Category Archives: Repair and healing

REPAIR OF FRACTURE OF BONE

REPAIR OF FRACTURE OF BONE

Types of fracture of bone:

A- Simple fracture: in which the covering skin is not wounded, and may be complete or incomplete.

B- Compund fracture: occurs when there is a wound in the skin.

How repair of fracture occurs:

(steps of repair of fracture bone):

The healing of a fracture occurs by regeneration with formation of a bony union between the ends of fractured bone which takes place as follows:

1.     The fractured bone should be put in proper alignment and then fixed in plaster.

2.     The gap between the fractured ends is filled with haematoma, within 48 hours there is hyperaemia of vessels with infiltration of the area by polymorphs and macrophages.

3.     The osteoclasts and macrophages will phagocytose and remove any fragments of bone, blood clots and debris.

4.     This is followed by replacement by new tissue called osteoid tissue or non-lamellar bone formed by osteoblasts.

 

■       Osteoid tissue: contains masses of collagen, osteoblasts, and masses of calcium.

■       Functions of osteoblat:

a- It produces alkaline phosphatase leading to calcification.

b- It contains a specialized ground substance of mucoprotien known as osseomucin.

 

5.   The osteoid tissue becomes condensed and acts as splint
and is arranged in three layers each one is called callus:

a-  External callus: to the outside underneath the periosteum.

b-  Internal callus: in medullary canal.

c-  Intermediate or permanent callus: found in between the two ends of fractured bones.

6.      The osteoid tissue is gradually removed by invasion of many osteoclasts. At the same time the osteoblasts of the intermediate callus only will form the adult type of lamellar bone containing the Haversian system.

7.      Finally the external and internal calli will be gradually absorbed or removed by the osteoclastic activity. The repaired part of the bone is very strong. Complete repair of bone takes place in a period from 4 weeks- 4 months.

 

 

Abnormalities of fracture healing:

1.      Non-union: due to presence of pieces of muscles that prevent union.

2.      Delayed union: due to infection, poor blood supply and incomplete immobilization.

3.      Fibrous union: when immobliziation is not complete the osteoblasts will behave as fibroblasts and union takes place by fibrous tissue. This occurs most commonly in case of fracture of tibia. Rarely with increased movement, the fibroblasts differentiate into synovial cells and a false joint may develop known as pseudo-arthrosis.

 

 

Repair of the nervous system:

1-       The central nervous system: the nerve cells are permanent cells which do not regenerate. When a nerve cell is damaged, the entire neurone with the related axon, is necrosed, liquified and disappears. It is replaced by proliferated microglia, specially astrocytes and this process is known as gliosis which is analogous to fibrosis in other parts of the body.

2-       The peripheral nerves: are reparied by a process known as (the Wallerian degeneration)

 

-    Following the section of a peripheral nerve, the nerve cell swell and the Nissel granules disappear, and this is called (chromatolysis). The nucleus takes an eccenteric position. Three weeks later, the cell recovers and the granules reappear.

-    Within the first 48 hours, the axis cylinder of both the proximal and the distal segments up to the level of the first node of Ranvier, become irregular and the myelin sheath breaks into droplets which are phagocytosed by the macrophages.

-    The neurilemmal cells in both the proximal and the distak ends, proliferate and unite together forming a tube in which new myelin is formed. A new axis cylinder grows from the proximal segment, elongates gradually untill it reaches the required length in about 3-4 months.

- Finally the myelin sheath forms gradually.

The final function of the injuried nerve after repaire, depends on the degree of the injury:

1-     If the injury affects the axon only while the nerve trunk is not cut, recover may be complete.

2-     If the nerve trunk is completely cut, recovery is not complete unless carfull surgical suture is done and infection is prevented.

 

 

Organization of a thrombus:

Gradually the peripheral part of the thrombus is liquified and is replaced by granulation tissue and this continues untill all the thrombus is completely replaced by this tissue which ends in fibrosis. In most cases, the lumen is completely occluded by the fibrous tissue and this is known as organization without canalization. Rarely, some capillaries become widened and recommunicate the vascular channels on either sidesof the thrombus and restore the circulation. This is known as organization with canalization.

 

 

HEALING OF SKIN WOUNDS

HEALING OF SKIN WOUNDS

I. Healing of clean incised wound (surgical wound) is

known as healing by first intention or primary union, in which the edges are closely applied together by sutures. It occurs in the following steps:

1.     The two edges of the wound are approximated together by sutures but a small gap is still present between the two edges which is filled with clotted blood.

2.     Incision and sutures induce inflammation in both edges.

3.     Within 24 hours the basal cells of epidermis regenerate and cover the wound surface, subsequently other layers of epidermis form.

4.     Layers of granulation tissue will be formed from the periphery gradually replacing the clotted blood. This takes place when the blood clot is gradually liquefied and absorbed. Removal of clot and dead tissue occurs first by action of polymorph and later by macrophages.

5.     The gap is completely filled with granulation tissue in about seven days and then it ends in scar tissue. The wound edges are now firmly united. The covering epidermis is pale and does not have hair follicles, sweat or sebaceous glands.

 

II. Healing of large infected wounds: known as healing by second intention or secondary union. In this case the edges of the wound are not brought into apposition and are gapping. Healing takes place in the following steps:

1.     Wound contraction takes place to minimize the area of skin loss and healing becomes faster. Contraction i.e. movement of edges towards the center of the wound is brought about by contraction of fibroblasts which are now termed myofibroblasts. If contraction is prevented as in burns, administration of corticosteroids or exposure to ionizing radiation, healing becomes slow and a large ugly scar is formed.

2.     The blood clot is replaced by granulation tissue which progresses from the base upwards as well as from the edges inwards.

3.     The epithelium grows over the granulation tissue and completes the healing process. If the gap is small, it will be covered completely by skin, but if it is large a skin graft may be needed.

 

 

Difference between healing of clean cut and infected wounds:

 

Healing by first intention (Primary union) Healing by secondary intention (secondary union)
It occurs in clean cut wounds It occurs in septic wounds and abscesses.

There  is minimal loss  of tissue

There is marked loss of tissue

There is no gap or a very small one.

A wide gap is present

There is no foreign body or infection.

There is foreign body and/or infection.
Ends   with   formation   of minimal   granulation   tissue and thin scar. Ends with formation of abundant granulation tissue and thick scar.
No wound contraction Wound contraction is present
The complications are rare The complications are common.

 

 

Complications of Wound healing:

1.     Infection which may delay the healing or stop it completely if it is severe.

2.     Keloid formation: Excessive formation of fibrous tissue in the dermis produces a projecting swelling covered by thin epidermis. Recurrence of keloid after surgical removal is common. A keloid may follow secondary union or develops during the healing of a wound. The cause is unknown but may be related to individual susceptibility.

3.     Cicatrization or reduction in the size of the scar: It is a frequent complication of extensive burns of skin and may produce great deformity in the area.

4.     Weak scar in the anterior abdominal wall may lead to incisional hernia; Loops of intestines will protrude through this weak scar forming a hernia.

5.     Neuroma which is a painful mass formed of proliferation of neurilemmal cells and axis cylinders of cut peripheral nerves e.g. amputation neuroma.

6.     Sinus and fistula

Fistula: it is a tract formed of infected granulation tissue which connects two cavities together or one cavity to the outside and has a free ends.

Sinus: it is a tract formed of infected granulation tissue which connects a cavity to outside and has a blind end.

Factors affecting wound healing:

 

A.  Local factors:

Factors which will delay wound healing:

1.     Poor blood supply.

2.     Infection.

3.     Exposure to ionizing radiation. On the other hand, exposure of the wound to ultraviolet light increases the rate of healing.

 

B.  General factors:

1.     Age: wound healing is faster in young than old people.

2.     Nutrition: deficiency of protein and vitamin C leads to delay of wound healing. Deficiency of vitamin C leads to defects in collagen formation.

3.     Hormones: corticosteroids inhibit granulation tissue formation. Testosterone increases the rate of wound healing.

4.     Zinc deficiency delays healing because zinc is necessary for the synthesis of collagen.

5.     Wounds heal much more slowly in cold weather.

Repair and healing

REPAIR AND HEALING

Definition

It is the process by which the body forms new cells to replace structures damaged in a pathologic process.

This involves 2 processes, separately or often in variable combination:

■      Regeneration: Healing by cells of the same type.

■      Fibrosis  (organization):  Healing by  fibrous tissue scar developing form granulation tissue.

In order to understand the mechanism of repair we have to know the cell cycle.

Cell Cycle:

The period between 2 successive cell divisions divided into 4 unequal phases:

■      M (mitotic) phase: Interval between onset and conclusion of mitosis.

■      Gl (presynthetic) phase: Following mitosis. The cell is devoted to specialized activities.

■      S (synthetic) phase: Doubling of DNA.

■      G2 (premitotic) phase: Preceding next mitosis.

According to the proliferative potential of different cells, they are divided into three types:

■ Labile cells:

-   Proliferate throughout life.

-   Replace cells that are continuously lost.

-   Proceed in cell cycle from one mitosis to the other.

e.g. epidermal cells, lining of GIT, endometrial cells, and hemopoietic cells (bone marrow).

■ Stable cells:

-   Do not multiply under normal conditions.

-   Capable of rapid division after tissue loss i.e if stimulated.

-   Considered to be in the “G 0 phase”

-   Can re-enter the cycle at Gl after an appropriate stimulus (tissue loss).

e.g. liver cells, kidney cells, pancreatic cells, vascular endothelium, fibroblasts, osteoblasts, chondroblasts, and smooth muscle cells

■ Non-dividing (permanent) cells:

-   Do not multiply in postnatal life.

-   Considered to have “exited” the cycle at some point in intrauterine development.

e.g. nerve cells, cardiac muscle fibers, skeletal muscle fibers.

Most tissues in the body contain different proportions of the different cell types.

Regeneration occurs in tissues composed of labile or stable cells. Fibroplasia occurs in:

1.      Tissues composed of permanent cells.

2.      Presence of factors that prevent complete restoration e.g. interruption of blood supply

Control of cell growth:

Many mediators affect cell growth.

The most important are polypeptide growth factors:

■ Circulating in serum or produced locally.

■ Induce cell proliferation by affecting expression of genes involved in normal cell growth (proto-oncogenes).

■Most also stimulate cell migration and differentiation (pleiotropic effect).

Cell proliferation is directed by a family of proteins called cyclines (control phosphorylation of proteins involved in mitosis).

Growth factors:

■      Macrophage derived growth factor (MDGF)

■      Platelet derived growth factor (PDGF)

■      Epidermal growth factor (EGF)

■      Fibroblastic growth factor (FGF)

■      Vascular endothelial growth factor (VEGF)

■      Transforming growth factor-B (TGF-B)

Growth inhibitors:

■      Regulate cell growth e.g. decreased inhibitors lead to cell growth.

■      Are also largely polypeptide factors that use receptors.

■   The best studied are TGF-B and interferon gamma. Granulation Tissue:

Mesenchymal tissue consisting of:

■       Newly formed capillaries which arise from endothelial cells lining nearby blood vessels. These proliferate to form solid buds that branch, anastomose and become canalized.

■       Fibroblasts which arise from activation, proliferation and migration of nearby “fibrocytes”

■       Ground substance and small amount of young collagen formed by fibroblasts.

■       Few inflammatory cells and macrophages.

It is formed in: Wound healing, healing of abscess, chronic inflammation, replacement of fibrin and necrotic tissue (organization).

The granulation tissue appears soft, pink and granular. Progressive fibrosis then occur leading to the formation of a strong avascular fibrous scar.