TIS                         

HARD TISSUE: INJURIES AND HEALING

Bone is a specialized connective tissue, that provides structural support for the soft tissues, and act as levers for movement when acted upon by the various muscles. The ends of most bones form joint surfaces and serve as attachment sites for ligaments (Reid, 1992, p.103).

Articular cartilage is a tissue that covers the ends of long bones in synovial joints, whose primary function is to decrease friction and assist in absorbing shock. It contains no vasculature, acquiring nutrients from the synovial fluid within the joint, and no nervous structures. Articular cartilage contains chondrocytes and extracellular matrix, which is composed of proteoglycans, Type II collagen, and water (Wirth & Rudert, 1996).

BONE

Composition of Bone: normal adult bone is comprised of 30 percent organic material, primarily collagen, and 70 percent mineral, mainly calcium and phosphate. The organic components of bone give it flexibility and resiliency, while the inorganic components give bone its hardness and rigidity (Nordin & Frankel, 1989, p.3).

Bone Physiology: the primary cell responsible for ossification is the osteoblast, which produces the organic component of bones (Guyton, 1986, p.941). A small amount of osteoblastic activity occurs continually in all living bones, on about 4 percent of all bone surfaces at any given time, so that some new bone is being formed constantly (Guyton, 1986, p.942).

Bone is also continuously being absorbed, which is the function of osteoclasts. Osteoclasts are large multinucleated cells that are normally active at any one time on less than 1 percent of the bone surfaces (Guyton, 1986, p.942).

Bone, like soft tissues, responds to stress, with greater stresses producing a more dense bone, and a reduction of stress causing bone to be less dense. This is Wolff’s Law (Reid, 1992, p.103).

Inferences from Wolff’s Law:

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The functional unit of bone is the osteon, or haversian system. At the center of each osteon is a haversian canal, which contains blood vessels and nerve fibers. The osteon consists of concentric series of layers (lamellae) of mineralized matrix surrounding the central canal. Along the boundaries of each layer, or lamellae, are small cavities called lacunae, which contain a specifically-named osteoblast, called an osteocyte (Reid, 1992, p.105, Nordin & Frankel, 1989, p.4).

Types of Bone

Cortical bone forms the outer shell of the bone.

Cancellous bone within this shell of cortical bone is composed of thin plates, or trabeculae, in a loose mesh structure. Cancellous bone has a richer blood supply than cortical bone, thus decreasing healing time when fractured.

Cortical bone always surrounds cancellous bone, but the relative quantity of each type varies among bones and within individual bones according to functional requirements.

Periosteum: the dense fibrous membrane that covers all bones, except for joint surfaces, which are covered with articular cartilage. Blood vessels and nerve fibers permeate the outer layer of periosteum. The inner layer of the periosteum contains osteoblasts, bone cells that are responsible for generating new bone during growth and repair. The periosteum allows for bone growth in width (Reid, 1992, p.105).

In the child, the periosteum is thick and loosely attached to the cortex, allowing for rapid production of new bone.

In the adult the periosteum is thinner and more adherent to the cortex, producing new bone less readily.

Gross Structure:

1. Long Bones
   Epiphysis: the expanded bone end that forms a support for the joint surface
   
   Epiphyseal plate (or physis): the growth plate, which permits longitudinal growth, and is located between the epiphysis and the metaphysis.
   
   Metaphysis: the transition area between the bulbous epiphysis and the shaft of the diaphysis.
   
   Diaphysis: the bone shaft; which forms the major site of attachment for muscle (Reid, 1992, p.109).


2. Short Bones



3. Flat Bones

Pathologies of Bone: Osteomalacia, Osteoporosis, and Fractures

• Osteomalacia: "softening of the bones" results from a decrease in deposition of calcium in the bone, and an increased production of unmineralized matrix (Aloia, 1989). Bone changes may become very sever, with the result that the markedly weak and "soft" bones gradually bend and become progressively deformed (Salter, 1983). Due to the increase in production of matrix, the bone is more likely to deform rather than fracture.



• Osteoporosis: a decrease in qualitatively normal bone, which renders the individual more susceptible to fractures (Bonnick, 1994). It is associated with an imbalance between bone resorption and bone formation. Osteoporosis results when the body has not obtained an adequate amount of mineral from the environment and when the mechanical load is insufficient for development of new bone due to physical inactivity (Aloia, 1989).
  
  
  Type I: "postmenopausal osteoporosis", a decrease in bone mineral density that develops when circulating estrogen levels decrease, as is the case in menopause. The prevalence of Type I osteoporosis is 6:1 between females and males (Edwards, 1994) and is most prevalent in people between the ages of 55 to 75 (Aloia, 1989). Type I osteoporosis affects primarily trabecular bone.
  
  Type II: "age-related osteoporosis" or senile / involutional osteoporosis; affects both men and women equally, usually over the age of 70 in which the loss of cortical and trabecular bone is proportional.

The best way to address osteoporosis, regardless of the type, is to prevent it as much as possible. The following are major factors that can have a significant impact on osteoporosis:

Hormones: Estrogen is a sex hormone that influences bone growth, including the ossification of epiphyseal plates (Seely, 1989). After puberty, estrogen plays a critical role in bone metabolism by regulating the removal of old bone and the production of new bone. If estrogen replacement therapy is ongoing after menopause, it can decrease the incidence of fractures (Cauley, 1992).

Hormone replacement therapy (HRT) with estrogen has been shown to decrease the incidence of atherosclerosis, but may increase the incidence of uterine cancer, breast cancer, and hypertension (Aloia, 1989). Some studies show that combining estrogen replacement with progestin replacement can decrease the incidence of uterine cancer (Aloia, 1989.)

Nutrition: Vitamin D and Calcium are important to bone metabolism.

Vitamin D is necessary for normal absorption of calcium into the blood stream from the intestines. The recommended daily allowance of Vitamin D is 200 units (Bonnick, 1994). Most people acquire an adequate supply of Vitamin D from the diet and from exposure to sunlight, however this may not be the case for sedentary persons (Rilin, 1987).

Calcium is the primary mineral composing bone. The skeleton stores 99.5% of the body’s calcium (Marcus, 1996) and bone supplies plasma with calcium in time of need. The body’s store of calcium peaks at about 30 to 35 years.

The recommended daily allowance for calcium is 800 mg for adults (Bonnick, 1994.) and 1000 mg for women who are postmenopausal (Heaney, 1991.)

One cup of regular, whole milk contains 291 mg of Calcium.
One cup of 2% lowfat milk contains 297 mg of Calcium.
One cup of plain yogurt contains 415 mg. of Calcium.
One ounce of american cheese contains 174 mg of Calcium.
Once cup of almonds contains 304 mg of Calcium.
Once cup of broccoli contains 136 mg. of Calcium.
(Aloia, 1989).

Exercise/activity: a decrease in activity coincides with a decrease in bone density (Doye, 1970). When stress is applied to bone, specifically physical activity, the tissue responds by increasing mass, density, and structural properties. Although we do not know the exact influence of exercise on bone mass, most researchers think that it stimulates osteoblast activity and partially inhibits osteoclast activity. (Kannus, 1996).

Exercise protocols that include high peak force and strain, short repetitions and training time, that overload the entire bone, and is progressive in nature may provide the greatest benefit in bone maintenance and enhancement (Kerr, Morton, Dick, & Prince, 1996, Vuori, et al., 1994). It is very important that therapists consider an individual’s bone density prior to prescribing a specific type of exercise. A person with a low bone mineral density may acquire fractures from an activity that is exceeds the strength of the bones (Snow-Harter, et al., 1992).

Weight training: the magnitude of load is more important than the number of repetitions (Kerr et al., 1996). Weightbearing activities performed 3 - 4 times per week for 45 minutes per session increases bone density in postmenopausal women (Brown , 1995). The bones that respond to weight bearing activities will be those that are directly stressed, for instance, a walking program will slow the rate of bone loss in the legs and spine, but not in the upper extremities (Krolner, et al., 1983).

Resistance training: limited studies indicate that a progressive weight training program can increase the bone mineral density in the specific areas trained (Pruitt et al., 1992.) Resistance training for extremities using equipment found in fitness gyms performed 2-3 times per week for 20 to 30 minutes increases bone density (Nelson et al., 1991). The training should emphasize high weights and low repetitions (Marcus et al., 1992).

Smoking and Alcohol consumption: both smoking and excessive intake of alcohol are positively linked with osteoporosis (Aloia, 1989).

Preventing Osteoporosis: the following is a summary of the preceding information, also known as "The Ten Commandments of Osteoporosis Prevention":

1. Get enough calcium in a balanced diet.
2. Get enough vitamin D in your diet and from sunshine.
3. Limit your intake of caffeine, salt, protein, and phosphorus.
4. Do not go on starvation diets.
5. Exercise regularly.
6. Take estrogen (progesterone after menopause if you are at high risk for osteoporosis).
7. Take estrogen if your ovaries have been removed surgically before menopause.
8. Avoid drugs that decrease bone mass.
9. Drink alcohol only in moderation.
10. Do not smoke.


(Aloia, 1989).

Fractures

A fracture is a break in the continuity of a bone due to an applied force.
A fracture always produces some degree of soft tissue injury.

Types of forces:

1. Bending (angulatory) Forces: causing transverse or oblique fractures, with the break usually occurring on the convex side of angulation.
2. Twisting: produce spiral fractures.
3. Traction: a "pulling" force that produces an avulsion fracture, in which a peace of the bone is pulled away either an attached tendon or ligament.
4. Compression.
5. Crushing.

Fracture Description

1. Site.
2. Extent: complete vs. incomplete.
3. Configuration: transverse, spiral, oblique, longitudinal.
4. Relationship of Fracture Fragments: apposition; rotated, distracted, impacted, overriding, comminuted, etc.
5. Relationship of Fracture to External Environment: open (compound) versus closed (simple).
6. Complications

complicated: infection, severe soft tissue damage (such as artery, nerve, etc.)
uncomplicated: minimal soft tissue injury

Epiphyseal Plate Fractures: the area of the epiphyseal plate is weaker than the surrounding bone, ligament, and joint capsule, and is subject to frequent injury. Because the growth plates are usually ossified by age 23, the majority of these fractures occur in children. Injury to the growth plate can lead to growth disturbances, resulting in limb length discrepancies (Salter, 1983).

Fracture Healing: bone is the only tissue in the human body that heals itself completely with tissue that is ultimately indistinguishable from the original bone. For this reason, bone healing has been referred to as bone regeneration, and is basically considered and exaggeration of the normal remodeling process that occurs throughout life. Fracture healing occurs in six stages:

1. The impact stage: occurs at the moment of injury and lasts until there is complete dissipation of energy (Reid, 1992, p.113).
2. The induction stage: following bony failure, cells possessing osteogenic potential are stimulated to form bone (Reid, 1992, p.113). Periosteal and intraoseous osteoblasts around the area of the break are activated, and large numbers of new osteoblasts are formed (Guyton, 1986, p.943).
3. The inflammation stage: begins shortly after impact and lasts until the bone ends are united by fibrous union, formed by increased osteoblast activity producing new organic bone matrix (occurs during the first and second weeks) (Guyton, 1986, p.943).
4. Soft callus stage: occurs when inflammation begins to subside and the bone ends become "sticky", and are held together by fibrous tissue and cartilaginous tissue (approximately two to three weeks). The minerals that comprise the inorganic component of bone are beginning to be deposited in the fibrous matrix.
Osteoclasts begin to appear in large numbers and absorb portions of dead bone fragments (Reid, 1992, p.115). Pain is greatly decreased by this time. The callus is not yet apparent on x-ray.
5. Hard callus stage: the callus continues to be "sticky" and is considered an "osteogenic sleeve" around the fracture fragments. The callus converts from fibrocartilaginous tissue to fiber bone. The bone begins to mature as mineralization continues and the callus begins to be absorbed by osteoclasts. The fracture fragments are firmly united by bone. The callus is apparent on x-ray, and the fracture is considered to have undergone clinical union. (Occurs at approximately three to five weeks) (Reid, 1992, p.116).
6. Stage of remodeling: occurs when the fracture is healed, and the diameter of the bone is nearing preinjury size. The callus has been or is close to being completely reabsorbed. At this point, the fracture has undergone radiographic union. The fiber bone is converted to lamellar bone and the medullary canal is reconstituted. The stage may take a few months to a few years to be complete (Reid, 1992, pp.113-116).

Age: because bone growth is more pronounced in children, fracture healing is more rapid in people under the age of 18-21. Fracture healing is essentially the same length for people over the age of 21.

Site and Configuration: bones surrounded by muscle heal faster than those surrounded by ligament.

Displacement of Fracture (initially and following reduction): the patency of the periosteum is critical to healing time: undisplaced fractures heal twice as fast as displaced fractures. Also, fractures that continue to experience movement between fragments will heal more slowly, if at all.

Blood Supply to Fracture Fragments: fragments with poor or interrupted blood supplies will necrose. Areas of bone with a good blood supply (such as cancellous bone) heals rapidly.

Management of Fractures

Non-intervention: in some cases, physicians will elect not to intervene when a person has acquired a fracture. This is due to a number of possible reasons, however in almost every case, the fracture is stable.

Closed Reduction: realignment of fragments externally, using physical traction, decreases the risk of infection. Casts or splints used to immobilize fracture site.

Open Reduction Internal Fixation (ORIF): surgical realignment of fracture fragments, with fragments being held in approximation by hardware such as plates, screws, pins, nails, intramedullary rods, etc. Bone grafts may also be used with fractures in which the fragments are not in close proximity to each other.

External Fixation: surgical application of appliances to reduce fractures externally. Associated with more severe fractures.

Traction: pins inserted in the distal fragment and weights applied to the fragment, to assist in realignment of the bone. Examples: Buck's traction, halo traction, etc.

External fixators: use of hardware to hold aligned fragments in place, usually consists of an external frame to which pins that are drilled through the various fracture fragments attach. Examples: Hoffman device.

Ilizarov and Debastiani procedures: a specialized external fixator (consisting of a frame attached to pins that are drilled into fracture fragments) through which traction can be applied to the bone fragments (usually larger pieces), to stimulate bone growth. This procedure is used to lengthen the bone, and is used when significant bone loss has occurred.

Atypical Fracture Healing

Mal-union: bone heals in the normal time frame, but in an unsatisfactory position.

Delayed union: bone healing takes longer to heal than normal, possibly due to poor circulation, movement of the fragments, etc.

Non-union: failure of the fracture to heal, resulting in a fibrous union of the fragments. Possibly due to poor reduction of the fragments, tissue caught between the fragments, poor circulation, infection, calcium and phosphorous deficiency, hormonal imbalances, osteoporosis, etc.

Use of cancellous bone grafts: harvested from ilium, etc.

Fracture Healing Complications

Vascular: arterial compromise/tearing; axillary, brachial, and femoral arteries commonly injured.

Neurological: brain, spinal cord, peripheral nerve damage

Avascular Necrosis: bone ischemia and/or death due to compromised blood supply; common in the femoral neck, scaphoid, and talus; results in delayed or non-union. Joint Stiffness or contracture: occurs primarily when joints are immobilized via casting, splints, etc.

Myositis Ossificans: due to significant bleeding within muscles; in which bony spicules are formed within the muscle.

Degenerative Joint Disease: frequently associated with intraarticular fractures.

Immobilization Effects: in addition to contracture of joints, also results in disuse atrophy of muscles, muscle imbalances, altered biomechanics.

ARTICULAR CARTILAGE

Articular cartilage has an incomplete capacity for self-repair. If an injury is superficial, it may produce a fibrous cartilage matrix, similar to scar tissue. If the injury is deep, ie, it reaches to subchondral bone, it may repair by using cells from the bone marrow or from the perichondrium to fill the defect. In any case, it does not replace the injured cells with Type II collagen, and thus it loses the original biomechanics of the injured tissue. Some studies report that fibrous cartilage may over a period of a year convert to hyaline cartilage, thus restoring the biomechanical properties of the tissue (Wirth & Rudert, 1996).

Orthopedic surgeons may attempt to stimulate cartilage regeneration by a number of methods including:

• Drilling into subchondral bone;
• Abrasion of the degenerated cartilage and shaving of the underlying bone;
• Excision of diseased cartilage and subchondral bone;
• Subchondral abrasion with continuious passive motion;
• Osteochondral progenitor cell transplantation;
• Chondrocyte transplantation (Wirth & Rudert, 1996).

Conclusion

Bone heals along similar time frames as does soft tissue. It heals in a similar fashion as soft tissue, yet with some significant differences. Bone, much like soft tissues, responds to the stresses placed upon it by becoming more dense. Current research indicates that articular cartilage has a limited ability to heal, and if it does so, the time frame in which it occurs is lengthy.

Therapists become involved with patients who have acquired injuries to their hard tissues to assist the patient to resume function, to stimulate tissue healing, or to address some other facet of the patient’s care. Again, knowledge of how these tissues heal plus an understanding of the patient’s unique circumstances will guide the therapist’s interventions.




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