The Toxic Tooth: APPENDIX C Causes of Cavitations and Associated Conditions Overview of Causes

 

APPENDIX C

Causes of Cavitations and Associated Conditions

Overview of Causes

Cavitation disease, or ischemic osteonecrosis, results from both systemic and local problems at a number of sites in the body. Although not so much a disease in it own right, ischemic osteonecrosis is the localized result of anything which significantly reduces the blood flow through the bone marrow.

Ischemic osteonecrosis of the head of the femur was once called “coronary disease of the hip” because of the associated marrow ischemia (reduced blood flow) and infarction (death of tissue from too little to no blood flow).

In cases of ischemic osteonecrosis involving the femoral head, the list of diseases and biological phenomena capable of producing this damage has continued to grow. Some of the etiologic factors are much more significant than others. Some factors are primary causes and other factors act as triggering mechanisms or “second hits” in persons otherwise susceptible to bone marrow blood flow problems.

Jaws are especially susceptible to cavitations and ischemic osteonecrosis for several reasons. The jaws are especially susceptible to reduced blood flow problems. Trauma and infection are the primary triggering events for osteonecrosis, and no other bones come close to the level of trauma and infection experienced by the jaws being subjected to an array of insults including: tooth and gum infections, tooth extractions, trauma (like a fist to the face), and oral or root canal (endodontic) or gum (periodontic) surgery.

Another cause of osteonecrosis can be added to those mentioned above, which is rather unique to dental procedures: the local anesthetics used to numb the jaw for tooth procedures or oral surgery. These drugs often contain powerful chemicals (vasoconstrictors, e.g. epinephrine) designed to

drastically reduce the blood flow in the area, thereby keeping the anesthetic in place longer and allowing more time to work.

These anesthetics are wonderful for the procedure itself but can be disastrous for someone with any one of the undiagnosed hypercoagulation disorders to be discussed. Moreover, the poor outflow characteristic of osteonecrosis means that the vasoconstrictor can remain in the area far longer than the few minutes needed for profound local anesthesia. And to add injury to insult, literally, the reperfusion of the bone after the vasoconstriction wears off releases large numbers of tissue-damaging reactive oxygen species. Normal tissues can withstand this onslaught nicely, but a nutrient-starved ischemic marrow does not maintain its marginal health status as well.

SPECIFIC CAUSES OF ISCHEMIC OSTEONECROSIS Hypercoagulation States

Hypercoagulation (a state where the blood clots more readily) is common. Some of the most common initiating factors are:

Undiagnosed coagulation disorders

The most important underlying, and almost always unappreciated, risk factor for cavitations comes from genetic coagulation disorders. Patients should be asked about a family history of clotting problems. This hypercoagulation problem might be suggested by a family history of stroke and heart attacks at an early age (less than 55 years), hip replacement or “arthritis” (especially at an early age), and deep vein thrombosis.

Hypercoagulation may be a life-threatening problem. Always keep in mind that the presence of a hypercoagulation state makes the patient susceptible to stroke, myocardial infarction, deep vein thrombosis, and other serious or life-threatening conditions. Usually a secondary problem or “triggering event” must occur, such as local infection, trauma, medications, etc.

Other associated diseases

There are other diseases associated with hypercoagulation. These include:

• Behçet’s disease
• Chronic fatigue syndrome • Fibromyalgia
• Irritable bowel syndrome • Sickle cell crisis
• Migraine headaches

The significance of these associations is not completely clear—direct studies are needed to prove these links—but these disorders appear to occur frequently in patients with ischemic osteonecrosis.

Hormones

Estrogen

Estrogen replacement therapy can be a cause of osteonecrosis. Estrogen enhances coagulation. In persons with a hypercoagulation state (at least 6% of the population) the risk of thrombosis from estrogen use increases, sometimes dramatically. For example, the risk for a person with a hypercoagulation disorder of forming a clot somewhere in the body (not just the jaws) is increased by more than 80 times when estrogen replacement is given. The orthopedic literature sometimes refers to this as estrogen-related ischemic osteonecrosis.

Pregnancy is associated with increased estrogen levels. Because of this, pregnant women are at an elevated risk of developing ischemic osteonecrosis, especially of the hip. A mild, self-limiting condition that is a precursor to osteonecrosis, transient ischemic osteoporosis, often spontaneously regresses with immobility after the birth of the child. Multiple joints may be involved, sometimes moving from one to another over time (migratory ischemic osteoporosis).

Hypercortisolism

Hypercortisolism (excess corticosteroid presence) is another cause of osteonecrosis. It can result from either excess natural production or from the common practice of prescribing prednisone or prednisolone to prevent swelling after oral surgical procedures. Corticosteroid use is the most

common cause of non-traumatic osteonecrosis. Although the risk appears to be magnified by higher doses and longer periods of administration, there are reports of striking hip osteonecrosis from a single week’s use of Medrol. The orthopedic literature contains articles pertaining to corticosteroid- induced osteonecrosis. The mechanism for this is not well-defined.

Hypothyroidism

Low levels of thyroid hormone have been associated with increased risk of developing ischemic osteonecrosis of the hip, probably because the diminished metabolism produced by this condition reduces blood flow rates throughout the body.

Miscellaneous Factors

Autoimmunity and Hypersensitivity

• Systemic lupus erythematosus • Antiphospholipid syndrome Maxillary sinus infections

Recurring maxillary sinus infections with the potential seeding of bacteria in the alveolar bone, producing osteomyelitis (bone infection), is a major risk factor. The inflammatory mediators at work in this chronic process are capable of increasing local and systemic coagulation. This is generally not a problem for a normal person but can be, again, disastrous for the 6% of the population who have undiagnosed or “silent” hypercoagulation states.

Gaucher’s disease

This lipid storage disease is associated with hyperviscosity, thrombocytopenia, and decreased factor IX and protein C. It has been suggested that when the very large lesional cells, Gaucher cells, enter the blood vessels they act as emboli and when they fragment their breakdown products they trigger excess intravascular coagulation, leading to thrombosis and hemorrhage (microinfarctions). Just before a crisis, there is

radioisotopic evidence of ischemia, but it may be days or several months after the acute pain onset before a biopsy will show obvious osteonecrosis.

Diseases and Conditions Associated with Osteonecrosis (any bone)

Disease or Etiologic Factor	Subcategories
Alcohol Abuse	Cirrhosis Pancreatitis
Arthritis	Subchondral cyst Subchondral marrow edema
Atmospheric Pressure Variations	Caisson’s disease

Deep sea diving

Blood dyscrasias

Disseminated intravascular coagulation (DIC) Sickle cell anemia

Cancer

Leukemia
Cancer-induced hypercoagulation Lymphoma
Metastatic intraosseous carcinoma Radiation therapy for cancer

Chronic Inactivity

Bedridden Full body cast Paraplegic

Corticosteroids

Hypercortisolism Inflammatory bowel disease Lupus erythematosus Transplants

Estrogen

Birth control pills
Estrogen replacement therapy Fertility drugs

Hypertension

Hypothyroidism	Incomplete removal of the periodontal ligament at the time of tooth extraction
Inflammation, intraosseous	Infection, bacterial and viral Trauma (mild or severe) Autoimmunity/hypersensitivity
Neurological damage	Brain injury/surgery

Pregnancy
Prostate chemotherapy Transient ischemic osteoporosis

Hypercoagulable state, local

Acute infections/inflammation Chronic infection/inflammation Increased intramedullary pressures

Hypercoagulable state, systemic

Antiphospholipid antibody syndrome Factor V Leiden gene mutation Hyperhomocysteinemia
Homozygosity for MTHFR* or CBS** Protein C deficiency

Protein S deficiency

Hyperlipidemia & embolic fat

Diabetes mellitus Dysbaric phenomena Fracture of bone Hemoglobinopathies Osteomyelitis, acute

Hypersensitivity reactions

Allograft organ rejection Anaphylactic shock
Immune globulin therapy Shwartzman reaction to endotoxin Transfusion reactions

Osteoporosis Regional or generalized Starvation Anorexia nervosa Storage diseases Gaucher’s disease Tobacco use Tobacco smoking

The above information has been reproduced, with some modifications, with permission of:

J. E. Bouquot, DDS
Director of Research, Maxillofacial Center for Education & Research
212 Tibbs Road
Morgantown, WV 26508
Adjunct Professor (Retired), Department of Diagnostic & Biomedical Sciences University of Texas School of Dentistry at Houston
Adjunct Professor, Department of Rural and Community Dentistry, School of Dentistry, West Virginia University
www.maxillofacialcenter.com

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