Bone formation and growth (hormones and minerals) Endochondral & Intramembranous ossification




Zone of resting

Zone of proliferating cartilage

Zone of hypertrophied cartilage

Zone of calcified cartilage

Newly formed part of diaphysis.

A bone fracture (sometimes abbreviated FRX or Fx, Fx, or #) is a medical condition in which there is a break in the continuity of the bone. A bone fracture can be the result of high force impact or stress, or trivial injury as a result of certain medical conditions that weaken the bones, such as osteoporosis, bone cancer, or osteogenesis imperfecta, where the fracture is then properly termed a pathologic fracture.

Although broken bone and bone break are common colloquialisms for a bone fracture, break is not a formal orthopedic term.


In orthopedic medicine, fractures are classified in various ways. Historically they are named after the doctor who first described the fracture conditions. However, there are more systematic classifications in place currently.

All fractures can be broadly described as:

Closed (simple) fractures are those in which the skin is intact

Open (compound) fractures involve wounds that communicate with the fracture, or where fracture hematoma is exposed, and may thus expose bone to contamination. Open injuries carry a higher risk of infection.

Other considerations in fracture care are displacement (fracture gap) and angulation. If angulation or displacement is large, reduction (manipulation) of the bone may be required and, in adults, frequently requires surgical care. These injuries may take longer to heal than injuries without displacement or angulation.
Compression fractures usually occurs in the vertebrae, for example when the front portion of a vertebra in the spine collapses due to osteoporosis (a medical condition which causes bones to become brittle and susceptible to fracture, with or without trauma).

A greenstick, buckle or torus fracture is a fracture in a young, soft bone in which the bone gets eaten away and partially breaks. This is owing in large part to the thick fibrous periosteum of immature bone. A person's bones become harder (calcified) and more brittle with age and the periosteum becomes thinner and less restrictive. Greenstick fractures usually occur most often during infancy and childhood when bones are soft. The name is by analogy with green (i.e., fresh) wood which similarly breaks on the outside when bent. There are three basic forms of greenstick fracture.

In the first a transverse fracture occurs in the cortex, extends into the mid portion of the bone and becomes oriented along the longitudinal axis of the bone without disrupting the opposite cortex.
The second form is a torus or buckling fracture, caused by impaction.
The third is a bow fracture in which the bone becomes curved along its longitudinal axis.

Signs and symptoms of Greenstick fracture

Some clinical features of a greenstick fracture are similar to those of a standard long bone fracture- greenstick fractures normally cause pain at the injured area. As these fractures are specifically a pediatric problem, an older child will be protective of the fractured part and babies may cry inconsolably. As per a standard fracture, the area may be swollen and either red or bruised. Greenstick fractures are stable fractures as a part of the bone remains intact and unbroken so this type of fracture normally causes a bend to the injured part, rather than a distinct deformity, which is problematic.

Other types of fracture are:

Complete fracture: A fracture in which bone fragments separate completely.

Incomplete fracture: A fracture in which the bone fragments are still partially joined. In such cases, there is a crack in the osseous tissue that does not completely traverse the width of the bone.

Linear fracture: A fracture that is parallel to the bone's long axis.

Transverse fracture: A fracture that is at a right angle to the bone's long axis.

Oblique fracture: A fracture that is diagonal to a bone's long axis.

Spiral fracture: A fracture where at least one part of the bone has been twisted.

Comminuted fracture: A fracture in which the bone has broken into a number of pieces.

Impacted fracture: A fracture caused when bone fragments are driven into each other.


Bone healing, or fracture healing, is a proliferative physiological process in which the body facilitates the repair of a bone fracture.

Generally bone fracture treatment consists of a doctor pushing dislocated bones back into place via relocation with or without anaesthetic, stabilizing their position, and then waiting for the bone's natural healing process to occur.


In the process of fracture healing, several phases of recovery facilitate the proliferation and protection of the areas surrounding fractures and dislocations. The length of the process depends on the extent of the injury, and usual margins of two to three weeks are given for the reparation of most upper bodily fractures; anywhere above four weeks given for lower bodily injury.

The process of the entire regeneration of the bone can depend on the angle of dislocation or fracture. While the bone formation usually spans the entire duration of the healing process, in some instances, bone marrow within the fracture has healed two or fewer weeks before the final remodeling phase.

While immobilization and surgery may facilitate healing, a fracture ultimately heals through physiological processes. The healing process is mainly determined by the periosteum (the connective tissue membrane covering the bone). The periosteum is one source of precursor cells which develop into chondroblasts and osteoblasts that are essential to the healing of bone. The bone marrow (when present), endosteum, small blood vessels, and fibroblasts are other sources of precursor cells.

Phases of fracture healing

There are three major phases of fracture healing, two of which can be further sub-divided to make a total of five phases;

1. Reactive Phase
i. Fracture and inflammatory phase
ii. Granulation tissue formation

2. Reparative Phase
iii. Cartilage Callus formation
iv. Lamellar bone deposition

3. Remodeling Phase
v. Remodeling to original bone contour


After fracture, the first change seen by light and electron microscopy is the presence of blood cells within the tissues adjacent to the injury site. Soon after fracture, the blood vessels constrict, stopping any further bleeding. Within a few hours after fracture, the extravascular blood cells form a blood clot, known as a hematoma. All of the cells within the blood clot degenerate and die. Some of the cells outside of the blood clot, but adjacent to the injury site, also degenerate and die. Within this same area, the fibroblasts survive and replicate. They form a loose aggregate of cells, interspersed with small blood vessels, known as granulation tissue.


Days after fracture, the cells of the periosteum replicate and transform. The periosteal cells proximal to the fracture gap develop into chondroblasts which form hyaline cartilage. The periosteal cells distal to the fracture gap develop into osteoblasts which form woven bone. The fibroblasts within the granulation tissue develop into chondroblasts which also form hyaline cartilage. These two new tissues grow in size until they unite with their counterparts from other parts of the fracture. These processes culminate in a new mass of heterogenous tissue which is known as the fracture callus. Eventually, the fracture gap is bridged by the hyaline cartilage and woven bone, restoring some of its original strength.

The next phase is the replacement of the hyaline cartilage and woven bone with lamellar bone. The replacement process is known as endochondral ossification with respect to the hyaline cartilage and bony substitution with respect to the woven bone. Substitution of the woven bone with lamellar bone precedes the substitution of the hyaline cartilage with lamellar bone. The lamellar bone begins forming soon after the collagen matrix of either tissue becomes mineralized. At this point, the mineralized matrix is penetrated by channels, each containing a microvessel and numerous osteoblasts. The osteoblasts form new lamellar bone upon the recently exposed surface of the mineralized matrix. This new lamellar bone is in the form of trabecular bone. Eventually, all of the woven bone and cartilage of the original fracture callus is replaced by trabecular bone, restoring most of the bone's original strength.


The remodeling process substitutes the trabecular bone with compact bone. The trabecular bone is first resorbed by osteoclasts, creating a shallow resorption pit known as a "Howship's lacuna". Then osteoblasts deposit compact bone within the resorption pit. Eventually, the fracture callus is remodelled into a new shape which closely duplicates the bone's original shape and strength. The remodeling phase takes 3 to 5 years depending on factors such as age or general condition


[Match the phases of bone healing, the i - v stages within the 3 phases with the diagram above]




From Wikipedia, the free encyclopedia
Osteolysis refers to an active resorption of bone matrix by osteoclasts as part of an ongoing disease process.

Osteolysis in joint replacement

While bone resorption is commonly associated with many diseases or joint

problems, the term osteolysis generally refers to a problem common to artificial joint replacements such as total hip replacements, total knee replacements and total shoulder replacements. Osteolysis can also be associated with the radiographic changes seen in a person with bisphosphonate-related osteonecrosis of the jaw.
There are several biological mechanisms which may lead to osteolysis. In total hip replacement the generally accepted explanation [1] for osteolysis involves wear particles (worn off the contact surface of the artificial ball and socket joint). As the body attempts to clean up these wear particles (typically consisting of plastic or metal) it triggers an autoimmune reaction which causes resorption of living bone tissue. Osteolysis has been reported to occur as early as 12 months after implantation and is usually progressive. This may require a revision surgery (replacement of the prosthesis).

Although osteolysis itself is clinically asymptomatic, it can lead to implant loosening or bone breakage, which in turn cause serious medical problems.

Distal clavicular osteolysis

Distal clavicular osteolysis (DCO) is often associated with problems weightlifters have with their acromioclavicular joints due to high stresses put on the clavicle as it meets with the acromion. This condition is often referred to as "weight lifter's shoulder". [2]

A common surgery to treat recalcitrant DCO is re-sectioning of the distal clavicle, removing a few millimetres of bone from the very end of the bone. [2]


1. Sanjeev Agarwal (2004). "Osteolysis - basic science, incidence and diagnosis".

Current Orthopaedics 18: 220±231.

2. D E Schwarzkopf R, Ishak C, Elman M, Gelber J, Strauss DN, Jazrawi LM (2008).

"Distal clavicular osteolysis: a review of the literature"


Osteosclerosis, an elevation in bone density,[1] is normally detected on a Radiograph as an area of increased opacity; that is, where more mineral is present in the bone to absorb or deflect the X-ray beam. Localized osteosclerosis can be caused by injuries that compress the bone, by osteoarthritis, and


Osteopenia is a condition where bone mineral density is lower than normal. It is considered by many doctors to be a precursor to osteoporosis. However, not every person diagnosed with osteopenia will develop osteoporosis. More specifically, osteopenia is defined as a bone mineral density T-score between -1,-0 and -2,5.


Osteoporosis ("porous bones", from Greek: οστούν/ostoun meaning "bone" and πόρος/poros meaning "pore") is a disease of bones that leads to an increased risk of fracture.[1] In osteoporosis the bone mineral density (BMD) is reduced, bone microarchitecture deteriorates, and the amount and variety of proteins in bone is altered. Osteoporosis is defined by the World Health Organization (WHO) as a bone mineral density that is 2.5 standard deviations or more below the mean peak bone mass (average of young, healthy adults) as measured by DXA; the term "established osteoporosis" includes the presence of a fragility fracture.[2] The disease may be classified as primary type 1, primary type 2, or secondary.[1] The form of osteoporosis most common in women after menopause is referred to as primary type 1 or postmenopausal osteoporosis. Primary type 2 osteoporosis or senile osteoporosis occurs after age 75 and is seen in both females and males at a ratio of 2:1. Finally, secondary osteoporosis may arise at any age and affect men and women equally. This form of osteoporosis results from chronic predisposing medical problems or disease, or prolonged use of medications such as glucocorticoids, when the disease is called steroid- or glucocorticoid-induced osteoporosis (SIOP or GIOP).

Osteoporosis risks can be reduced with lifestyle changes and sometimes medication; in people with osteoporosis, treatment may involve both. Lifestyle change includes diet and exercise, and preventing falls. Medication includes calcium, vitamin D, bisphosphonates and several others. Fall-prevention advice includes exercise to tone deambulatory muscles, proprioception-improvement exercises; equilibrium therapies may be included. Exercise with its anabolic effect, may at the same time stop or reverse osteoporosis. Osteoporosis is a component of the frailty syndrome.


Osteomalacia is the softening of the bones caused by defective bone mineralization secondary to inadequate amounts of available phosphorus and calcium, or because of overactive resorption of calcium from the bone as a result of hyperparathyroidism (which causes hypercalcemia, in contrast to other etiologies). Osteomalacia in children is known as rickets, and because of this, use of the term osteomalacia is often restricted to the milder, adult form of the disease. It may show signs as diffuse body pains, muscle weakness, and fragility of the bones. The most common cause of the disease is a deficiency in vitamin D, which is normally obtained from the diet and/or from sunlight exposure.

Bone and it’s Role in HOMEOSTASIS in progress

Endochondral and Intramembranous Bone Growth has been discussed earlier.

Appositional Bone Growth is another type of Bone Growth which occurs from the periosteum inward,

increasing the bone in thickness. This layer is less fixed than the growth attained by endochondral growth, and this bone can be accessed for an emergency supply of calcium. Calcium can be redeposited when there is an abundance again. The levels of blood calcium determines whether Ca is deposited or withdrawn. Two hormones regulate this process and it can be diagrammatically be depicted as follows.

Hypercalcaemia - Calcitonin

Ca deposition in bone s.a. vertebrae


Parathyroid hormone

1. Stimulates osteoclast activity in resorbing bone

2. Activates Vit D to increase Ca absorption from GIT

3. Increases reabsorption of Ca from renal tubules

The feedback mechanisms in play:
Stimulus: Hypocalcaemia

Receptors cells relay condition to integration centre

Effector: Parathyroid glands

Response: Secretes parathyroid hormone

Targets: Bone - increases osteoclast activity

GIT - Vit D stimulated to increase Ca absorption

Kidneys - increased reabsorption of Ca from renal tubules

Monitoring: Receptors cells relay condition

Feedback: Negative - When very close to normocalcaemia PTH secretion will be halted
The effect of calcitonin on bone redeposition is very limited, unlike previously thought, thus not much calcium is returned to particularly bone shafts. (Vander, Sherman, Luciano 1994 Human Physiology Sixth Ed(Int) , McGraw-Hill, USA)