Bone Modelling and Remodeling for Vet Rehab Therapists

The skeleton is a dynamic structure that undergoes continuous adaptation in response to mechanical forces. This adaptability is crucial for the performance and longevity of equine and canine athletes, as their bones must withstand significant mechanical stress during training and competition. Bone modeling and remodeling are two fundamental processes that maintain skeletal integrity and optimize bone structure. 

This article explores the principles of bone physiology, the impact of mechanical stress on equine and canine bone adaptation, and how these processes relate to exercise, training and immobilisation.

An exclaimer before we begin: I am currently re-studying my Veterinary Physiotherapy degree through Equine Librium College, and as a second-year student Veterinary Pathophysiology is one of my subjects. This blog was written during the course of my studies, to help me learn through the process of ‘teaching’. I have been using ChatGPT as a tutor and quizbot, and this article was partly written with ChatGPT during an expanded study session. I take full responsibility for the accuracy of the information in this article – everything has been written, rewritten, edited or checked by myself. This information is not a reflection of Equine-Librium College or their course curriculum.

I would love your feedback at the end of the article – do you think this blog is up to our usual standard, better, or lacking in some essentially human ways?

 

Bone Structure and Function in the Athlete

Bone serves multiple functions, including structural support, locomotion, mineral storage, and protection of vital organs. They are categorized into long bones, short bones, irregular bones, and flat bones, with long bones primarily contributing to locomotion. Long bones consist of three primary regions:

• Diaphysis: The main shaft composed of cortical bone, which provides rigidity and strength.
• Metaphysis: The transitional zone between the diaphysis and the epiphysis, rich in trabecular bone. This is where growth plates are located.
• Epiphysis: The widened ends of the bone that form articular surfaces, distributing load to minimize stress concentrations​.

The bone matrix consists of organic and inorganic components. The inorganic component includes hydroxyapatite, a calcium-phosphate mineral providing rigidity and strength. The organic component includes collagen, proteoglycan, glycoproteins and water which provides a measure of elasticity. This composite structure allows bone to be both strong and resilient​.

 

How Bone Develops During Growth

Bone development primarily occurs through two processes: intramembranous ossification and endochondral ossification. Most bones in the equine skeleton form via endochondral ossification, where a cartilage template is gradually replaced by bone.

 

Endochondral Ossification (Growth of Long Bones)

In the embryo, osteoprogenitor cells differentiate into chondrocytes, creating a cartilage template for each bone, or a cartilage model.

The primary ossification center is the first site of bone formation at the center of the diaphysis of long bones.  Blood vessels invade the area, osteoblasts follow the blood vessels depositing bone matrix, and forming the diaphysis or shaft of the bone during fetal development.

Secondary ossification centers form at the epiphysis after birth, allowing growth to occur from the growth plates or physes. This allows the creation of the metaphysis and epiphysis of the bones and longitudinal growth of the bones.

Growth plates contain specialized resting, proliferative, hypertrophic, and ossification zones, where chondrocytes divide, enlarge, mineralize, and are replaced by bone. Growth continues until skeletal maturity when the growth plates close, and the remaining cartilage becomes articular cartilage.

 

Bone Growth in Width (Appositional Growth)

Bone will thicken through appositional growth, where osteoblasts in the periosteum lay down new bone matrix on the external surface of the bone. During this process, osteoclasts will resorb bone from the endosteum or the inner surface of the bone, enlarging the medullary cavity. This process allows bone to strengthen while maintaining it’s proportional shape.

 

Bone Remodeling and Wolff’s Law

Bone remodeling is an ongoing process that allows the skeletal system to adapt to mechanical demands, repair microdamage, and regulate calcium homeostasis. This process involves the coordinated actions of the three main cell types in bone:

1. Osteoblasts – Bone-forming cells that synthesize and mineralize the bone matrix.
2. Osteocytes – Former osteoblasts embedded in bone matrix, acting as mechanosensors to regulate remodeling.
3. Osteoclasts – Large, multinucleated cells responsible for bone resorption, breaking down bone tissue to release minerals.

 

The bone remodeling cycle consists of several phases:

1. Activation: Osteocytes detect mechanical strain or microdamage and signal the recruitment of osteoclast precursors. This process starts within hours of stress, and can last for days.
2. Resorption: Osteoclasts attach to bone surfaces and secrete enzymes that dissolve the mineral matrix, forming resorption pits known as Howship’s lacunae. Bone is at its weakest during this phase as structural integrity is compromised. This process can last for 1-3 weeks.
3. Reversal: A transition phase where mononuclear cells prepare the bone surface for new formation. Osteoclasts undergo apoptosis, and mononuclear cells smooth the resorbed surface. Osteoblasts begin migrating to the site in preparation for new bone formation. The bone remains weaker than normal during this phase as it has not yet been rebuilt. This phase lasts for 1-2 weeks.
4. Formation: Osteoblasts lay down new osteoid (unmineralized bone matrix), which gradually mineralizes. Initially, the new bone is weak and immature (woven bone), but it gains strength as it matures. This phase lasts for 1-3 months.
5. Quiescence: The remodeled bone enters a resting phase until further remodeling is triggered.

Bone remodeling is regulated by mechanical forces, hormonal signals (e.g., parathyroid hormone, calcitonin), and local growth factors (e.g., transforming growth factor-beta, bone morphogenetic proteins).

 

When is Bone at Its Weakest?

Bone is at it’s weakest during the resorption and early reversal phase (weeks 1-5) because old bone is being removed before new bone is sufficiently deposited. Bone regains much of its strength during formation (1-3 months) as new bone is mineralized. Full strength is achieved during quiescence (3-6 months or longer) when the bone fully remodels into a lamellar structure.

 

Wolff’s Law: Bone Adapts to Mechanical Stress

Wolff’s Law, formulated by German anatomist Julius Wolff in 1892, states that bone remodels itself in response to the mechanical stresses placed upon it. This means that bone structure is dynamic and adapts to optimize strength based on the loads it experiences.

Key Aspects of Wolff’s Law:

• Increased Load → Bone Strengthens: When bone experiences greater mechanical stress (e.g., weight-bearing exercise, resistance training), osteoblasts increase bone formation, leading to denser and stronger bone.
• Decreased Load → Bone Weakens: In the absence of sufficient mechanical loading (e.g., immobilization, prolonged rest), osteoclast activity dominates, leading to bone loss (osteopenia or osteoporosis).
• Site-Specific Adaptation: Bone thickens in areas of high stress (e.g., the cortical thickening in a racehorses metacarpus) and resorbs where stress is minimal.

 

How Exercise Impacts Remodelling

Bone is a mechanosensitive tissue, meaning it adapts its structure based on mechanical loading, following Wolff’s Law—bone is deposited where needed and resorbed where not needed.

In young horses exposed to a gradual mechanical load, trabecular bone will become denser and cortical bone thicker. Subchondral bone will strengthen in areas subjected to frequent impact such as the fetlock, carpus, metacarpus and metatarsus. As a result, young horses who have access to free exercise on different surfaces will develop stronger bones that can provide a protective mechanism for future loading.

Training and exercise will stimulate bone modelling and remodelling in response to the loads placed on the bone. An increase in exercise intensity will result in enhanced bone mineral density and stronger trabecular structures. High-impact training such as galloping will stimulate remodelling of cortical and subchondral bone. Low-impact training including walking and trotting will maintain bone turnover without excessive stress.

 

Overtraining

Excessive or sudden increases in training load without adequate time for adaptation can result in an accumulation of microdamage. When bone resorption outpaces bone formation, stress fractures or subchondral bone sclerosis can develop. When horses are trained on hard surfaces without adequate recovery periods, they are at a higher risk of developing fatigue fractures.

 

Response to Specific Forces

Bone is a viscoelastic material, meaning its response to forces depends on both magnitude and duration of the load​.

 

Compression

Compression occurs when bone is pushed together, such as in weight-bearing areas.

Compression stimulates osteoblasts to deposit more bone, particularly in trabecular regions such as the subchondral bone in joints and weight-bearing areas of the skeleton​. When a bone experiences high compressive stress, it thickens and strengthens in that region through adaptive remodelling (Wolff’s Law).

Excessive or repetitive compression can lead to subchondral bone sclerosis and fatigue fractures.

 

Tension

Tension forces occur when bone is pulled apart, such as at muscle insertions (e.g., tibial tuberosity, olecranon). Cortical bone is stronger in tension than trabecular bone. While tension can stimulate bone deposition, it more often triggers bone resorption to redistribute forces. In areas of high tensile stress, osteoclasts may remove bone, allowing for structural adaptation. Stress fractures, for example, will always occur on the tension side of a bending force. Avulsion fractures also occur as a result of tension forces from a tendon pulling on a bony attachment point – instead of thickening, these areas can weaken over time when overloaded.

 

Combined Forces: Bending and Shear

Many bones experience both compression and tension simultaneously. The dorsal metacarpal cortex in galloping horses undergoes compression on one side and tension on the other, leading to conditions like dorsal metacarpal disease (bucked shins)​. Shear forces, common in joints, can lead to cartilage degradation and osteoarthritis.

 

Forces in Summary:

Compression → More Bone Formation

Tension → Less Bone Deposition, More Remodeling.

Combination of Both (Bending) → Adaptation to Load Distribution

 

This is why trabecular bone becomes denser in weight-bearing areas (compression) and why tensile areas are more prone to stress fractures rather than hypertrophy.

 

Conclusion

Bone modeling and remodeling are vital processes that shape and maintain the equine skeleton in response to mechanical stress. Understanding these processes allows veterinary physiotherapists to optimize training protocols, minimize injury risk, and manage bone-related pathologies effectively. By implementing evidence-based conditioning programs, proper nutrition, and regular veterinary assessments, equine athletes can achieve peak performance while maintaining long-term skeletal health.

 

The author generated this text in part with ChatGPT. The author reviewed, edited, and revised all generated content and takes ultimate responsibility for the content of this publication.