Findings:
Image 1 is an axial STIR. Image 2 is a coronal T1.

The arrows on image 1a identify fluid surrounding the biceps tendly. The arrowhead identifies the biceps tendon, which demonstrates slightly increased signal.

The arrows on image 2a are identifying a normal variation appearance to the trochlear notch. See the section on articular cartilage abnormalities.

Diagnosis:
Tendinosis/tendonopathy of the biceps tendon, with associated paratendinitis and cubital bursitis.

Discussion:
In adults, the myotendinous junction is usually the weakest point and typically tendon strength fails at the myotendinous junction in adults. In children, muscle and tendon strength as well as ligament and capsular attachment site strength are greater than the strength in the unfused apophyses, and therefore avulsion injuries result.

However, in adults most tendon failures of the distal biceps tendon are surprisingly not at the myotendinous junction, but are within the distal substance of the tendon at or near the radial tuberosity insertion. This may be due to several factors. Repetitive mechanical impingement of the distal biceps tendon on the radius and ulna occurs. The space between the radius and ulna narrows by approximately half in the pronation position. Also, the distal one centimeter portion of the biceps tendon is believed to be less well vascularized.

These factors, as well as aging, degeneration, and repetitive stresses lead to underlying biceps tendon degeneration/tendinosis and an abnormal arrangement of collagen fibers in the distal biceps tendon. Instead of inflammatory cells and healing collagen fiber deposition, which are produced in a more acute injury, fibroblasts are produced in this more chronic repetitive stress environment. As the collagen fibers tear, scar tissue is deposited and a weaken tendon is produced. See image 3.

It is thought that the small tears that are produced with too much activity are not able to properly heal because of the environment of constant strain and overuse, which continually re-injures the tendon. Scar tissue is alternatively produced by the angiofibroblastic reaction. The tendon weakness that results is due to partial thickness tendon tears which have not properly healed with collagen fibers, but which have healed with fibrous scar, in a failed tendon healing response. Histologically, partial thickness tendon tears are seen in the presence of the angiofibroblastic reaction. Moreover, chronic renal disease, steroid use, and diabetes are believed to weaken tendons.