9. PMID: 31034380
Lespasio MJ, Sultan AA, Piuzzi NS, Khlopas A, Husni ME, Muschler GF, Mont MA
Perm J 2018;22:17-084. doi: 10.7812/TPP/17-084. PMID: 29309269Free PMC Article
Murphy NJ, Eyles JP, Hunter DJ
Adv Ther 2016 Nov;33(11):1921-1946. Epub 2016 Sep 26 doi: 10.1007/s12325-016-0409-3. PMID: 27671326Free PMC Article
Aresti N, Kassam J, Nicholas N, Achan P
BMJ 2016 Jul 6;354:i3405. doi: 10.1136/bmj.i3405. PMID: 27383835

Therapy

Goh SL, Persson MSM, Stocks J, Hou Y, Lin J, Hall MC, Doherty M, Zhang W
Ann Phys Rehabil Med 2019 Sep;62(5):356-365. Epub 2019 May 21 doi: 10.1016/j.rehab.2019.04.006. PMID: 31121333Free PMC Article
Hunter DJ, Bierma-Zeinstra S
Lancet 2019 Apr 27;393(10182):1745-1759. doi: 10.1016/S0140-6736(19)30417-9. PMID: 31034380
Zhu X, Sang L, Wu D, Rong J, Jiang L
J Orthop Surg Res 2018 Jul 6;13(1):170. doi: 10.1186/s13018-018-0871-5. PMID: 29980200Free PMC Article
Gay C, Chabaud A, Guilley E, Coudeyre E
Ann Phys Rehabil Med 2016 Jun;59(3):174-183. Epub 2016 Apr 1 doi: 10.1016/j.rehab.2016.02.005. PMID: 27053003
Bartels EM, Juhl CB, Christensen R, Hagen KB, Danneskiold-Samsøe B, Dagfinrud H, Lund H
Cochrane Database Syst Rev 2016 Mar 23;3(3):CD005523. doi: 10.1002/14651858.CD005523.pub3. PMID: 27007113Free PMC Article

Prognosis

Pincus D, Jenkinson R, Paterson M, Leroux T, Ravi B
JAMA 2020 Mar 17;323(11):1070-1076. doi: 10.1001/jama.2020.0785. PMID: 32181847Free PMC Article
Karachalios TS, Koutalos AA, Komnos GA
Hip Int 2020 Jul;30(4):370-379. Epub 2019 Oct 31 doi: 10.1177/1120700019883244. PMID: 31672068
Lu M, Phillips D
J Am Acad Orthop Surg 2019 Apr 15;27(8):275-285. doi: 10.5435/JAAOS-D-17-00775. PMID: 30289797
Pereira D, Peleteiro B, Araújo J, Branco J, Santos RA, Ramos E
Osteoarthritis Cartilage 2011 Nov;19(11):1270-85. Epub 2011 Aug 24 doi: 10.1016/j.joca.2011.08.009. PMID: 21907813
Busija L, Bridgett L, Williams SR, Osborne RH, Buchbinder R, March L, Fransen M
Best Pract Res Clin Rheumatol 2010 Dec;24(6):757-68. doi: 10.1016/j.berh.2010.11.001. PMID: 21665124

Clinical prediction guides

Ohashi Y, Uchida K, Fukushima K, Satoh M, Koyama T, Tsuchiya M, Saito H, Takahira N, Inoue G, Takaso M
Biomed Res Int 2021;2021:9212585. Epub 2021 Sep 18 doi: 10.1155/2021/9212585. PMID: 34589551Free PMC Article
Yoo JI, Cha YH, Kim KJ, Kim HY, Choy WS, Hwang SC
BMC Musculoskelet Disord 2019 Feb 8;20(1):63. doi: 10.1186/s12891-019-2450-2. PMID: 30736783Free PMC Article
Iagnocco A, Naredo E
Clin Exp Rheumatol 2017 May-Jun;35(3):527-534. Epub 2017 Feb 10 PMID: 28229810
Nilsdotter A, Bremander A
Arthritis Care Res (Hoboken) 2011 Nov;63 Suppl 11:S200-7. doi: 10.1002/acr.20549. PMID: 22588745
Salaffi F, Stancati A, Silvestri CA, Ciapetti A, Grassi W
Eur J Pain 2004 Aug;8(4):283-91. doi: 10.1016/j.ejpain.2003.09.004. PMID: 15207508

Recent systematic reviews

Saueressig T, Owen PJ, Zebisch J, Herbst M, Belavy DL
JAMA Netw Open 2021 Feb 1;4(2):e210254. doi: 10.1001/jamanetworkopen.2021.0254. PMID: 33635329Free PMC Article
van Doormaal MCM, Meerhoff GA, Vliet Vlieland TPM, Peter WF
Musculoskeletal Care 2020 Dec;18(4):575-595. Epub 2020 Jul 9 doi: 10.1002/msc.1492. PMID: 32643252
Goh SL, Persson MSM, Stocks J, Hou Y, Lin J, Hall MC, Doherty M, Zhang W
Ann Phys Rehabil Med 2019 Sep;62(5):356-365. Epub 2019 May 21 doi: 10.1016/j.rehab.2019.04.006. PMID: 31121333Free PMC Article
Gay C, Chabaud A, Guilley E, Coudeyre E
Ann Phys Rehabil Med 2016 Jun;59(3):174-183. Epub 2016 Apr 1 doi: 10.1016/j.rehab.2016.02.005. PMID: 27053003
Bartels EM, Juhl CB, Christensen R, Hagen KB, Danneskiold-Samsøe B, Dagfinrud H, Lund H
Cochrane Database Syst Rev 2016 Mar 23;3(3):CD005523. doi: 10.1002/14651858.CD005523.pub3. PMID: 27007113Free PMC Article

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      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Curated

    • NICE, 2022
      UK NICE Guideline NG226, Osteoarthritis in over 16s: diagnosis and management, 2022

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