Histomorphologic Changes of the Long Head of the Biceps Tendon in Common Shoulder Pathologies

Abstract

To assess molecular and histologic differences between the proximal (intra-articular) and distal (extra-articular) portions of the long head of the biceps (LHB) tendon in 3 different disease states (biceps instability, tendinosis, and degenerative joint disease [DJD]) compared with a healthy tendon (fresh frozen). We used 32 LHB tendons of patients undergoing tenodesis (mean age, 54.7 ± 10.1 years) and 9 harvested tissue donors. Tendons were divided according to 4 diagnostic groups: (1) biceps instability, (2) tendinosis, (3) DJD, and (4) normal control. After sectioning, tendons were fixed in formalin and stained with H&E and alcian blue for histologic analysis. Measurements of collagen organization by use of polarized light microscopy was then performed, and protein expression for type I and type III collagen, tenascin C, and decorin was determined. There were no statistical differences found for protein expression of type I or type III collagen, tenascin C, or decorin. The proximal and distal regions of the tendons had statistically significant differences in alcian blue staining, with the proximal portion containing a higher amount of proteoglycan (instability, P = .001; tendinosis, P = .005; DJD, P = .008; control, P = .011). When compared with the nonpathologic control tendons, a significant increase in alcian blue staining for the proximal region was seen in all 3 groups. Total polarized light analysis showed that the distal tendon had a significantly higher intensity (organization) compared with the proximal tendon (P < .001); this was also seen in all of the diagnostic groups (instability, P = .010; tendinosis, P = .013; DJD, P = .07; control, P = .028). This study showed a greater degree of degeneration of the proximal (intra-articular) regions of the LHB tendon when compared with the distal regions in all pathologic groups. However, no major differences at the cellular level were found among groups. The pathomechanisms of the various forms of known LHB diagnoses are not yet fully understood and basic science studies may help in understanding their etiology and therefore optimizing treatment options.