Presentation on Medical Sciences. (Joint issues by Rajad Bhatt)

1. Osteoarthritis
Rajat Bhatt MD

2. 1 32
Epidemiology EtiopathogenesisClinical features

3. Incidence
Age and sex-standardized incidence rates of symptomatic radiographic OA in the
in adults aged ≥20 years and older
Hand OA = 100 per 100,000 person years. Knee OA = 240 per 100,000 person years
Hip OA = 88 per 100,000 person years.

4. Because of the aging of our society and the obesity
epidemic, the burden of OA will continue to increase
over the next 20 years

5. 1.Idiopathic
Localized
Medial Compartment Lateral Compartment
Patellofemoral Compartment
(e.g., chondromalacia)
Eccentric (superior) Concentric (axial, medial)
Diffuse (Coxae senilis)
Apophyseal Intervertebral(disk)
Spondylosis (osteophytes)
Ligamentous (hyperostosis
[Forestier disease or DISH])
Generalized: include three or more
areas listed above (Kellgren-Moore)
Hands (e.g.,Heberden and Bouchard nodes [nodal], erosive
interphalangeal arthritis [nonnodal]): Scaphometal,
scaphotrapezial )
Feet (e.g.,Hallux valgus, hallux rigidus, contracted toes
[hammer/cock-up toes]):talonavicular
Knee
Hip
Spine (particularly cervical and lumber
Other single sites (e.g., shoulder temporomandibular,
sacroiliac, ankle,wrist, acromioclavicular)
Small (Peripheral and Spine)
Large (Central and Spine)
Mixed (Peripheral and Central)

6. 2.Secondary
Posttraumatic
Congenital or
developmental diseases
Localized
Hip Diseases (e.g.,
Legg-Calve-Perthes,
congential hip
dislocation, slipped
capital femoral
epiphysis, shallow
acetabulum)
Mechanical and Local
Factors (e.g., obesity
[?], unequal lower
extremity)
Generalized
Bone dysplasias (e.g
epiphyseal dysplasia,
spondyloapophyseal
dysplasia)
Metabolic diseases
(e.g., hemochromatosis,
ochronosis, Gaucher
disease,
hemoglobinopathy,
Ehlers-Danlos-Danlos
syndrome)
Calcium deposition
disease
Calcium
pyrophosphate
deposition disease
Apatite arthropathy
Destructive
arthropathy (shoulder,
knee)
Other bones and joint
disorder (e.g.,
avascular necrosis,
rheumatoid arthritis )
Other Deseases
Endocrine diseases
(e.g., diabetes mellitus,
acromegaly,
hypothyroidism,
hyperparathyroidism
necrosis, rheumato)
Neuropathic
arthropathy (Charcot
joints)
Miscellaneous (e.g.,
frostbite, Kashin-Beck
disease, caisson disease)

7. OA can be defined pathologically, radiographically, or
clinically,

8. American College of Rheumatology criteria for osteoarthritis
(OA) of the hand, hip, and knee

9. Item Required for presence of OA
Hand(Clinical)
Hand pain, aching, or stiffness
for most days of prior month
(1,2,3,4 or 1,2,3,5)
Hard tissue enlargement of
> 2 of 10 selected hand joints
MCP swelling in < 2 joints.
Hard tissue enlargement of
> DIP joints
Deformity of >1 of 10
selected hand joints.
Hip(Clinical &
Radiographic)
Hip pain for most days of
the prior month. (1,2,3 or
1,2,4 or 1,3,4)
ESR <20 mm / hr
(laboratory)
Radiographic femoral and /
or acetabular osteophytes.
Radiographic hip joint space
narrowing
Knee(Clinical)
Knee pain for most days of
prior month
Crepitus on active joint
motion
Morning stiffness <30min in
duration
Age >38yr
Bony enlargement of the
knee on examination
Knee (Clinical &
radiographic)
Knee pain for most days of
prior month
Osteophytes at joint margins
(radiograph)
Synovial fluid typical of OA
(laboratory)
Age >40yr
Morning Stiffness <30 min
in duration
Crepitus on active joint
motion

10. Radiographic osteoarthritis
Definitions
Kellgren-Lawrence (KL) radiographic grading scale and atlas have been in use for more
than five decades.

11. Grade Classification Description
0 Normal No features of osteoarthritis
1 Doubtful Minute osteophyte, doubtful signification
2 Minimal Definite osteophyte, unimpaired joint space
3 Moderate Moderate diminution of joint space
4 Severe Joint space greatly impaired with sclerosis of subchondral bone
Kellgren-Lawrence radiographic grading system
for osteoarthritis
Adapted from Kellgren JH, Lawrence JS, editors. The epidemiology of chronic rheumatism, atlas of standard radiographs.
Oxford: Blackwell Scientific 1963.

12. Example of semiquantative. Radiographics assessment with use of the Kellgren-Lawrence and Osteoarthritis Research-Society International (OARSI) grading scheme. (a)
Kellgren-Lawrence grade 3. No lateral femoral and tibial osteophytes are seen (OARSI grade 0). A medial femoral osteophyte OARSI 1 (white arrow), a medial tibial
osteophyte OARSI grade 2 (White arrowhead). Lateral tibiofemoral joint space width OARSI grade 0, and medial tibiofemoral joint space narrowing OARSI grade 2
(black arrows) are depicted.(b) Kellgren-Lawrence grade 2. A lateral femoral osteophyte OARSI grade 2 (white arrow), a lateral tibial Osteophyte OARSI grade 2 (white
arrowhead), a medial femoral osteophyte OARSI grade 3 (black arrowhead), a normal lateral tibiofemoral joint space width OARSI grade 0, and medial tibiofemoral joint
space width OARSI grade 1 (gray arrow) are shown.

13. Lack of perfect congruence between radiographic
findings of OA and clinical symptoms. Up to 60% of
individuals with radiographic knee OA may not
complain of pain.

14. Sometimes individuals may curtail symptom-inducing
activities and that even “asymptomatic” radiographic
OA is not without consequence.

15. Higher mortality associated with increasing age, male sex, walking disability, and self-
reported comorbidities (diabetes, cancer, cardiovascular disease) but not with joint
affected, previous joint replacement, obesity, nonsteroidal antiinflammatory drug use,
depression, or baseline hip or knee pain.
Reduced physical activity and a chronic inflammatory state in OA patients may contribute
and should be aggressively managed

16. Overview: Primary OA
DIP Joints
PIP Joints
CMC Joints
AC joints
Hip Joints
Knee Joints
1st MTP joints
Facet / apophyseal joints of the C- and L-spine

17. Risk Factors

18. Risk Factors for
osteoarthrits
Increasing
age (All sites)
Trauma, and some
occupation involving
repetive activities
(Specific sites)
Obesity (most sites, but
more marked for the
knee than other joints)
Genetic
predisposition
(All sites)
Race of ethnicity
(Variable at
different joint sites)
Female sex or gender
(Some sites
particularly knee and
hand)

19. A framework for understanding systemic and local
risk factors for osteoarthritis
Systematic factors affecting joint
vulnearability
1.Age
2.Female Gender
3.Race
4.Genetic susceptibility
5.Nutritional factors
Susceptibility to osteoarthritis
Use (loading) factors acting on joints:
1. Obesity
2. Injurius physical
3.Activities
Osteoarthritis or its progression
Intrinsic joint vulnerabilities (Local
enviroment):
1. Previous damage (e.g., meniscectomy; ACL tear)
2.Bridging muscle weakness
3. Cartilage not responsive
4.Malalignment
5.Proprioceptive deficiencies

20. Person with OA in one joint is at high risk of getting it in others, even other joints distant
from the first.
Systemic risk factors

21. With age, chondrocytes, which do not replicate throughout life, become senescent and
become less responsive to regulatory growth factors in the cartilage matrix
environment,and the cartilage matrix itself changes in ways that make it more vulnerable
to injury.
The local joint environment also changes with age in ways that make the joint susceptible
to damage. With age, muscles become weaker and less well conditioned. Reaction times
slow so that incipient injury to a joint from an oncoming weight-bearing load may not be
buffered or shock absorbed as competently in an older joint as in a younger one

22. Even if it does not have direct effects on joint structure, vitamin D deficiency may have
indirect effects on joint health by lowering the threshold for joint pain. Vitamin D
deficiency has been linked with generalized pain, and vitamin D deficiency may impair
muscle function so that rehabilitation is difficult

23. Some of the changes in local joint environment may be more
prominent in women (e.g., loss in strength and conditioning), and
hormone-related changes that occur in postmenopausal women may
increase disease risk, although the data on estrogen loss and its
relation to the development of OA are mixed

24. Factors in the local joint environment
In all joints, cartilage and other structures in the joint are designed to bear a certain amount
of stress (force per unit area) during loading and joint use. When the direction of the
transarticular load changes or when the joint becomes misshapen, altering loading patterns
inside the joint, focal loads within the joint transcend physiologic parameters and joint
damage can occur

25. In some joints such as the ankle and the wrist, which are only rarely affected by OA, most
disease is caused by major joint injury
In joints more commonly affected by OA such as the knee and hip, major joint injuries,
perhaps even unrecognized ones, also are likely to be major causes of disease
In the knees, the common joint injuries with important effects on subsequent joint function
and disease are anterior cruciate ligament (ACL) tears and meniscal tears.
Factors in the local joint environment

26. Neuromuscular factors and
osteoarthritis
Proprioception
Muscle strength

27. Hip dysplasia in which there is an underdevelopment of the acetabulum leading to
undercoverage of the femur and excess focal stress where the edge of the acetabulum
contacts the femur.
Others include a nonspherical femoral head or an acetabulum that extends too far around
the femoral head; both of these latter problems can cause femoroacetabular impingement
(FAI)
Hip osteoarthritis and abnormalities of joint shape

28. OA occurs when that loading occurs in an environment in which the joint is already
injured or impaired or in which the loading is so excessive or injurious that even a normal,
well-functioning joint cannot tolerate it without injury
Risk factors relating to loading of the joint

29. Obesity has a far greater effect on knee OA than it has been shown to have on hand OA,
which suggests that most of the effect of obesity can be explained by its effect in
producing excess load
For hip OA the relation of obesity is less strong and less clear. The development of new-
onset symptomatic OA is increased in persons who are obese, as is the risk of developing
bilateral radiographic disease, although there is no significant or consistent relationship
between obesity and the development of unilateral OA of the hip.
Obesity

30. Physical activity does not consistently increase the risk of OA
Risk Factors
First, as noted earlier, elite marathon runners—those on Olympic teams and who run professionally—are
at a high risk of developing knee and hip OA at a relatively early adult age (in their 30s or 40s).
Second, those whose jobs require manual labor with repetitive activities that load a specific joint
excessively and repeatedly tend to get OA in the overused joint (e.g., cotton pickers in hand joints; miners
in backs and knees), which suggests that even normal joints can develop OA if these joints are forced to do
the same laboring task for hours every day and many weeks each year over many years.
Lastly, marathon runners who have already had meniscal tears are at high risk of advanced OA if they
continue to run
Physical activity: injurious or protective?

31. High bone mineral density increases the risk of knee and hip OA independently of other
factors such as obesity and strength
Unclear reason
The peculiar case of bone mineral density: is it
systemic or local?

32. Clinical features of
osteoarthritis

33. SymptomsandSignsofosteoarthritis
Symptoms
Pain
Discomfort
Depression
Stiffness
Reduced function
Weakness
Grinding or clicking
Instability / buckling
Signs
Alter gait
Tendenrness
Hard tissue enlargment
Swelling with / without effusion
Crepitus
Limitation of motion
Deformity
Ligamentous instability

34. The presence or absence of an obvious cause (Primary or Secondary OA).
The distribution between joints and number of joints affected (localized or generalized OA).
The amount of bone formation around the joints, or, conversely or bone attrition (hypertrophic or atrophic OA),
and the related presence or absence of diffuse idiopathic skeletal hyperostosis
The presence of absence of overt inflammation (inflammatory OA)
The presence or absence of chondrocalcinosis (pyrophosphate arthropathy) or of basic calcium phosphate crystal
deposition (apatite-associated arthropathy).
The rate of progression (rapidly progressive osteoarthritis).
The main factors that have been considered as
indicative of possible subsets have included
1
2
3
4
5
6

35. Pain of OA changes during the day and has been demonstrated to vary by 20% within a
given week and from week to week.Pain in OA is also influenced by pain at other sites and
by patient adaptation and avoidance strategies, and it is inextricable from function.The
pain of OA is associated with poor sleep, fatigue, changes in mood, and impaired quality
of life.
Joint pain is often referred distally; for example, hip pain may be referred into the thigh or
knee

36. Anatomic Site Mechanism
Cartilage (defective or lost)
Synovial: inflammation induced by cartilage “char” fragments, cartilage crystal
shedding, cartialage release of cytokines (e.g., interleukin-1), enzymes (e.g.,
metalloproteinases)
Subchondral bone: Mechanical stress (see below)
Instability: Stress on capsule.
Menisci Tear or degeneration: stretch at insertion to the joint capsule, catch between surfaces.
Synovial cavity Stretch of joint capsule, transport of inflammatory mediators between synovium and
cartilage.
Synovium Inflammation, hypertrophy
Subchondral bone Ischemia with increased subchondral pressure, decreased, oxygen tension, and
increased pH.
Avascular necrosis.
Regeneration or repair of infarcted bone.
Osteophytes Periosteal elevation
Neural impingement.
Table: Relationship between anatomic site and possible physiologic pain in osteoarthritis

37. Anatomic Site Mechanism
Osteophytes Periosteal elevation
Neural impingement
Joint capsule Stretch from joint distention.
Stress at insertion to periosteal and bone.
Bursae Inflammation, with or without classification
Muscle Spasm, contracture
Nocturnal myoclonus
Central nervous
system
Depression, anxiety, fibromyalgia, non-restorative sleep.
General Ethnic and cultural factors, coping skills, prior pain experience, abuse
Altered function placing stress on other areas of the musculoskeletal system
Table: Relationship between anatomic site and possible physiologic pain in osteoarthritis

38. Pain can be measured through standardized testing.
For the hip or knee, the Western Ontario McMaster Universities (WOMAC) Osteoarthritis Index quantifies pain,
stiffness, and function in separate subscales.
http://www.rheumatology.org/I-Am-A/Rheumatologist/Research/Clinician-Researchers/Western-Ontario-
McMaster-Universities-Osteoarthritis-Index-WOMAC
The algofunctional index of Lequesne measures hip or knee pain and function in a single scale.
The WOMAC index has been incorporated into the Hip Dysfunction and Osteoarthritis Outcome Score (HOOS)
and the Knee Dysfunction and Osteoarthritis Outcome Score (KOOS).
Because of the often cyclic nature of OA, an 11-item tool, the Measure of Intermittent and Constant Osteoarthritis
Pain (ICOAP), has been developed.
For the hand, validated scales include the Australian-Canadian Hand Osteoarthritis Index (AUSCAN) and the
Functional Index for Hand Osteoarthritis (FIHOA)

39. Damaged articular cartilage indirectly causes pain due to loss of its structural integrity,
alteration in biomechanics, cartilage debris, and release of inflammatory mediators.
Structural damage to cartilage causes uneven surfaces, which results in a grinding
sensation felt by the patient and crepitus on examination, often accompanied by pain
Damage to articular cartilage

40. Although synovial inflammation is most often less severe than in
the traditional “inflammatory” arthritides (e.g., rheumatoid
arthritis), activation of inflammatory responses always occurs in
OA joints, at both the synoviocyte and chondrocyte level (which
justifies the term osteoarthritis)

41. In cases in which cartilage is fissured and the subchondral bone is exposed, hydroxyapatite
crystals from bone or cartilage may leach or be sheared into the synovial cavity. In
addition, the absence of articular cartilage allows loosening and instability of the joint and
exposure to subchondral bone.
Other loose bodies in the joint, such as “joint mice” or osteochondromatosis, are potential
indirect causes of pain. The disrupted portion of torn menisci can be displaced, stretching
the joint capsule.

42. Synovial fluid can indirectly cause pain by serving as a transport medium, distending the
joint capsule, and/or limiting joint function. In OA the synovial fluid may act as a reservoir
for inflammatory cytokines, cells, and crystals. In addition, excess synovial fluid distends
the joint, which potentially compresses synovial blood vessels and stimulates pressure
receptors in the capsule.25 A distended joint compromises the normal transport of nutrition
and gases by synovial fluid between cartilage and synovium. The residual waste products
linger in the synovial space and perpetuate inflammation.
Role of synovial fluid

43. The synovium contains nerve fibers. These include Aβ (large myelinated
mechanoreceptor), Aδ (large myelinated mechanoreceptor/nociceptor), and C
(small nonmyelinated nociceptor) fibers.20 The latter can release both substance P
and calcitonin gene–related peptide (CGRP). Substance P stimulates both the pain
response and inflammation

44. Osteophytes are the most consistent pathologic and radiographic finding associated with
the presence of pain.31 Osteophytes may cause pain directly by distending the periosteum;
pain can sometimes be elicited by applying pressure over an osteophyte about the knee or
interphalangeal joint of the hand
The pain of ischemic bone is aching and deep seated. In OA, subchondral cysts and
sclerosis are radiographic evidence that localized osteonecrosis has taken place.

45. The joint capsule and periarticular ligaments are stretched by synovial effusions, abnormal
menisci, or instability and may cause pain through mechanoreceptors and nociceptors.
Stress at the ligamentous insertion on the periosteum stimulates nociceptors. When the
periarticular tissues are distorted, the ligaments may be abnormally stressed, which
induces contractures that result in decreasing function and increasing pain from stress at
ligamentous insertions and periarticular muscle spasm.
Damage to meniscus, capsule, and related tissues

46. Muscle spasm is probably a common source of pain
in OA. Muscle spasm may occur in the form of
nocturnal myoclonus, altering sleep patterns and
resulting in fibromyalgia-like symptoms. Muscle
spasm of the lower extremities must be
differentiated from pain related to vascular causes
(e.g., night cramps) or restless leg syndrome and
pain of spinal radicular origin. Joint contractures in
OA can cause pain on stretching of the periarticular
ligaments and muscles.

47. Periarticular bursae may become inflamed and hence be a
source of pain (e.g., anserine bursitis medial and inferior
to the knee). Bursal inflammation is sometimes associated
with calcium formation (e.g., calcific bursitis).

48. Pain is complicated by the presence of coexistent or induced psychological distress, such
as depression
Psychological factors and pain

49. Stiffness may be defined as a sensation of a gelling or tightening of the involved joint that
usually occurs after inactivity, such as in the morning or when rising after sitting for a
prolonged period. The stiffness in OA usually lasts only a few minutes and almost always
less than 30 minutes, in contrast to the diffuse stiffness of rheumatoid arthritis. Also, the
stiffness in OA is usually confined to the symptomatic joints.
Stiffness

50. Impaired function of a weight-bearing joint places stress on the
contralateral weight-bearing joints. It is not uncommon for the patient
with impaired right knee function (perhaps with pain) to have
difficulty with the left hip and vice versa.

51. Patients may complain of enlargement of the joints of the hand or knee. They
may also complain of increasing deformity of the knees, such as knocked
(valgus) or bowed (varus) knees. There may be a click or grinding sensation
with joint motion, and this grinding may be associated with pain. In the knee,
instability is often associated with a feeling that the knee is “giving out.”

52. Inactivity secondary to pain may lead to significant weakness
and can be compounded by periarticular muscle atrophy.

53. Signs

54. Gait
OA of the hip or knee frequently is associated with significant changes in the periarticular
muscles, often with atrophy and weakness. Reduced muscle strength is compounded by
reduced proprioception

55. Tenderness
There may be tenderness of soft tissues (e.g., synovium, capsule, bursae, and
periarticular muscles) or periosteum at the insertion of capsule or ligaments.

56. There may be enlargement of the joint from synovitis, synovial effusion, or bony
enlargement. Effusions are usually cool or slightly warm to palpation. Effusion of the
distal interphalangeal (DIP) joint may present as a cystic herniation ; aspiration often
reveals a jelly like material reminiscent of a ganglion cyst. Swelling of the joint from an
effusion frequently leads to loss of extension.
Joint swelling

57. Grinding, crunching, or cracking may be heard over a joint with OA. Crepitus is caused by
movement of uneven surfaces across each other and is best demonstrated with active
motion of the joint. This contrasts with the benign “cracking” of the proximal
interphalangeal (PIP) joints that occurs when smooth cartilage surfaces are separated,
which creates a vacuum sound with release of nitrogen gas.
Crepitus

58. There may be loss of function with reduced motion as a result of pain, synovitis/effusion,
or periarticular soft tissue contractures. When motion of a weight-bearing joint is limited,
additional stress is placed on ipsilateral and contralateral weight-bearing joints
Limitation of motion

59. Deformity may be present in any of the peripheral joints with OA. However, it is most
notable in the interphalangeal joints of the hands with enlargement and subluxation, in the
first CMC joint, in the knees (varus/valgus deformity), or in the hips (shortened
extremity). Deformity may be associated with joint fusion or instability.
Deformity

60. Range-of-motion examination may reveal instability in various planes of motion. For
example, instability of the knee may be demonstrated in the anteroposterior planes
(cruciate ligament laxity or deficiency) or in the mediolateral planes (loss of meniscus,
collateral ligament laxity, loss of medial compartment bony stock).
Instability

61. OA of the knees and hips occurs in a monarticular or oligoarticular distribution. OA of the
hands and OA of the feet are generally present in the same individual to varying degrees.
There is a subgroup of patients who have OA in three or more joint groups, which is
known as generalized OA.
Patterns of joint involvement

62. Shoulder pain is sometimes related to glenohumeral OA. Pain is typically aching and is
associated with extremes of motion or occurs after activity of the shoulder. OA of the
shoulder usually coexists with, and is difficult to differentiate from, other abnormalities of
the shoulder (e.g., rotator cuff abnormalities, adhesive capsulitis, labrum, and bursitis).
Shoulder

63. A peculiar destructive arthropathy (Milwaukee shoulder) is associated with
persistent shoulder pain, large synovial effusions, and demonstration of a variety
of synovial fluid calcium crystals
Acromioclavicular joint OA can produce pain that can be aggravated by weight
bearing or other stressful activities. Painless enlargement of the acromioclavicular
and sternoclavicular joints is commonly associated with reduced shoulder motion.

65. Classification of hand OA into nodal (noninflammatory) OA and erosive interphalangeal
(inflammatory) OA.
Erosive inflammatory osteoarthritis is localized to the DIP, PIP, and first CMC joints of
the hands. It causes more pain, tenderness, and soft tissue swelling than does typical
nodal osteoarthritis. Patients with this variant experience rapid loss of motion from
joint destruction that may lead to bony ankylosis. This localized form of
osteoarthritis is the most common cause of an asymmetric non-infl ammatory
polyarthropathy.
Hand OA

66. DIP joints are typically involved, with slow bony enlargement over a period of years
(Heberden nodes)
On occasion, the evolution of interphalangeal OA may be indistinguishable from early-
onset rheumatoid arthritis or psoriatic arthritis.

67. Clinical photograph of a patient with nodal,
generalized osteoarthritis showing the typical
swellings of the distal interphalangeal joints
(Heberden’s nodes) and of the proximal
interphalangeal joints (Bouchard’s nodes),as
well as squaring of the thumb base due to OA
and subluxation of the carpometacarpal joint.
(From Women’s Health Service, University of
Maryland Medical School, with permission).

68. X-rays

69. Examination demonstrates hard tissue (bony) enlargement and
deformities of the interphalangeal joints. There may be tenderness and
occasionally other signs of inflammation. There is often a partial loss
of range of motion and subluxation

70. A predominantly palmar subluxation may give the appearance of a mallet finger
OA of the first CMC joints (trapeziometacarpal and trapezioscaphoid) is common. There is
a tendency for osteophytes to develop on the distal ulnar surface of the trapezoid,
associated with radial subluxation of the proximal head of the first metacarpal. This gives
the base of the thumb a “squared” or “knobby” clinical appearance

71. Hips
Patients with hip OA most often have groin or anterior hip pain that radiates into the thigh.
Pain is associated with early ambulation and weight bearing and is lessened or relieved by
rest. Examination most often reveals difficulty rising from a seated position, altered gait
favoring the arthritic hip, and reduced range of motion on examination, with pain on
motion, particularly internal rotation.

73. Both lumbar spine and hip OA may be painful when the patient rises from a seated or
reclined position and during early ambulation. Pain from lumbar stenosis often has its
onset after ambulation for a distance and, because of radiation to the thighs, is more
suggestive of claudication (pseudoclaudication). More severe hip OA may be painful at all
times, even at rest. Pain is usually localized to the groin or medial thigh but may be lateral,
suggesting (and associated with) trochanteric bursitis and/or meralgia paresthetica.

74. Hip OA is associated with an antalgic gait, one in which the patient overshifts the weight
while walking to reduce the pain
The Trendelenburg sign may be present: standing on the involved extremity leads to a
drop in the contralateral hip from weakening of the ipsilateral hip abductors. Another late
sign is shortening of the extremity as the femoral head migrates superiorly and axially into
the acetabulum, in association with a flexion contracture of the hip.

75. Most hip OA is slowly progressive. However, there is a subset of
patients, estimated at 10%, with a rapidly progressive form of
hip OA that evolves over a few months.

78. Knee
Patients often experience an insidious onset of pain about the knee, particularly with
weight bearing and stair climbing (gonarthritis). The patient may have noticed knee
swelling and/or varus/valgus deformity. Examination sometimes reveals swelling with loss
of the usual crease in the skin and soft tissues over the inner (null) facet between the
patella and the femoral condyle, in addition to a bulging suprapatellar sac. When present,
the effusions are usually cool to palpation
Hips

80. Crepitus on motion is best detected on active joint motion.
Occasionally distention of the popliteal semitendinosus bursa
(popliteal or Baker cyst) may be present.

81. Marginal osteophytes, intrasynovial loose bodies (joint mice), or
moveable bodies (osteochondromas) may be palpable. Medial narrowing
of the joint space (radiographic interbone distance) may lead to or
aggravate a varus deformity, whereas lateral joint space narrowing may
lead to a valgus deformity

83. Knee OA also has been associated with quadriceps weakness, reduced knee
proprioception, and increased postural sway
Knee OA may be associated with pain at the distal medial joint margin (anserine bursitis at
the insertion on the pes anserinus of the tibia).
Other structures affected in Knee OA

84. Adult patellofemoral OA is not commonly symptomatic. Anterior knee pain is aggravated
by sitting in low chairs (e.g., at movie theaters) and can be precipitated by pressure with
mediolateral movement of the patella in the intercondylar groove (patellar apprehension or
grind test).
OA of the knee may be associated with varying degrees of subchondral spontaneous
osteonecrosis of the knee.

87. Talonavicular and subtalar joint OA is usually secondary to trauma with or without
ligamentous damage or to an old ankle fracture. Patients complain of ankle pain on weight
bearing. Examination reveals swelling of the ankle that must be distinguished from a
variety of conditions, such as Achilles bursitis, plantar fasciitis, talocalcaneal coalition,
painful os trigonum, posterior tibial tendinitis, and pedal edema.
Ankle

88. Patients with OA of the feet most often present with pain of the first metatarsophalangeal
(MTP) joint, particularly with walking. Examination commonly reveals an enlarged joint,
with medial subluxation and lateral deviation of the big toe (bunion deformity). There are
sometimes signs of inflammation over the involved joint, with tenderness and loss of
dorsiflexion.

89. There is often painful and tender swelling of foot joints. Associated
contractures of additional toes (cock-up deformity) with loss of plantar fat
pads are often seen. Disabling pain on ambulation may ensue. Pes planus,
with relaxation of the transtarsal ligament and a pronator forefoot
deformity, aggravates the symptoms

90. The talonavicular joint is at the pinnacle of the arch of the foot and is
particularly prone to OA in the dorsal portion of the joint.

95. OA variants
1.Menopausal, inflammatory, nodal, generalized (or erosive) OA.
2.Rapidly progressive hip or knee OA.
3.Neuropathic arthropathy (Charcot’s joints).
4.Diffuse idiopathic skeletal hyperostosis (DISH)

96. This condition is characterized by the formation of bridging enthesophytes in the
spine, as well as enthesophytes and osteophytes in peripheral joints, and people with it
often have OA
DISH

97. No single lab test diagnoses OA by itself
Synovial fluid from patients with OA is usually clear and colorless or with a slight yellow
tinge. The polymorphonuclear leukocyte content is usually less than 2000 cells/mL.
Crystals may be present in as many as 70% of synovial fluid specimens from patients with OA.Although all calcium crystals
have been shown to precipitate inflammation, the relationship of hydroxyapatite and several forms of basic calcium phosphate
to the synovitis that is present in patients is not well established.
Evaluation

98. Cause of Secondary OA Laboratory Test
Underlying joint disease
ESR, CRP raised in inflammatory desease; autoantibodies such as RF and ANA in
connective tissue disease
Systemic metabolic or endocrine disorder
Ochronosis Presence of homogentisic acid in urine which turns black on exposure to light or on
alkalinization
Wilson’s disease Reduced serum caeruloplasmin; increased urinary excretion of copper
Hemochromatosis Raised serum iron; raised serum ferritin
Acromegaly Raised growth harmone with lack of suppression with a glucose tolerance test.
Hyperparathyrodism Raised serum calcium; low phosphate; raised parathyroid hormone levels.
Hypothyroidism Low serum thyroxin; raised thyroid-stimulating hormone Raised serum urate
Neuropathic disorder
Tabes dorsalis Positive VRDL; positive TPHA and FTA-ABS test.
Diabetes mellitus Abnormal glucose tolerance test
Laboratory tests in secondary osteoarthritis

99. Conventional radiography
In OA, subchondral sclerosis and osteophytosis are generally the earliest radiographic
features. They increase with time in both extent and size and precede radiographic joint
space narrowing which occurs at a later stage of the disease
Imaging

100. Pathology
Increased activity of
subchondral bone
Increased activity at the
articular margins
Altered bone
biochemistry
Altered articular cartilage
biochemistry
Cartilage fissuring and
rupture
Early disease
Bone alters early in
the disease due to the
blood supply
Later disease stage
Biomechanically
weaker bone
Early disease stage
Cartilage
biomechanically
weaker
Later disease stage
Focal loss and
removal of Cartilage.
Radiology
Increased subchondral cortical
plate and trabecular thickness
Incresed subarticular
trabecular osteoporosis
Osteophytosis
Remodelling of joint surface,
cyst formation, and later
altered joint alignment
Narrowing of joint space due
to cartilage compression
Loss of joint space
The pathologic features of
osteoarthritis determines the
characteristic radiographics
features

101. a) Pathologic changes in osteoarthritis and the corresponding
characteristic radiographic features visualized in plain
radiographs of joints with early- and late-stage disease.
b) Radiograph of a healthy knee.
c) Radiograph of a knee with late disease showing most of the
features listed in (a).

102. Osteophytes form as outgrowths at articular margins, capsular insertions, and central
articular regions in the unloaded region of joints
Osteophytes

103. Increased subchondral cortical plate thickness and subjacent trabecular sclerosis are
among the earliest changes in OA. Subchondral bone also demonstrates trabecular loss,
which becomes marked with advancing disease and increased local bone turnover results
in younger, less highly mineralized bone.
Radiolucencies noted in the subchondral bone may be juxtaarticular erosions or
subchondral cysts, which tend to occur in more advanced OA at sites of increased
mechanical load and frequently communicate with the articular surface.
Subchondral bone changes

104. Joint space narrowing is focal and not uniform, reflecting asymmetric cartilage loss across
the articular surface.1 This feature can prove useful in distinguishing early OA from other
arthritides such as rheumatoid arthritis.
Joint space narrowing

105. Subchondral bone in OA patients is mechanically weaker than that in individuals with
nonarthritic joints. It is detected radiographically as flattening and increased congruity
between the articular surfaces . With cartilage loss in the load-bearing compartment,
tongue-and-groove corrugation may develop, and with complete loss of cartilage the
subchondral bone is further flattened . Ultimately, the surfaces become deformed, with the
collapse of the bone leading to altered limb alignment and deformity.
Bone remodeling and attrition

106. Imaging in OA

107. The most reliable and reproducible method for imaging the tibiofemoral compartment of
the knee is the standing semiflexed view.
The patellofemoral compartment can be assessed using either a lateral or a “skyline”
(axial) view
Hip radiographs are conventionally taken with the hip in 15 to 20 degrees of internal
rotation.
The optimal view for imaging the hand is a dorsopalmar view with the fingers in line with
the forearm when laid flat on the x-ray detector holder.
Radiographic views

108. Kellgren-Lawrence (KL) grading system remains the most widely used scale to quantify
radiographic OA lesions. The KL system grades radiographic findings on a scale of 0 to 4
by assessing the presence and severity of osteophytes, joint space width, subchondral bone
sclerosis, and deformity of bone contour.
Radiographic grading systems

109. Discordance among radiographic change, clinical symptoms, and the degree of disability
experienced by patients;
Relation to clinical features

110. At present, given the absence of structure-modifying therapies, MRI has little use in the
routine clinical management of OA
MRI OA of the knee can be defined as the presence of both full-thickness cartilage loss
and definite osteophyte formation
MRI

111. The most common MRI-detected subchondral bone abnormality is manifested as a high-
signal area seen on fat-suppressed T2-weighted or short tau inversion recovery (STIR)
sequences and has been referred to as a bone marrow lesion (BML)
Changes noted on MRI

112. Coronal T2-weignt fat suppressed magnetic resonance image
of the knee demonstrating bone marrow lesion and cartilage
loss on both sides of the medical joint.
The medical meniscus is markedly degenerate with
maceration and abnormality increased signal (straight
arrow) compared with the normal lateral meniscus (curved
arrow). Abnormally increased signal is also seen on both
sides of the medical collateral ligament (arrowheads).

113. Changes noted on MRI
Subchondral bone marrow changes
Bone attrition
Cartilage abnormalities
Fibrocartilage and ligament abnormalities
Synovitis and joint effusion
Erosion
Osteophytes

114. US has been shown to be more accurate than radiography at detecting cortical erosions in
inflammatory arthritis
US can detect early bone changes in OA as a hyperechoic signal in the area of the
attachment of the joint capsule to the bony cartilaginous margin. This corresponds with the
eventual appearance of osteophytes seen on the conventional radiograph
Ultrasound

115. US readily demonstrates joint effusion and synovitis, although this is easier in some joints
than in others
Synovitis and effusion were particularly prevalent in those with erosive OA rather than
nonerosive OA

116. Sonogram of the knee joint (taken
longitudinally through the suprapatellar
pouch). The anterior cortex of the femur is
shown (black arrow head). A knee joint
effusion (Eff) and synovitis are apparent in the
suprapatellar pouch (white arrows)

117. US is more sensitive than clinical examination at detecting
synovial hypertrophy and effusions, and US detection of gray-
scale synovitis has been validated against arthroscopic biopsy
results and MRI detection of synovitis in large-joint OA.

118. US is highly operator dependent, and adequate training is required.
The current roles of US in OA may be acting as a tool for guiding intraarticular injections,
helping to differentiate OA from inflammatory diseases, and confirming the presence of
osteophytes to support a diagnosis of OA.
Clinical use of ultrasound

119. CT does not yet have an established role in OA trials or clinical practice and has the
drawbacks of low soft tissue contrast and radiation exposure.
Particularly effective at depicting cortical bone and may be useful when detailed
presurgical planning is required. CT has an established role in assessing facet joint OA of
the spine. CT arthrography, using a contrast medium, has the ability to clearly image the
articular surface of a joint, and this technique is comparable to MRI for qualitative
assessment of knee cartilage.
Computed tomography / Computed tomographic arthrography

120. Assessment of pain
The instruments most often used to date to evaluate pain in OA include both generic pain
measures, most notably a visual analogue scale or numeric pain rating scale,12 the McGill
Pain Questionnaire,13 and the SF-36 bodily pain scale,14 and arthritis-specific measures,
including the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC)
pain scale (specific to hip and knee OA)15 and the Australian-Canadian Hand
Osteoarthritis Index (AUSCAN; specific to hand OA)
Physical function :The most commonly used generic measure for hip and knee OA is the
physical function subscale of the SF-36
Outcome measurement

121. Measure ICF Domain
Impairments Activity limitation Participation restriction
Generic Measures
SF-36 Pain +Stiffness Physical Functioning Social functioning.
Arthritis- and osteoarthritis-specific measures
WOMAC Pain+
Stiffness
Pain++
Physical function
KOOS/HOOS Symptoms
Stiffness Pain
Quality of life.
Pain
Function, daily living
Function, Sports and
recreational activities
Quality of life+
Lequesne indices Pain + Stiffness ADL knee
ADL hip++
Pain++
Walking
ADL hip+
OAKHQOL Pain / Sleep
Mental health
Physical Activity Social activities
ICF Domains assessed by selected outcomes measures.

122. No Disease
Preclinical
Biochemical markers
Preradiographic
Sensitive imaging
markers
Radiographic
Progression
markers
Preclinical OA
Primary Prevention
(no detected disease)
Secondary Prevention
(those with serologic
abnormalities, not just
traditional risk factors).
Tertiary Prevention
(those with disease).
OSTEOARTHRITIS CONTINUUM AND TREATMENT

123. Pathogenesis

124. ACTIVATED INNATE
IMMUNITY AND
IMPAIRED WOUND
HEALING
POTENTIATORS
INSULTS
Activated
Macrophages
Complements
Alarmins
Extrinsic Inciting Agents
Macroinjury
Microinjury
Environment
Intrinsic Risk Factors
Age
Obesity
Gender
Genetic susceptibility
Level of repair and innate
immune responses OA
Preclinical Preradiographic Radiographic
This model depicted osteoarthritis (OA) as
a condition incited by the mechanical
insults of microinjury, macroinjury, and
environmental factors. The interaction of
extrinsic inciting insults with potentiating
intrinsic factors determines the relative
susceptibility to progression of disease
mediated by a biologic innate immune
inflammatory reasons. Analogous to a
chronicle wound. The resulting pathology
is a manifested first as a preclinical (not
clinically recognizable) entity. With
progression in some individual to
Preradiographic stages (detected by
sensitive imaging modalities) and
eventually to readiographic stages. The
interacting cogwheels, able to turn
intermittently depict the penchant for OA
activity to wax and wane. The exact timing
of the onset of the illness of OA that
includes symptoms in this continuum of
OA pathogenesis is unclear at present.

125. Pathogenesis and pathology of osteoarthritis

126. Joint Destruction
Primary (No major causative
reasons known )
Secondary
Articular gout Bone infarction
Endocrine disorder
(e.g.,hyperparathyroidism, hypothyroidism)
Hemophilia
Intraarticular infections
Joint instability (e.g., ligament and
meniscus)
Neuropathic arthritis (e.g., Charcot joint)
Overload causing excessive wear (Work,
Sports, Varus or Valgus deformity)
Paget disease Trauma

127. In osteoarthritis (OA) the articular
cartilage is lost or severely thinned,
the (subchondral) bone is sclerotic,
the joint capsule is thickened, and
the synovial membrane is activated.
(Courtesy E.Bartnik, Frankfurt.)
Scheatic view of the main structures of a healthy (left) and
osteoartritic (right joint.)

128. Macroscopic
appearance of the
femoral condyles of
a normal knee.
Femoral condyles of
a severely damaged
knee.
Arthroscopic image
of a cartilage defect
of the femoral
condyle within the
knee joint.

129. Conventional histologic
preparations show fibrillation
and matrix los in
osteoarthritic (OA) cartilage
(b) compared with normal
cartilage (a). In severely
damaged areas nearly all
articular cartilage is
destroyed. Also a moderate
(d) to severe (e) loss of
proteoglycans blue staiming.
Besides changes in articular
cartilage, changes in the
subchondral bone plate (f)
compared with normal (c).

130. The lymphocytic infiltrate in the subsynovial stroma appears to correlate directly with
interleukin-1β (IL-1β) in the synovial fluid as well as matrix metalloproteinase-1
expression by synoviocytes, which suggests a direct stimulatory role of the inflammatory
cells on the activity of the synovial lining cells. The presence of inflammation in a
significant portion of OA patients points to the option of antiinflammatory therapy for
some subsets of OA patients.
Inflammatory OA

132. The hallmark of OA cartilage degeneration is a loss of
cartilage matrix homeostasis.

135. CHONDROCYTE BEHAVIOR

136. Interaction between synovium and cartilage in OA

139. Chondrocytes sense and respond to mechanical stimuli transmitted through the matrix. The
mechanical forces are recognized by mechanoreceptors such as integrins and stretch-
activated ion channels. Activation of these transmembrane molecules by physiologic
mechanical loads results in stimulation of a series of regulatory molecules and intracellular
signal cascades including FAK, PKC, JAK/STAT and MAP kinases that ultimately leads
to changes in gene expression and protein production. Thus an anabolic response is
produced that maintains, and in some circumstances improves, cartilage structure and
function.
Response to mechanical forces

140. Anabolic responses resulting in increased expression of aggrecan and inhibition of
protease production involve α5α1 integrin and release of locally acting mediators that
include interleukin-4 and substance P.

141. In contrast, overloading induces a stress response with molecular and biomechanical
changes that shift the balance of tissue remodeling in favor of catabolic over anabolic
activity

142. Stimulation of stress-induced intracellular pathways leads to the production of
proinflammatory cytokines such as IL-1 and TNF-α and increased production of MMPs
and aggrecanases. Interestingly, chondrocytes from OA cartilage show an altered
responsiveness to mechanical loads because they fail to show an anabolic response to
physiologic loading but instead demonstrate a proinflammatory IL-1β-dependent response.
This may further accelerate disease progression and attenuate cartilage repair.

143. Relevance of the genetic aspects of OA joint disease is still under debate.
Genetics

146. There are many different hypotheses that try to explain cartilage and joint degeneration,
including chronic mechanical (over)load, matrix proteolysis, age-induced changes in the
cartilage matrix and the chondrocytes, and increasing damage to the genomic DNA of the
chondrocytes leading to a deranged cellular phenotype.
Biomechanical factors are essential in the pathogenesis of OA. Altered joint biomechanics
are generated by joint incongruity, laxity, muscle weakness, and impaired proprioception
in addition to trauma and heavy physical load.
The production of proinflammatory cytokines as well as the activation of cellular
inflammatory signaling pathways, including interleukin-1 and the MAP kinases, likely
play an important role in OA pathogenesis.
Summary

147. Question