1
Background
In 1921, Sinding–Larsen and Johansson described a syndrome in adolescents that associated pain at the distal patella with fragmentation of the patellar pole on X-rays [ ]. At one point, Sinding–Larsen–Johansson syndrome (SLJS) was considered as type I bipartite patella [ ].
SLJS is a type of osteochondrosis that is histologically similar to Osgood-Schlatter disease (OSD) [ ] and caused by repeated traction microtrauma and excessive prolonged stress occurring on a particular skeletal region which is mechanically weak.
This syndrome appears when stress applied during sports activity exceeds intrinsic resistance and repair capacities of the bone tendon junction unit.
SLJS typically occurs in adolescent males between 10 and 14 years of age [ ].
The diagnosis is not always obvious. SLJS is used as a general term for all pain conditions at the pole of the patella, but its etiology remains unclear.
In this syndrome, pain is due to abnormal motion of the synchondrosis area that appears mainly after repeated microtrauma in adolescent athletes [ ]. This theory was based on research in patients with cerebral palsy as a high incidence of SLJS was found in this population ranging from 11% to 28% [ , ], among these spastic patients, 57% had coexisting OSD without a documented injury event.
The histology of SLJS is very similar to OSD, but it is very different from type II or III bipartite patella [ ].
Patients can be treated conservatively by immobilization or surgically with loose fragment excision [ ]. Pain generally disappears with appropriate conservative treatment, allowing for rapid return to sports activities. Surgical treatment can be considered if the conservative treatment fails [ ].
2
Clinical Study
2.1
Symptoms
The affected child usually complains of pain at the tip of the patella. This symptom could have appeared either progressively or brutally, and in this case, it impairs sports activities.
A history of knee trauma can be found, but most often it is minimal. The onset of pain can follow a live impulse such as a jump or a sprint [ ].
This pain is characterized by an increase in intensity during flexion combined with loading of the knee joint.
2.2
Physical Examination
The main clinical features on physical examination are swelling of the infrapatellar soft tissues and knee range of motion (ROM) limitations [ ].
Palpation of the patellar tip, forced flexion of the knee, and resisted contraction of the quadriceps awaken the pain.
If the condition is present for a long time, there may be an amyotrophy of the thigh.
In case of acute symptoms, the examiner can note a swelling of the knee with local inflammation signs [ ].
Frequently, there is a retraction of the rectus femoris muscle associated with an increased heel-buttock distance ( Fig. 13.1 ).
It is important to examine the tip of the contralateral patella since this affection is quite often bilateral and can remain functionally asymptomatic.
Likewise, the palpation of the tibial tuberosity can reveal pain in relation with an associated OSD since, as mentioned earlier, the association of the two diseases in the same subject is possible [ ].
3
Differential Diagnosis
The differential diagnosis of SLJ disease includes:
3.1
Sleeve Fracture
A history of knee trauma is usually found.
3.2
Osteochondritis Dissecans (OCD)
Pain and swelling of the knee often initiated by sports or physical activity are the most common initial symptoms of OCD. Advanced cases may present with joint catching or locking.
3.3
Stress Fracture of the Patella
This fracture usually occurs after an increase in the intensity of training. The patient may report a sudden onset of a sharp anterior knee pain.
3.4
Patellar Tendinopathy
Pain in the anterior aspect of the knee is the first symptom of patellar tendinopathy. This pain is worsened by sports activities that require knee extension. On physical examination, there is tenderness on the proximal insertion of the patellar tendon.
4
Imaging
4.1
Standard X-rays
An X-ray examination may show patellar fragmentation and, in late stages of the disease, calcification of the patellar tendon with possible opacification of the adjacent portions of Hoffa’s fat pad [ ] ( Fig. 13.2 ).
