all about knee OA

1. Tugas Mini-Cex

2. Quadriceps angle (Q-Angle)
Khasawneh RR, Allouh MZ, Abu-El-Rub E (2019) Measurement of the quadriceps (Q) angle with respect to various body parameters in young Arab population. PLOS ONE 14(6): e0218387. https://doi.org/10.1371/journal.pone.0218387
• The quadriceps angle (Q angle), formed between the
quadriceps muscles and the patella tendon
• supply very useful information concerning the
alignment of the pelvis, leg, and foot
• normal Q angle should fall between 12 and 20
degrees; the males are usually at the low end of this
range; while females tend to have higher
measurements (ec wider pelvis)
• the values should be as low as 10 degrees or >20°to
reflect problems
Center of
patella
Weight-bearing position

3. Quadriceps angle (Q-Angle)
• excessive Q angle  excessive pronation of the foot  excessive
internal rotation of the tibia  change the quadriceps pull and
lateral tracking of the patella
• Value  based on gender and height (weight factor not
significant)
Khasawneh RR, Allouh MZ, Abu-El-Rub E (2019) Measurement of the quadriceps (Q) angle with respect to various body parameters in young Arab population. PLOS ONE 14(6): e0218387. https://doi.org/10.1371/journal.pone.0218387

4. Risk of patellofemoral pain female>male

5. Abnormal Gait in OA
• Antalgic gait  stance phase pada sisi sakit < sisi
sehat untuk mengurangi beban axial loading
pada painful knee
• Stride length and walking speed are
decreased in OA (attempt to reduce pain by
minimizing the impact on their knees)
• The gait of knee OA patients is also
characterized by higher knee adduction
moment (KAM), a marker of medial joint
loading and known risk factor for progression
of OA  varus thrust saat stance phase
•Relationship between foot function and medial knee joint loading in people with medial compartment knee osteoarthritis DOI: 10.1186/1757-1146-6-33

6. Gait deviation in knee OA
PFOA has been found to be independently
associated with quadriceps muscle weakness 
quadriceps weakness gait
attempt to reduce pain by limiting the external
knee flexion moments and compressive loading of
the PF joint  knee remain extend in loading
response
Altered Gait Biomechanics and Increased Knee-Specific Impairments in Patients with Coexisting Tibiofemoral and Patellofemoral Osteoarthritis doi:10.1016/j.gaitpost.2014.08.014

7. Source of Pain
• Sources of joint pain may be classified into
two anatomic categories:
• articular structures
• joint capsule with synovial membrane/synovium
(filled by synovial fluid)
• Subchondral bone
• Meniscus
• ACL and PCL
• periarticular structures (structures superficial
to the joint capsule).
Lamberson, M., & Lowery-North, D. (2012). Joint pain. In S. Mahadevan & G. Garmel (Eds.), An Introduction to Clinical Emergency Medicine (pp. 437-448). Cambridge: Cambridge University Press.
doi:10.1017/CBO9780511852091.038

8. Joint cartilage
principal function  provide a smooth,
lubricated surface for articulation and to
facilitate the transmission of loads with a low
frictional coefficient
composed of a dense extracellular matrix
(ECM) with a sparse distribution of highly
specialized cells called chondrocytes
ECM 
- water, collagen, and proteoglycans
- noncollagenous proteins and glycoproteins
(smaller amount)
Lack of blood vessels, lymphatics, and nerves
 limited capacity for intrinsic healing and
repair
STZ  superficial Tangensial Zone, tensile area (ec tight collagen) and resist shear force
Middle  first line to resist compressive force
Depp  main area to resist compressive force (ec high proteoglycan)

9. Intra-articular problem

10. Source of Pain
• OA-related pain is the result of a complex
interaction between local tissue damage,
inflammation, and the peripheral and
central nervous systems
• Pain mechanism  nociceptive and
neuropathic
• stimulation of peripheral nociceptors 
three fibers: myelinated Aδ (group III) and
unmyelinated C fibers (group IV),
myelinated Aß fibers (group II)

11. • myelinated Aδ (group III) and unmyelinated C fibers (group IV
synovial membrane, joint capsule, periarticular ligaments, menisci,
adjacent periosteum and subchondral bone (activated by noxious
mechanical, chemical or thermal stimuli)
• myelinated Aß fibers (group II)  synovial membrane, joint capsule,
periarticular bursae, fat pad, ligaments, menisci and adjacent bony
periosteum (activated by joint movement)
• BUT cartilage is avascular and aneural, and so damaged cartilage
cannot generate pain directly

12. • Degeneration cartilage in OA  matrix degradation  inflammation
marker (cytokines (e.g. tumor necrosis factor) and mediators (pro-
inflammatory interleukins, chemokines, nerve growth factor,
leukotrienes, prostaglandins and matrix metalloproteinases)) release
in joint  peripheral sensitization, stimulation nociceptive primary
afferent neuron, hyperexcitability of nociceptive neurons in the
central nervous system
• Local joint damage leads to the involvement of peripheral nerves 
neuropathic pain

13. The bone changes in OA usually occur in two phases:
1. destructive phase (i.e. bone eburnation and/or deformation and cyst
formation, especially at level of the joint exposed to pressure)
2. productive phase (i.e. progressive remodeling, such as osteophytes).

15. Diagnostic Criteria (ACR)
Presence of knee pain along
with at least 3 of 6 items:
Age>50 years old
Morning stiffness < 30 minutes
Crepitus on knee motion
Bony tenderness
Bony enlargement
No palpable warmth
•Presence of knee pain with at
least 1 of 3 items along with
osteophyte in knee X-Ray:
•Age > 50 years old
•Morning stiffness < 30
minutes
•Crepitus on knee motion
•Presence of knee pain along with at
least 5 of 9 items:
Age > 50 years old
•Morning stiffness < 30 minutes
•Crepitus on knee motion
•Bony tenderness
•Bony enlargement
•No palpable warmth
•ESR<40mm/hr
•RF<1/40
•Synovial fluid compatible with OA:
clear, viscous, leucocyte
<2000//mm2