NAVICULAR DISEASE. 345 



trivial accident. In other instances the destructive process is 

 limited (see No. 4, Fig. 61, page 343) by ossification of the 

 cancellated spaces limiting the boundaries of the cavities by 

 a more or less solid osseous wall. Not only are the natural 

 areolae of the interior structures solidified, but the vascular canals 

 within the trabeculse are blocked up by osseous material, the more 

 effectually to arrest the process of destruction ; and for the same 

 purpose, and to limit motion as much as possible, the tendon be- 

 comes adherent to the bone. This adhesion of the tendon occurs 

 in two ways : — 1st. Its fibres are lacerated and present loose ends. 

 These are imprisoned by lymph thrown out from the exposed 

 interior of the bone, and are united to it by a new connecting 

 fibrous tissue. 2d. By the formation of a false membrane, 

 which is very vascular, similar to that already described 

 (Goodsir's false membrane), extending from the synovial fringes, 

 both on the inferior surface of the bone, and superior surface 

 of the tendon, creeping by slow degrees over the whole articu- 

 lar surfaces, destroying their smoothness, and becoming a bond 

 of union between them. In some specimens all semblance 

 to a bursa has been destroyed by the parts becoming completely 

 united together, and secretion of synovia, being no longer 

 required, has entirely ceased. In the earlier stages the synovial 

 secretion seems to be augmented, and this was considered by 

 Professor Dick to give rise to the fulness which is sometimes 

 observable in the hollow of the heel. In some rare instances 

 the navicular and pedal bones become anchylosed by spicules of 

 bone from the inferior border and extremities of the navicular, 

 and from the posterior part of the pedal bone. 



The changes in the tendon are indicated by, first, softening 

 and fibrillisation of its superior surface ; the splitting up is not 

 altogether due to friction against the roughened surface of the 

 diseased bone, but to degeneration of the structure of the ten- 

 don, from the inflammatory action having extended to it from 

 the bone, and increased vascularity ctf its connecting tissue. 

 This splitting up or rupture of the fibres is manifested by the 

 surface of the tendon being covered by tufts of loose, stringy, 

 whitish fibres, with their free extremities floating in the secre- 

 tion of the synovial membrane, until an exudate is formed, by 

 which they are at a later stage united to the bone. 



The synovial membrane, at a very early stage, is involved in 



