Elsevier

The Journal of Hand Surgery

Volume 34, Issue 8, October 2009, Pages 1429-1435
The Journal of Hand Surgery

Scientific article
Correlations Between Clinical Presentations of Adult Trigger Digits and Histologic Aspects of the A1 Pulley

https://doi.org/10.1016/j.jhsa.2009.05.015Get rights and content

Purpose

We aimed to report by light microscopy the normal histology of the A1 pulley, describe the histologic abnormalities of A1 pulleys in trigger digits, and look for possible correlations between these findings and the severity of the disease.

Methods

In a series of 104 trigger digits operated on in 80 adult patients, the A1 pulleys were removed and histologically studied. The findings were compared with 55 normal A1 pulleys obtained from fresh-frozen cadaveric specimens.

Results

The normal A1 pulley was composed of 3 layers: layer I, an inner, avascular, concave unicellular or bicellular gliding layer containing cartilage-like cells; layer II, a middle layer, also avascular, characterized by spindle-shaped fibroblasts; and layer III, an outer, richly vascularized layer, continuous with the membranous tendons sheath. We used a 3-grade classification, increasing in severity, to describe the histologic abnormalities observed in trigger digit A1 pulleys. Mild abnormalities (grade 1) were those with a fibrocartilaginous gliding surface almost intact. The margin between the fibrocartilaginous and membranous portions of the pulley was well delineated. In moderate abnormalities (grade 2), the avascular fibrocartilaginous gliding surface appeared fissured and thinner. The inner layer (I) was interrupted and replaced by fibrous tissue, with fissures that did not cross through the middle layer (II). A mild vascular network hyperplasia was observed in the outer layer (III), which began to invade the fibrocartilage. In severe abnormalities (grade 3), the fibrocartilaginous gliding surface was thin, discontinuous, or even completely destroyed. The vascular network hyperplasia became excessive and reached the synovial space of the flexor tendon sheath. The histologic features were correlated with the severity of the clinical symptoms (p < .001).

Conclusions

The histologic abnormalities observed in the A1 pulley of trigger digits are characteristic and not related to inflammation. As the trigger digit worsens, the gliding surface begins to wear and is gradually replaced by a secondary invasive hyperplasia from the outer layer. These abnormalities could be caused by a modification or an increase of the mechanical stresses along the flexor tendons.

Section snippets

Materials and Methods

We obtained 55 normal A1 pulleys from all digits of 11 fresh-frozen adult cadaver hands. The proximal border of the pulley was at the metacarpophalangeal skin crease of the thumb, proximal palmar crease of the index finger, halfway between the proximal and distal palmar creases for the long finger, and distal palmar crease for the ring and little finger.11 To recognize the distal border of the pulley, we searched for the separation between the A1 and A2 pulleys, present in 95% according to

Results

In normal A1 pulleys, we observed a 3- layer structure (Fig. 1A, B). The innermost layer (I), forming the gliding surface in contact with the flexor tendons, was characterized by collagen bundles oriented parallel to the long axis of the digit. Ovoid cells (cartilage-like cells),8 arranged in a unicellular or bicellular layer, were strongly stained with Alcian blue. They were grouped in a striking linear orientation with the long axis of the collagen bundles (Fig. 1C). The immediately palmar

Discussion

The precise histologic structure of the normal flexor tendon pulleys has not been well established in the literature. Amis and Jones5 reported that the membranous portion of the sheath has no insertion on the proximal or distal borders of the annular pulleys. In contrast, Lundborg and Myrhage7 observed that the membranous portion inserts on the palmar superficial surface of the pulleys. A concept of 2 layers, 1 superficial, membranous portion and 1 deep, fibrocartilaginous retinacular layer,

References (34)

Cited by (0)

No benefits in any form have been received or will be received related directly or indirectly to the subject of this article.

View full text