Hans K. Uhthoff

Calcifying tendinitis: a new concept of its pathogenesis.

To elucidate the pathogenesis of calcifying tendinitis, clinical and morphological investigations were done on 46 surgically treated cases. Contrary to the prevalent concept of degeneration preceding dystrophic calcification, we found no evidence for an active or a healed degenerative process. The affected tendon was transformed into fibrocartilage with a predilection for calcification. The formative phase of calcification was followed in course of time by a resorptive phase during which the deposits were surrounded by phagocytosing cells. There was a concomitant proliferation of vascular channels. We found a significant correlation between severe pain and histological signs of resorption. The pathogenetic mechanism of calcifying tendinitis should be reassessed as a unique disorder of the musculotendinous cuff.

Internal plate fixation of fractures: short history and recent developments

Metal plates for internal fixation of fractures have been used for more than 100 years. Although initial shortcomings such as corrosion and insufficient strength have been overcome, more recent designs have not solved all problems. Further research is needed to develop a plate that accelerates fracture healing while not interfering with bone physiology.The introduction of rigid plates had by far the greatest impact on plate fixation of fractures. However, it led to cortical porosis, delayed bridging, and refractures after plate removal. These unwarranted effects were said to be caused by bone–plate contact interfering with cortical perfusion. Consequently, further plate modifications aimed to reduce this contact area to minimize necrosis and subsequent porosis.The advocates of limited-contact plates have not published measurements of the contact area or proof of the temporary nature of the porosis. Moreover, clinical studies of newer plate types have failed to show a superior outcome. Histomor-phometric measurements of the cortex showed no difference in the extent of necrosis under plates having different contact areas. Necrosis was predominant in the periosteal cortical half, whereas porosis occurred mostly in the endosteal cortical half. No positive correlation was found between either.The scientific evidence to date strongly suggests that bone loss is caused by stress shielding and not interference with cortical perfusion secondary to bone–plate contact. Consequently, an axially compressible plate (ACP) incorporating polylactide (PLA) inserts press-fit around screw holes was designed. The bioresorbable inserts should allow for (1) increased micromotion in the axial plane to promote healing during the union phase and (2) gradual degradation over time to decrease stress shielding during the remodeling phase.Results of ongoing experimental results are encouraging. Only plates allowing dynamic compression in the axial plane can lead to a revolution in fracture fixation.

Acromial enthesopathy and rotator cuff tear. A radiologic and histologic postmortem investigation of the coracoacromial arch.

Changes of the coracoacromial ligament (CAL) at its insertion into the undersurface of the acromion were studied radiologically and histologically in 76 autopsy specimens. Two changes were noted: (1) a downward, bony projection of the acromion, an anatomic variant limited to the area covered by the CAL, which might reduce the height of the subacromial compartment, and (2) a thickened layer of fibrocartilage, constituting a potential cause for narrowing of the subacromial space. The former might act as a predisposing factor for the impingement syndrome, whereas the latter could develop in response to pressure from constituents of the subacromial compartment. The acromial spur was a result of enchondral bone formation. A possible correlation between these changes and rotator cuff tears was investigated. The incidence and severity of cuff tears increased with age. However, there was no correlation between aging and degenerative changes of the undersurface of the acromion, except possibly in very advanced cases. Rotator cuff tears are unlikely to be initiated by impingement; rather, they develop as an intrinsic degenerative tendinopathy.

PATHOLOGY OF FAILURE OF THE ROTATOR CUFF TENDON

In failure of the rotator cuff tendon, interference with its function prevents the rotator cuff from fulfilling its physiologic role. Trauma in younger individuals, calcifying tendinitis, degenerative changes of cuff tendon, and partial- or full-thickness tears cause cuff failure intrinsically. Degenerative changes constitute the most frequent cause of cuff failures and correlate with tendon tearing. An acromial spur, long coracoid process, subacromial bursitis, and thickening of the corocoaromial ligament causes cuff failure extrinsically.

MECHANICAL FACTORS INFLUENCING THE HOLDING POWER OF SCREWS IN COMPACT BONE

1. Cell differentiation around screws manufactured by two American and two Swiss companies and inserted into seventy femora in forty-one adult mongrel dogs has been observed over periods varying between two weeks and nine months. 2. This study reveals that, despite their excellent holding power, such screws are not everywhere in firm contact with the surrounding bone at the time of insertion. Indeed, only part of the thread surface facing the head of the screw touches the compact bone, all other surfaces being separated by a space up to 150 µ in thickness. 3. These spaces result both from the surgical technique employed and from the inaccurate measurements of drills, screws and taps. 4. Migrating cells invade these spaces during the first two weeks. In the absence of movement, these cells differentiate into osteogenic cells; movement leads to differentiation into fibroblasts, chondroblasts and osteoclasts, and failure of fixation ensues. In contrast, callus formation by osteogenic cells firmly anchors screws in four to five weeks, well before callus uniting the bone fragments has been established. 5. Extremities should be protected from undue stresses during those first few weeks after osteosynthesis, whatever the technique. 6. This study clearly demonstrates the importance oftesting screws in living bone to ascertain their holding power at all stages of fracture healing.

Early reattachment does not reverse atrophy and fat accumulation of the supraspinatus--an experimental study in rabbits.

Introduction: Reattachment of the supraspinatus (SSP) tendon after spontaneous rupture leads to improved shoulder function. Whether this improvement of function is due to a reversal of muscle atrophy and fat accumulation known to occur after SSP rupture is still debated. Our previous study of late reattachment of SSP (12 weeks) failed to confirm a reversal of muscle atrophy and of fat accumulation.

Histologic evidence of degeneration at the insertion of 3 rotator cuff tendons: A comparative study with human cadaveric shoulders

We determined on histologic examination the degree of degeneration at the insertion of 3 rotator cuff tendons in 76 cadaveric shoulders, 17 of which had a partial tear of the supraspinatus. Fiber thinning, the presence of granulation tissue, and incomplete tearing of fibers, all evidence of degeneration, were quantified separately for each tendon. Among the shoulders that were intact on macroscopy, no significant difference in degeneration score could be found. In all 3 tendons degeneration was more prominent on the articular sides compared with the bursal sides (P < .0001). The degeneration score of partially torn supraspinatus was significantly higher than that of the intact tendons (P < .0001). The extent of granulation tissue, 1 criterion of degeneration, seemed to contribute mostly to this difference. Intrinsic degeneration occurred foremost in the articular side of the rotator cuff and might constitute the primary cause of rotator cuff tearing.

Intra-articular fractures of the calcaneus.

The results of computed tomography, combined with those of plain radiography, permit comprehensive assessment of the pattern of the fracture and, therefore, accurate classification and possible alteration of the mode of treatment

The development of synovial plicae in human knee joints: An embryologic study

An embryologic study about the development of the human knee joint cavity was carried out with special attention to the formation of synovial plicae, using a total of 116 knees of embryos and fetuses. The incidence of synovial plicae in the fetal stage was also investigated. Formation of joint space starts at the middle of the interzone at around 8 weeks of gestation. Multiple small cavitations around the femoral condyle and patella coalesce to form larger cavitations. At around 10 1/2 weeks, the knee joint consists of a single cavity with synovial lining. At certain sites, such as at the medial part of patello-femoral and the infrapatellar regions, mesenchymal tissue strands remain. They may become plica. In the fetal stage from 11 to 20 weeks, an infrapatellar plica was found in 50% of specimens, a suprapatellar plica in 33%, and a mediopatellar plica in 37%. Only the infrapatellar plica showed a decrease in incidence.

Calcifying tendinitis, an active cell-mediated calcification

Biopsy specimen from 18 patients suffering from calcifying tendinitis were stained with different histologic and histochemical techniques. The results of these examinations seem to indicate that we are not dealing with a dystrophic calcification, but with a cell-mediated calcification of a living tissue. The process resembles an incomplete endochondral ossification. Histologische und histochemische Untersuchungen der Supraspinatussehne von 18 Patienten mit calcifizierender Tendinitis. Der Verkalkungsprozeß wird eingeleitet durch eine Transformation der Tendinocyten in Chondrocyten begleitet von einer Anreicherung alkalischer Phosphatase. In einer zweiten Phase kommt es, unter Mitwirkung der Chondrocyten, zur granulären Verkalkung und gelegentlich auch zur Ossifikation vergleichbar der enchondralen Ossifikation. Für die Annahme einer dystrophischen Sehnenverkalkung ergeben sich keine Hinweise.