X Ray Core pathology: Is it a hard of soft callous during bone healing?Question.
A healthy young man suffered a fracture of the tibia and fibula 6 weeks ago, which has been treated in a below elbow plaster cast. The cast is removed at fracture clinic for repeat X-ray. Which of the following statements is correct regarding the pathophysiology of bone repair at this stage in fracture healing?

a.bone repair cells differentiate from the bone marrow
b.chondroblasts alone form the initial soft callous
c.osteoblasts lay down lamellar bone before woven bone
d.osteoclasts are not yet present at the fracture site
e.radiologically visible hard callous is produced by osteoblasts

 

 

Answer.
The correct answer is e. Osteoblasts lay down hard callous, which after 6 weeks is sufficiently mineralised to be visible on plain x-ray (fig 1).
 
Explanation.

Like wound healing, healing of a fractured bone occurs in distinct but overlapping stages. These are the reactive phase, the repair phase and the remodelling phase. The repair phase is often subdivided into the soft callous and hard callous phases.

Additional points to note are:
• the periosteum is well innervated and produces the severe pain of bone fracture.
• bone is also well vascularised. Nutrient arteries penetrate the bone cortex passing into the medullary cavity to supply the inner 2/3rds of mature bone. The outer 1/3rd of bone is supplied with blood from periosteal vessels via capillaries in the haversian canals.
• The pluripotent cells of the periosteum and endosteum differentiate into the cells required for bone repair – chondroblasts, osteoblasts and osteoclasts.

The first event in fracture healing is bleeding and subsequent formation of a haematoma at the fracture site. The following phases then occur,

1. Reactive phase (0-7 days)
Within a few hours post-fracture a haematoma develops at the fracture site. Numerous inflammatory cells – neutrophils, macrophages and lymphocytes – migrate into the haematoma and generate an inflammatory response. Over the course of a few days, fibroblasts infiltrate the fracture haematoma and lay down new granulation tissue between the bony ends.

2. Repair phase

a. Soft callous phase (4 days to 3 weeks): Cytokines and growth factors released during the inflammatory response stimulate nearby periosteal cells to divide and differentiate into chondroblasts and osteoblasts. Fibroblasts and chondroblasts migrate into the new granulation tissue and produce hyaline cartilage, a simple form of cartilage consisting mostly of type II collagen and chondroitin sulphate. Osteoblasts similarly relocate and secrete woven bone, a mineralised but structurally weak form of bone characterised by highly disorganised collagen fibres. The mass of newly synthesised hyaline cartilage and woven bone expand from both bone ends to loosely unite the bone with soft callous.

b. Hard callous phase (2 to 6 weeks): Osteoblasts differentiate from periosteal progenitors in greater numbers and act to resorb the woven bone replacing it with much stronger and harder lamellar bone (where the collagen is arranged in ordered sheets). After 6 weeks or so, hard callous is radiologically visible and is usually sufficiently strong to allow recovery of function (clinical union). The hard callous closely resembles the trabeculae of cancellous bone.

3. Remodelling phase (6 weeks to a year)
Bone remodelling begins in the latter half of the repair phase and continues well beyond clinical union. Osteoclasts (bone resorbing cells) migrate from the periosteum into the fracture callous and resorb the weak lamellar and trabecular bone. Osteoblasts activity continues with secretion of mature bone matrix and mineral to form the hardest form of bone, compact bone. Remodelling over time also refashions the gross bone appearance as close as possible back to its original shape.