Knee osteoarthritis

Dr. Zahraa Hussein

Epidemiology
 Osteoarthritis (OA) is by far the most common form of arthritis
and is a major cause of pain and disability in older people.

 The prevalence rises progressively with age and it has been

estimated that 45% of all people develop knee OA at some
point during life.
 marked increase in prevalence among women after 50 years.

 Radiographic and symptomatic knee OA were more common

among African Americans compared with white people.
 At the knee, Osteoarthritis (OA)
principally targets the
patellofemoral and medial
tibiofemoral compartments, but
eventually spreads to affect the
whole of the joint.
 It may be isolated or occur as part
of generalized nodal OA.
 Most patients have bilateral and
symmetrical involvement.
 Pathophysiology
 OA is a complex disorder, with both genetic and environmental
components.
 Degeneration of articular cartilage is the defining feature of OA.
 Chondrocytes in OA start dividing to produce nests of metabolically active
cells, Initially, producing matrix components at an increased rate.
 But there is ↑ degradation of the major structural components of cartilage
matrix, including aggrecan and type II collagen.
 Then concentration of aggrecan ↓ and makes the cartilage vulnerable to
load-bearing injury →Fissuring of the cartilage surface then occurs →
development of deep vertical clefts, localized chondrocyte death and
decreased cartilage thickness.
 This is initially focal( maximum load-bearing part of the joint), but
eventually large parts of the cartilage surface are damaged.
 Subchondral bone becomes sclerotic + subchondral cysts.
 Fibrocartilage is produced at the joint margin, which undergoes
endochondral ossification to form osteophytes
 Hyperplastic synovium and may be the site of inflammatory change.
 The outer capsule thickens and contracts, usually retaining the
stability of the remodeling joint.
 The muscles surrounding affected joints commonly show evidence of
wasting and non-specific type II fiber atrophy.
Clinical features
 The main presenting symptoms are pain and functional
restriction.
 The pain is usually localized to the anterior or medial aspect
of the knee and upper tibia.
 Patello-femoral pain is usually worse going up and down
stairs or inclines.
 Posterior knee pain suggests the presence of a complicating
popliteal cyst (Baker’s cyst).
 Prolonged walking, rising from a chair, getting in or out of a
car, or bending to put on shoes and socks may be difficult.
 Physical examination
 a jerky, asymmetric (antalgic) gait with less
time weight-bearing on the painful side
 a varus or, less commonly, valgus and/or a
fixed flexion deformity
 joint-line and/or periarticular tenderness
(secondary anserine bursitis and medial
ligament enthesopathy, causing tenderness
of the upper medial tibia)
 weakness and wasting of the quadriceps
muscle
 restricted flexion and extension with
crepitus
 bony swelling around the joint line.
 Investigations
 OA is diagnosed clinically, and laboratory testing is rarely required.
 A plain X-ray of the affected joints, standing anteroposterior X-rays
taken to assess tibio-femoral cartilage loss and a flexed skyline
view to assess patello-femoral involvement.
 providing diagnostic information + assessing the severity of
structural change, which is helpful if joint replacement surgery is
being considered.
 typically show osteophytes, joint space narrowing, sclerosis, and
cysts of subchondral bone.
Normal knees x-rays
Radiographic OA is at least twice more common than symptomatic
OA
 Management
 Education: nature of the condition, risk factors such as obesity, heredity and
trauma and prognosis (better for knee than hip OA).
 Lifestyle advice: Weight loss, exercises, Shock-absorbing footwear, pacing of
activities, offload braces, foot orthotics, walking stick, and built-up shoes to
equalize leg lengths.
 Occupational therapy
 Local physical therapies
 Pharmacological therapy: If symptoms do not respond to non-pharmacological
measures, paracetamol should be tried. Addition of a topical NSAID and then
capsaicin can also be helpful. Oral NSAIDs should be considered in patients who
remain symptomatic. These drugs are significantly more effective than
paracetamol and can be successfully combined with paracetamol or compound
analgesics if the pain is severe.
 Nutraceuticals: Chondroitin sulphate and glucosamine sulphate
:can improve knee pain to a small extent (3%–5%) compared
with placebo.
 Intra-articular glucocorticoid injections: are effective in the
treatment of knee OA.
 Surgery:
 considered for patients whose symptoms and functional
impairment impact Significantly on their quality of life despite
optimal medical therapy and lifestyle advice.
 Total joint replacement surgery is by far the most common
surgical procedure.
 ANTERIOR CRUCIATE LIGAMENT
 Origin: lateral femoral condyle
 Insertion: anterior and between the
intercondylar eminences of the tibia.
 two bundles: anteromedial and
posterolateral.
 It prevents anterior translation of the tibia
relative to the femur
 Anterior displacement of the tibia is
resisted by the anteromedial bundle of the
ACL, while the posterolateral part tightens
as the knee extends.
ANTERIOR CRUCIATE LIGAMENT INJURY
 The ACL is one of the most frequently injured structures in the
knee, particularly in women.
 Common mechanisms of injury include a direct blow to the
lateral side of the knee (the “clipping” injury in football) , as
well as noncontact injuries that occur during cutting, pivoting,
and jumping. (axial-loading twisting injury on a slightly flexed
knee)
 Risk factors include joint hypermobility, genetic
predisposition, elevated BMI and increased tibial slope.
 Clinical features
 Patients often report an audible “pop” accompanied by the acute
onset of knee swelling.
 The bleeding associated with ligament rupture will cause an acute
hemarthrosis and the patient will describe swelling almost
immediately.
 Pain deep in the knee joint.
 Initial inability to weight bear, "give way", especially during pivoting
movement
 Multiple tests have been described to evaluate the ACL. The most
sensitive tests for diagnosis of an ACL injury include the anterior
drawer, and Lachman.
 Imaging
 Plain X-rays: may reveal associated fractures or bony
avulsions that can occur in conjunction with a ligament injury.
 Magnetic resonance imaging: is the gold standard imaging
tool for the assessment of knee ligament injuries.

 Computed tomography: have high specificity and sensitivity

in detecting ACL disruption. It helps characterize the avulsed
bone fragment when it is present.
 Treatment
Treatment individualized to patient based on activity level, age,
demands, and concomitant pathology.
 Nonoperative: physical therapy, bracing and lifestyle
modifications. Indicated for low demand patients or recreational
athlete not participating in cutting/pivoting activities.

 Operative: ACL reconstruction: for patients with persistent

symptomatic instability in order to provide a functionally stable
knee with reduced potential for secondary injury and long-term
morbidity.
Prognosis

 Natural history: ACL deficient knees believed to lead to an

accelerated progression of arthritis.

 Survival with treatment:

 near complete restoration of native kinematics following
reconstruction.
 high level of return to sport at all levels of competition.
COMMON PERONEAL NERVE (COMMON FIBULAR
NERVE)
 It is one of 2 major branches off the sciatic
nerve (in the distal posterior thigh proximal
to the popliteal fossa) and receives fibers
from the posterior divisions of L4 through
S2 nerve roots.
 The nerve curves around the fibular neck
before dividing into two branches:
1- superficial peroneal nerve:
 Motor: Lateral compartment (Peroneus
longus and Peroneus brevis) and
 Sensory: Anterolateral distal third of the leg and the
majority of the dorsum of the foot (except the first
webspace).
2- deep peroneal nerve: Motor: Anterior compartment
(Tibialis anterior, Extensor hallucis longus, Extensor
digitorum longus, and Peroneus tertius), and Sensory: First
dorsal webspace.

 These two nerves are essential in the eversion of the foot

and dorsiflexion of the foot, respectively.

 Common peroneal nerve: Sensory: lateral aspect of the

leg just distal to the knee.
 COMMON PERONEAL NERVE INJURY
Etiology
 Trauma or injury to the knee: Knee dislocation, direct impact, penetrating
trauma, or laceration, Fracture of the proximal fibula.
 Anatomic risk factors: a fibrous band at the origin of the peroneus longus.
 External compression sources: Tight splint/cast, Compression
wrapping/bandage, Habitual leg crossing, Prolonged bed rest, Positioning
during anesthesia and surgery.
 Intraneural ganglion
 Peripheral nerve tumor
 Iatrogenic injury
 systemic illnesses: Diabetes mellitus, Inflammatory conditions
Epidemiology

 Commonest mononeuropathy encountered in the lower limbs

and the third most common focal neuropathy encountered
overall, after median (carpal tunnel syndrome) and ulnar
neuropathies.

 Traumatic injuries most commonly afflict young athletic

patients (e.g., football, soccer) and adult patients following
high energy trauma (e.g., motor vehicle collisions).
 Clinical presentation
 The most common presentation: weakness of ankle dorsiflexion and
the classic resultant foot drop or catching the toes while ambulating.
 Foot drop can develop acutely or over days to weeks, depending on
the etiology.
 Numbness or paresthesia present along the lateral leg, dorsal foot,
and/or the first toe webspace.
 Pain may also be present in traumatic cases but is not always
present.
 High steppage gait to prevent dragging their toes on the ground due
to nerve injury.
 Evaluation
 When the history and physical examination is indicative of a
potential injury to the common peroneal nerve, plain radiography
should be part of the initial workup.
 CT scans can be used to evaluate further osseous abnormalities,
and MRI/ultrasound can be used to assess soft-tissue sources or
masses.
 Electrodiagnostic studies, including nerve conduction velocity
(NCV) tests and electromyography tests (EMG), can be used to
diagnose peroneal nerve palsy. They are also helpful in the
localization of nerve injury.
Treatment
 Non-operative treatments include ankle-foot orthoses and
physical therapy.
 Direct injuries of the common peroneal nerve and its
branches should be explored and repaired or grafted
wherever possible.
 Traction injuries from a knee dislocation may damage the
nerve over a large length, needing a graft so long that
recovery is hopeless. Splintage and tendon transfers are
required.
Prognosis
 Prognosis depends on etiology.
 Some transient common peroneal nerve neuropathies often
improve or resolve over time with nonsurgical measures.
 common peroneal nerve palsy following traumatic knee
dislocations results in inferior outcomes with a poor prognosis
long-term recovery of nerve function.