Dr.

Tag
Knee

Normally:
Children are born with genu varum then as they stand and walk, it transfers to
genu rectum then genu varus within the age of 2-3 years old.
NB: Abduction: Distal segment moves away from the Axis.
Adduction: Distal segment moves to the Axis
Valgum: Distal segment moves away from the midline.
Varum: Distal segment moves towards the midline.
This only classified in this way happens on the level of Toes and fingers, because the midline and axis
are separated.

Physiological Varum:

Physiological genu varum is associated with wide BOS, because the tibia is
perpendicular on the ground. Tibia is perpendicular on the ground, because knee
and ankle are modified hinged joint, so to make provide normal weight bearing in
compression and make the joints leveled, which will prevent loading with shear.
While in pathological genu varum, it is associated with narrow BOS, which is
because of the diagonal orientation of the tibia on the floor.

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Wide BOS Narrow BOS
Stability More Stability Less Stability
Grace Lesser Grace Better Grace
(Shape of the Gait)
Energy Expenditure High Energy Expenditure Less Energy Expenditure
( To move COG from Rt.
to Lt.) 1
Age During the age of Genu After the disappearance
Varum of Genu Valgum ER
NB: Genu valgum does not form except after standing and walking.

Analysis of quadriceps force on the knee joint:

Quadriceps muscles exerts an extension moment on the tibia in addition to an
abduction moment that aims to cause joint deformation, This is mainly the cause
of the formation of genu valgum. If it continues, it should cause massive OA due
to the crushing of articular surfaces toward each other.
But this does not happen, because of THE PATELLA

Functions of the patella:

1- Deflection of the valgus stress of the quadriceps from the tibia to the
patellofemoral joint.

Stability of PFJ:
(A) Bony:
1- Shape of the patella: Congruency of patella2 with the trochlea anchors
the patella on the femur and prevent its lateral movement, so it is ready
to deliver the forces applied on it by the quadriceps to the tibia as pure
extension forces.
2- Height of the patella: Normal height of the patella provide normal
patellar tracking3 then prevent the liability to dislocate by the lateral

1
Translation of COG during gait happens in an angulatory (Sinusoidal) shape:
From Rt. to Lt: If you are looking from the horizontal plan, its magnitude depends on the size of BOS.
Up and down: If you are looking from the sagittal plan.
2
Its Wedge shape
3
While the quadriceps is exerting its highest tension, the patella exists in the deepest part of the trochlear groove
and vice versa

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Knee
tracking forces applied by the quadriceps, because it is too deep and
congruent to dislocate4. (at about 30° knee flexion)
3- Size of the patella: Normal size of the patella, that is occupying the
trochlear space, is very important for its stability5.
4- Normal size, height and shape of the trochlear sulcus.

(B) Soft tissue:

1- Ligaments: MPFL and LPFL:
(α) Medial: From the medial corner of the patella to the adductor
tubercle. It is horizontal in direction to resist lateral subluxation
(β) Lateral: From the lateral corner of the patella to the ITB.
2- Muscles:
(α) Quadriceps: It has five heads, and the most important part is VMO,
because its attachment of the patella is almost horizontal, so it will
make medial pull on the patella and stabilize it against the lateral pull
of the quadriceps.

4
In case of patella alta, patella become more shallow during the maximum quadriceps tension, so lateral patellar
dislocation may happen
5
Dysplastic patella is one of the most known causes of PFJS/D

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NB: The high compress forces across the patellofemoral joint that is due to the
contraction of quadriceps, is prevented by the anterior tibial step off6.

Patella
Lateral side is higher than the medial side, which makes the lateral side higher
than the medial side and the tibia internally rotated. It also meets the lateral
femoral condyle, which all prevent subluxation laterally7.
NB: PCL tear is associated with PFPS because of the loss of the step off causing
more compressive forces on the patella and pain in the patellofemoral joint (As it
is a disease of disability not instability).

Patellofemoral joint instability (PFJI):

Types: 1- Congenital 2- Traumatic 3- Habitual 4- Recurrent
Traumatic Patellar instability:
MOI: By pivoting (Change of direction 180° suddenly or cutting (Change of
direction 90°)
Causes:
1- Increase in Q angle due to the internal rotation of the patella associated
with femoral internal rotation (Dynamic increase of Q angle >> Increase in
valgus vector due to increase the forces on the horizontal axis >> Patellar
subluxation if it was in shallow position)
Treatment:
1- Restore the normal position of the patella, then put the patient in a cylindrical
extension cast for 8 weeks to allow healing of the soft tissue of the knee.
2- In case of recurrent dislocation >> Reconstruction of the medial
patellofemoral ligament.

6
It is 1 cm anterior translation of tibia on the femur, its function is decreasing the compression forces caused by
the quadriceps contraction on the patellofemoral join it near to full extension (for the first 30° of flexion).
7
High lateral forces on the lateral part of the patella is normalized by bigger surface area of the lateral side more
than the medial side.

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Knee

Habitual:
There is no pathoanatomy, but the patient suffers from abnormal pattern of of
quadriceps activation due to abnormal quadriceps wiring ( Lateral part of the
quadriceps is activated more than the medial part >> Leads to shift of the line of
force laterally >> Increase of Q angle >> Subluxation)
Treatment:
Electrical reeducation of the quadriceps muscle.

Recurrent:
Patellofemoral joint instability recognizable abnormality in joint stabilizers or
abnormal stresses on the joint.
(A) Abnormal stresses:
(α) Increased IR of femur due to persistently high femoral anteversion8,
associated with patella in >> Apex of Q angle become more medial >>
Increase in Q angle
(β) Pathological genu valgum
(γ) ITB contracture >> Leads to IR of the tibia >> Increases the Q angle
(ζ) Patella Alta (Supra): Increases Q angle and puts the patella in the shallow
part during the period of high quadriceps tension >> Patellar instability.
(B) Abnormal Stabilizers:
(α) Hypoplastic patella or patellar groove
(β) Patella Alta
(γ) Hypoplastic lateral femoral condyle
(ζ) Ligamentous laxity (MPFL) >> E.g. Down syndrome
(θ) Absent VMO

8
Means anterior twisting of the head of femur.

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Knee

S/SX of recurrent instability

1- Apprehension (Anxiety form experiencing impending dislocation), mainly at
any position that requires rotation (Rounding of corners)
2- Giving way, which cause falling due to loss of the extensor mechanism of
quadriceps due to its inhibition.

Post-diagnostic tests
Patellar tracking test: Ask the patient to do full flexion.
Positive findings: patellar mal-tracking ( J sign9).
Patellar apprehension test: The examiner places the knee to be examined into full
extension or semi-extended (20°). A lateral force is applied to the medial edge of
the patella with the examiner's thumb.
Positive finding: Apprehension

Radiological examination:
Lateral X-ray: For assessing patellar height.
Using Lateral Salvati method:
Height of the patella from the upper pole to the lower pole equal to the height from
the lower pole to the tibial tuberosity.(1:1).
If the latter is more than the first, then the patella is in higher position (Patella
Alta10).
Skyline view (Multiple level, till 120° knee flexion): For assessing the PFJ itself.
Disadvantage: Expose patient’s genitalia to a lot of radiation.

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The J-sign refers to the inverted ‘J’ track the patella takes from extension to early flexion (or vice versa) in a mal-
tracking patella. The laterally subluxated patella suddenly shifts medially as it engages the trochlear groove of the
distal femur. The J-sign on clinical examination is suggestive of patellar mal-tracking and potential instability
10
Patella Alta causes recurrent lateral patellar instability and Extensor lag (Which is incomplete active ROM with
the passive ROM maintained), that is caused by active insufficiency.
Active insufficiency: The length between the origin and insertion is less than the length of a fully contracted
muscle. During extension it is prevented by a pump in the distal femur, that raise the patella at the end of the
range and then the lever arm increase to compensate the decrease of the force by riding of the patella in distal
femur. This property is lost in Patella Alta.
Excursion: The distance that the muscle able to short (Difference between fully contracted and fully relaxed
muscle.

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CT Axial (Dynamic Patellofemoral CT scan): By taking multiple knee cut-sections.
Findings:
(A) Trochlear sulcus angle: Normally it is 138±6. If it is less, the sulcus is shallow
(Trochlear sulcus hypoplasia).
(B) Congruence angle: Normally it is -6 to the medial side.

Treatment of PFJI:
According to the Cause:
(A) Treatable:
1- High femoral anteversion >> Femoral derotational osteotomy.
2- Patella alta >> Infrapatellar plication.
3- Genu Valgum >> Medial Closing-Wedge Distal Femoral Osteotomy.
4- ITB Contracture >> ITB release surgery.
(B) Untreatable:
1- Lateral condylar hypoplasty
2- Patellar hypoplasia
3- Ligamentous hyper-laxity.
Treated by Realignment of the extensor mechanism.

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Knee
Proximal Extensor mechanism Distal Extensor mechanism
realignment realignment
(Galeazzi's modified technique for
recurrent patellar instability)
Tenodesis of the semitendinosus Medialization of tibial tubercle >>
tendon: By cutting the semitendinosus Obliteration of Q angle.>> No valgus
from its insertion in pes anserinus, stress on the patella.
move it proximal and attach it through
a tunnel through the quadriceps
tendon above the patella and suture it
into it >> Prevents the lateral patellar
subluxation.
Done in immature patients that are in Done only in mature patients to avoid
high risk of bone growth arrest. bone growth arrest.

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Knee

Genu Valgum/Varum
Facts about normal knee angulation:
Genu Varum after the 3rd year, the child can stand and walk, is considered
pathological.
Genu Valgum before the 2nd year is considered pathological.

(A) Criteria of physiological genu varum:

1- Bilateral
2- Symmetrical
3- Its course is regressive11.
4- Not focal (Gentle and Curvy, Curved tibial shine12,)
5- No clinical nor radiological abnormalities.
6- Child is < 3 Years.
7- Not associated with lateral thrust13 during gait.

Causes of Genu Varum:

1- Rachitic14 Genu Varum:
Rickets Definition: Category of symptoms (body out-crying, Mainly
musculoskeletal symptoms), caused by abnormal levels of Calcium15,
Phosphate and Vitamin D metabolism
Types of rickets:
1- Vitamin D Deficient: It is due to lack of vitamin D in the child metabolism.
Labs: Serum calcium and phosphate are low normal.
Treated by administration of a non-activated form of vitamin D.
2- Vitamin D Dependent: Happens due to a problem in the activation of
vitamin D, mainly due to

11
If Progressive, it is considered pathological
12
If straight tibia, it can be pathological.
13
It happens in case of pathological genu varum, due to laxity of knee lateral collateral ligament, caused by high
load on it in mid-stance during gait and then lead to lateral thrust due to lateral subluxation of knee joint during
mid-stance.
14
Rachitic bone is a painful bone (unlike Primary post-menopausal OP, while secondary is painful).
15
Has both vital job (Contractility of muscles, coagulation, an enzymatic catalyst, the 2 nd most important secondary
messenger in the body after cyclic AMP)

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Knee
(A) A problem in the enzymes that activate it.
(B) End organ insensitivity to the indigenously activated vitamin D.
Labs: Low serum calcium, phosphate. ( In some cases, it can be normal).
vitamin D16 dependent patients is not associated with tetany due to
acidosis17 that is present with those patients.
Treated by administration of an external activated form (Isozyme) of
vitamin D.
3- Vitamin D Resistant: It is mainly due to abnormal serum phosphate level
and it has 2 types:
(A) Hypophosphatemic: Decreased phosphate levels, deficiency in
Hydroxyapatite needed for bone mineralization.
Labs: Calcium18 may be low with it, due to other associate problems
such as lactose intolerance but it is mainly normal, Low serum
phosphate levels
(B) Hyperphosphatemic: Mainly due to renal failure.
Renal failure >> Increase phosphate level in blood>>Block calcium
absorption from the stomach and it will be lost in defecation
process>> decreased serum calcium level >> Stimulating
Parathormon19 >> Vitamin D20 activation in kidney>> Vitamin D
stimulate carrier proteins formation in the intestinal mucosa but it
cannot absorb calcium from the intestine so it tries to restore serum
calcium level by doing bone resorption and also increase the
16
Sources of Vitamin D: Diet, Sun exposure and dietary supplement. Recommendation of WHO is to give Vitamin D
supplements from 2 Months to school age (4 years old), to replace the amount needed by sun exposure then again
at senior age (45 Years) till death.
17
Because there is an inverse relationship between calcium level and PH level, due to the retention of H+ ions in
the body, decreasing blood PH, Increasing the level of free calcium, preventing tetany.
18
Balance between calcium and phosphate: For calcium to be absorbed, carrier proteins that are made by
activated form of vitamin D should be present. Vitamin D itself needs parathormon to be activated and
parathormons are released only in case of low serum calcium. (Facilitated diffusion of calcium)
So, any problem involves calcium absorption, is mainly related to vitamin D.
Phosphate deficiency are not common as calcium deficiency (Highly available in diet and enters blood by simple
diffusion).
Calcium and phosphate level is regulated by kidney (phosphate is moved out of the body and reabsorb what only
the body needs, so in case there is phosphate problem, there is a problem in the kidney)
19
Increase serum calcium level while decreases serum phosphate level >> Encouraging calcium absorption.
20
Increase remolding cycle (decrease serum calcium level while increase phosphate level) >> Inhibiting calcium
absorption but stimulate the osteoclastic activity and bone remolding.

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phosphate excretion through kidney >> Osteoporosis21 ( because
whatever the calcium that will be provided from the bone, it cannot
provide the daily requirements of calcium , so hypocalcemia will
persist.
Labs: Hyperparathyroidism, Low serum calcium levels.
So in this case, the patient suffers from Vitamin Hyperphosphatemic
resistant rickets, secondary hyperparathyroidism, secondary
osteoporosis and renal failure.
NB: It is not associated with tetany, because in case of phosphate
retention >> H+ retention will happen >> Acidosis >> Increase free
calcium level >> No tetany.
Difference between the administrated types of vitamin D22:
1- Non-activated type:
(A) Inexpensive
(B) Can be stored in the body
(C) Used in the treatment of vitamin D deficient type of rickets.
2- Activated isozymes of vitamin D:
(A) Expensive
(B) Cannot be stored in the body.
(C) Used in the treatment of vitamin D dependent type of rickets.

NB: Solubility product: simplified equilibrium constant defined for equilibrium

between a solids and its respective ions in a solution.
If Calcium × phosphate concentration in blood is > solubility product, they will not
be sedimented. (As in Blood)
If Calcium × phosphate concentration in blood is < solubility product, they will be
sedimented in bone for mineralization. (As in Bone).

21
Osteoporosis (Rickets): Bone mass is normal, but every unit is under mineralized, while osteomalacia bone is
normally mineralized but with low bone mass.
22
In case of inability to identify the type, treatment start with giving the patient the non-activated form of vitamin
D, and if there are signs of healing on the X-ray, it is considered as the dependent type. If it is not, labs should be
done to know if it is deficient or resistant type.

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Solubility product is affected by PH, as PH increase (Alkaline), as the solubility
product decrease and as PH decrease (Acidic) as the solubility product increases23.

Clinical Picture of Rickets:

MSK Manifestations:
1. Myopathy like appearance (Sluggish gait with positive Gower’s sign),
caused by calcium deficiency.
2. Severe muscle weakness that is more proximal than distal.
3. Buddha Posture.
4. Very irritable to touch or movement, due to pain in bone and muscle.
5. Obese child.
6. Face: Craniotabes24 and Caput Quadratum25.
7. Chest: Pigeon Chest.
8. Diaphragm: Harrison sulcus26.
9. Abdomen: Belly abdomen and rachitic catback deformity27, due to
weak abdominal muscles.
10.Limbs: Rachitic Genu Varum (Not before 3 years).
Rachitic Genu Varum Rachitic Genu Valgum
 Rickets developed in neonates.  Rickets developed later in
(Sometimes because polycystic age, 8 years is the most
kidney disease). common age (after the
 More Common, children are development of standing and
very vulnerable for vitamin D walking).
deficiency.  Caused by renal failure.
 Less Common.

11- Bone Cupping or fraying (Cupped Metaphysis): Due to

undermineralizedbone >> Caused by calcium resorption from the bone.

23
That is what makes prostatic metastasis (Secreting acid phosphatase) osteolytic.
24
Softening or thinning of the skull in infants and children, which may be normally present in newborns. It is seen
mostly in the occipital and parietal bones. The bones are soft, and when pressure is applied they will collapse
underneath it.
25
Rounded prominence of the frontal and parietal bones in an infant’s cranial vault.
26
horizontal groove along the lower border of the thorax corresponding to the costal insertion of the diaphragm
(out-flared lower chest).
27
Long, smooth dorsal kyphosis.

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Bone Growth:
Width: By intramembranous ossification.
Length: By Inchondral ossification, How?

Physeal plate28 forms chondrocytes by the division of germinal zone of cells in the
direction away from blood supply (forming the proliferative zone) >>as a
continuation of cell division, Ischemia happens in the distant cells due to the
increasing distance between the cells and BS and cells increase in size (hypertrophic
zone) >> More ischemia that leads to cell death and explosion then deposition of
calcium forming a layer called (zone of provisional calcification) that is rich with
blood supply >>> Osteoclasts formation from monocytes >>> Remove of the dead
cartilage and stimulate the osteoblastic activity>> Bone formation.

In Rickets.
The development arrests at the zone of hypertrophy, due to the inability to deposit
calcium. So in Rickets, Findings on X-ray are:
(A) In case of active Rickets:
1- Wide Physeal Plate.
2- Loss of the provisional zone of calcification29.
(B) In case of Healing Rickets:
1- Decrease in Physeal plate width. (But still not normal)
2- Zone of provisional calcification appears.
(C) In case of Healed Rickets
1- Normal Physeal plate width
2- Provisional calcification appears as a thin line.

28
Slipped epiphysis normally happens in normal children at the weak point between the layer of provisional
calcification and zone of hypertrophy (Stress riser). In rickets there is no documented cases of slipped epiphysis
due to higher matrix ratio in the zone of division and informed zone of hypertrophy.
Stress riser: It is a point at which there is a change in the mechanical structure, direction, mechanical properties
and tissue formation (It is the point that at which failure happens in case of high change in the previously
mentioned properties).
29
Normally it appears as a thin bright line at the level of metaphysis (brighter than the original bone).

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Treatment:
(A) Nonsurgical:
1- Deficient: Administration of Inactive Vitamin D
2- Dependent: Administration of active endogenous form of vitamin D.
3- Resistant:
(A) Hypophosphatemic: Administration of inorganic Phosphate
(B) Hyperphosphatemic: Renal dialysis or transplantation then treat rickets.
(B) Surgical:
NB: Active rickets and rachitic genu varum is not treated surgically before the
rickets is healed and remodeling arrest (Arrest in the changes, decrease, in the
intercondylar distance). ICD30 is measured every 3 months. In case of arrest of ICD
for 6 months, surgery is indicated.
1- Wedge osteotomy.
Disadvantage: 1- High risk of compartment syndrome, so fasciotomy should
be accompanied with it.
2- High risk of overcorrection ( Genu Valgum).

30
Intercondylar distance.

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2- Partial temporary Epiphysiodesis31
Disadvantage: Parents aren’t satisfied, because the correction is not
immediate.
(C) Criteria of physiological genu valgum32:
1. Bilateral.
2. Symmetrical.
3. Not before the age of 2 years old.
4. Focal.
Why is it focal?
To align the mechanical axis of tibia with the
mechanical axis33 of the femur, which will allow
the normal transfer of weight.
5. Disappear with knee flexion34
6. Not associated with any clinical or radiological
abnormalities.
NB: 1- How to locate the origin of pathological genu valgum:
1- Femoral origin: If valgum disappears with knee flexion.
2- Tibial origin: if valgum persists with knee flexion.
3- Mixed combined origin: If valgum does not disappear but only decreases
with knee flexion.
4- Mixed contradictory origin: If valgum is present with knee extension but
increases with knee flexion (in this case the defect in tibia was compensated
by a defect in the femur, and its effect disappeared with flexion).
2- The angle between:
(A) Mechanical axis of femur and tibia >> 0
(B) Anatomical axis of femur and tibia >> Q angle (14° in male, 17° in female).

31
Epiphysiodesis is the surgical ablation of a physis to stop its future growth
32
It is exaggerated at the age of 4-7 years then decrease again to normal (7°) till the age of 70 years. Then due to
mild osteoarthritis in the medial compartment of the knee, mild genu varum develops due to loss of the cartilage
>> Wider BOS. It is commonly associated with kyphotic posture to lower COG near the ground and provides more
stability (it also prevents SC stenosis by the increased the spinal canal wideness, caused by spinal flexion).
33
It is the line which along it the bone is loaded.
34
It appears only in extension, because of the difference in size between anterior parts medial and lateral
condyles, causing the valgum to appear in normal extended position. But flexion posterior femur become the more
apparent part of the articulating surface of the femur, causing valgum to disappear.

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Causes of pathological genu valgum:

Cozen's phenomenon (Post traumatic genu valgum), due to:
(A) Proximal tibial metaphysial fracture.
(B) Post-corrective osteotomy for genu varum, due to overgrowth of the
medial side of the physis.

Treatment:
Medial partial temporal epiphysiodesis.
NB: No surgery in case of active rickets.

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