OP Sheet #12 By Hanan Musleh

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OP Sheet #12 By Hanan Musleh

Post by Sura on 19/12/2011, 10:30 pm


عدد المساهمات : 484
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تاريخ التسجيل : 2010-09-29

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Re: OP Sheet #12 By Hanan Musleh

Post by Shadi Jarrar on 23/12/2011, 9:10 pm

Oral Pathology

Dr. Faleh

Lecture #12


Cherubism is a disorder characterized by abnormal bone tissue in the lower part of the face. Beginning in early childhood, both the lower jaw (the mandible) and the upper jaw (the maxilla) become enlarged as bone is replaced with painless, cyst-like growths.

In some cases the swelling in the maxillary region can lead to an upward pushing of the eyes which leads to the exposure of part of the sclera.

It affects the jaws. Clinically it affects males more than females. It's most often than not hereditary; autosomal dominant (AD). But there are some cases which present as new mutations (sporadic); there is no family history. Nevertheless most of the time it's AD.

The affected children are born healthy, however when they reach 2-4 years of age they start to experience swelling. This swelling involves part of the mandible; bilateral, symmetrical enlargement, progressive, painless bony swelling. It could affect part of the mandible and the main part of the maxillary tubrosity as well. It could be accompanied by an enlargement of the submandibular lymph nodes which produces circular enlargement of the face and this is a distinctive presentation. The age at which it occurs is distinctive as well (about 4 years of age). It's painless. The swelling continues until about the age of puberty, and then partial or even complete involution begins; the child returns back to health.

It is NOT soft tissue swelling, it is a bony swelling.

Some used to think that Cherubism is a hereditary type of fibrous dysplasia, because it has pretty much the same mechanism; there is in both types replacement of the bone with fibrous tissue which then undergoes calcification. However they have recently discovered that Cherubism is genetically different than fibrous dysplasia. So if you happen to read in any textbook that cherubism is considered as a hereditary type of fibrous dysplasia this is not correct.

Again it is a swelling in the bone, so it affects the teeth; it may lead to malocclusion, or failure of eruption of teeth. To confirm the diagnosis you have to take a radiograph which will show the bony swelling.

The first thing to do is to take a panoramic radiograph, and the image helps in the diagnosis due to the presence of bilateral, symmetrical, multilocular radiolucencies which is distinctive to cherubism.

This is during an early stage of the disease, so we can see that many teeth are still un-erupted. Also, displacement can occur to some teeth.

Since as we said usually this disease and it's swelling start to disappear at around the age of puberty, the dentist most of the time leaves it to regress on it's own without any intervention. So there's no need for any surgical interference in the management of cherubism, unless complete involution doesn’t occur, in this case interference may be in the form of cosmetic surgery. This is why the correct diagnosis is essential, so that we differentiate it from ameloblastoma and other more serious diseases, especially in some rare reported cases where the swelling actually starts unilaterally and then later on it progresses to the other side. This is a serious and dangerous case, because when you first see the unilateral swelling (before it's progression to a bilateral swelling) you won't consider cherubism as a likely cause, and when you take a biopsy it may resemble different diseases, and after they interfere surgically and the swelling progresses to the other side it becomes clear that there was no need for the surgery in the first place since Cherubism involutes on its own and it would've been preferable if no interference occurred.

More and more radiopacities start to appear in the region of the swelling with age, which may turn into a "ground-glass appearance", similar to what we saw in fibrous dysplasia.


Fibrous replacement similar to fibrous dysplasia; cellular fibrous tissue replacing the bone, there are a lot of multinucleated giant cells; we've seen this image before when we took the vascular, fibrous, and giant cell epulis and the peripheral giant cell granuloma.

Lots of giant cells, with fibrous cellular connective tissue, so this is considered as a giant cell lesion of bone, another one we previously took that’s also a giant cell lesion of bone is the aneurismal bone cyst which contains giant cells in the bone.

A pathognomonic sign of cherubism is that with time calcification may occur, and this differentiates it from other giant cell lesions, and the presence of eosonophilic vascular cuffing; where a ring of eosinophillic morphous material develops encircling the blood vessels.

{ Pathognomonic: is a term, often used in medicine, that means characteristic for a particular disease. A pathognomonic sign is a particular sign whose presence means that a particular disease is present beyond any doubt. Labeling a sign or symptom "pathognomonic" represents a marked intensification of a "diagnostic" sign or symptom……………Wikipedia

Metaplastic bone is seen with the giant cells, because as we said with time calcifications ensues and the development of a "ground glass appearance". ­ ALKP

Inflammatory diseases of bone:
Osteitis, osteomyelitis, periostitis
Their naming depends on the extent of bone that is affected (inflamed).

Osteomyelitis: the bone marrow spaces, cortical bone, and the other components are affected.

Periostitis: only the periosteum (the outer layer of bone) is affected.

Osteitis: such as cases when the area of bone beneath the tooth is inflamed, inside the bone trabeculae; it's usually localized.

Alveolar osteitis (Dry socket / السنخ الجاف ):

It is the most frequent painful complication of extraction. It happens when you extract a patient's tooth and then after about 2 days the patient comes back complaining of severe pain; in such cases you should suspect a dry socket is the cause. It doesn’t occur immediately after extraction, usually after a while (about 2 days). It is one of the most common complications that occur after extraction. All extractions can cause it, especially the extraction of the third molar; and mostly surgical extractions where there is more trauma than regular simple extractions, since some of the bone is removed and the tissues are traumatized. It follows 1-3% of all extractions; but especially the impacted mandibular 3rd molars. So when extracting an impacted mandibular 3rd molar you should expect that a dry socket is a highly possible complication, in Jordan university Hospital about 9.5% of cases of surgical extraction of impacted mandibular 3rd molars were complicated by a dry socket. This percentile is similar to that of other countries. Again for all teeth 1-3% of them are followed by a dry socket, but for 3rd molars; especially impacted mandibular 3rd molars the percentile may reach up to about 9.5%.


Usually following extraction, the area will be filled with blood, then clotting occurs, then organization (fibroblasts start to grow and produce collagen fibers then granulation tissue develops), and finally bone formation takes place, and the epithelium undergoes epithelialization and the wound closes up and heals. This is what normally happens following extraction. If the clot doesn’t develop then no organization will occur and consequently there will be no healing. If a clot does develop and then it's lost, the area will also remain empty and so the bone will undergo inflammation. So the predisposing factors are either no clot was formed in the first place, or a clot was formed but then an early loss of the organized clot took place. Either way exposure of bone takes place which leads to bone inflammation, necrosis, and since this area contains nerves severe pain will arise.

Again the predisposing factors are: failure of the clot formation, or early loss of the clot.

There are certain conditions that may facilitate this failure in clot formation, for example in osteosclerotic disease, similar to what we previously saw in osteopetrosis, there is dense bone with little vascularity. Or if the jaw underwent radiotherapy which reduced the vascularity and inhibits the formation of the clot. Or in Paget's bone disease where the vascularity is compromised as well.

Early loss mostly occurs if the patient exaggerated the use of a mouthwash following the extraction, or if he/she persisted in creating negative pressure in their mouth like the sucking movements that take place when drinking beverages using a straw, or if the patient spits a lot which also creates negative pressure; these may all lead to a dry socket.

Also if the surgical extraction included excessive trauma and destruction to the tissues and consequently many mediators are activated that may lead to the loss of the clot; which is why dry sockets mostly develop following the surgical extraction of third molars.

If you used an excessive amount of local anesthesia containing vasoconstrictors this may lead to dry sockets as well, especially in patients who have poor oral hygiene and periodontal disease and smokers these people have an increased risk to be affected by a dry socket. Females that are on oral contraceptive pills are also at an increased risk.


The patient comes complaining of a deep seated severe throbbing pain that doesn’t develop immediately following the extraction but after a few days usually about 2 days. This may last up to approximately 2 weeks. When you examine your patient you see that the socket is empty , and it contains food debris and necrotic material. The mucosa in the whole area of extraction is inflamed, red, and tender. In some cases you may find enlarged lymph nodes, fever, and malaise if the inflammation spread. Socket: no clot, whitish dead bone.

If you don't follow the right procedures during extraction; which include not extracting before removing any calculus that may be present so that after extraction the calculus and other foreign bodies won't spread to inside the socket, then you may need to clean the socket afterwards. But usually when the oral hygiene is good and there is no calculus then there shouldn’t be any need to clean the socket. Keep in mind that squeezing the socket after extraction is not the same as cleaning it; squeezing is a routine procedure following extractions; because after extraction the socket is dilated which alters the anatomy after healing takes place, so squeezing it just returns it back to normal. Again squeezing the socket is a routine procedure, whereas cleaning the socket with the use of an irrigant and such is something that is not usually done under normal situations, unless there are foreign bodies and calculus inside the socket and this rarely happens when following the correct ideal procedures of extraction. Sometimes an amalgam restoration may drop into the socket during extraction and this needs to be removed. So before extraction we should improve the oral hygiene by scaling if needed and instruct the patient to use a mouthwash.


It may take up to 2 weeks; so it’s a gradual process. We'll take its management in our surgery course.
Focal sclerosing (condensing) osteitis:

It’s a Bony reaction to a low-grade periapical inflammation. It’s a chronic periapical lesion, and then stimulation to the adjacent bone takes place to form more bone; the bone trabeculae in this area become thick and dense so when you take a radiograph there is a radiopacity beneath the root. The main condition for this to occur is that the tooth has to be non-vital, if the tooth was vital then the differential diagnosis would be Periapical cemental dysplasia*.


Lower first molars are the mostly likely teeth to be affected and young patients (< 20y) are more likely to be affected because they have a good haling ability. It's asymptomatic and doesn’t need any management.


Radiopague area below the apex sometimes referred to as a "bone scar" if it was found in the place of a tooth. It used to be a tooth and then periapical inflammation took place and then condensing osteitis developed.

It's basically an increase in the amount and thickness of normal bone trabeculae, lymphocytes, and fibrous marrow.

All of the above diseases are limited types of inflammation, whereas osteomyelitis is an extensive type of inflammation involving the bone marrow and is widely diffused inside it, it may reach the surface (the periosteum), and it may breach the cortex.

Osteomyelitis is uncommon. There are predisposing factors. Usually the source of the bacteria is the oral cavity, from the teeth and the areas surrounding the teeth. What makes the bacteria go into the bone and cause this extensive inflammation and infection? The predisposing factors, because as we recall bacteria frequently enters inside the periodontal ligament by exiting the root yet very rarely does osteomyelitis occur even though the bacteria may be all around the bone. The body responds by developing a granuloma or a cyst to isolate the area and inhibit the spread of the bacteria. Therefore the bacteria spreads when there are local or systemic factors.

Local factors:

Fracture in the mandible or maxilla, or if the patient underwent radiotherapy in the mandible and consequently the vascularity and immunity are compromised, or in the presence of an osteosclerotic disease: osteopetrosis or Paget's disease.

Systemic factors:

People with compromised immunity such as people suffering from acute leukemia, diabetes mellitus, alcoholics, and those who have malnutrition, anemia, or those on immunosuppressive drugs, or have HIV….these patients may be at risk to develop osteomyelitis.

The source of infection is as we said is from the teeth and from around them, if there was a fracture for example or a periapical lesion. It's usually caused by a group of bacteria not a single type so it's polymicrobial; Staph., Strep., anaerobic bacteria, bacteroids etc.


The mandible is more likely to develop osteomyelitis than the maxilla, in general the mandible is more susceptible to diseases than the maxilla. It's more susceptible to osteomyelitis because the only source of blood for the mandible is the inferior alveolar artery, so if the artery was cut then the whole area undergoes ischemia which increases the susceptibility to infection, whereas the maxilla gets it's blood supply from more than one vicinity so it's less susceptible to infections and the immunity is better. The patient comes in complaining from severe throbbing deep-seated pain, the pain feels like it's coming from inside the bone so you may suspect it to be an acute periapical infection. It leads to swelling and edema in the soft tissues which is also similar to an acute periapical abscess or cellulitis. The gingiva in the affected area is red, swollen, and tender. There are loose teeth and this is not seen in an acute periapical infection which may have the tooth directly above it loose, however in osteomyelitis an entire group of teeth are tender and loose and in this it's different from acute periapical infections/abscesses and cellulitis. Limitation of mouth opening and dysphagia occur as well with a difficulty in swallowing. Enlarged, tender lymph nodes which are also seen in an acute periapical abscess. Anesthesia or paraesthesia in the lip may occur and this indicates that the infection is very deep and surrounding the inferior alveolar nerve.

Again there is swelling and you may even see puss coming from around the teeth, the puss is present inside the bone, and after a while the diagnosis will be apparent from the radiograph.


In the beginning similar to the acute periapical abscess there are no radiographic changes, but after a while a "moth eaten appearance" develops, multiple irregular radiolucent areas and this may lead to a pathological fracture because the area becomes very weak.

{Cellulitis is just a swelling in the facial spaces, it may be caused by an acute periapical infection or from osteomyelitis. The acute periapical infection is around only one tooth whereas osteomyelitis is around several and it’s a deep-seated infection.


It's in the bone and extends into the bone marrow spaces, you also find puss and bacteria inside and may lead to separation of some parts of the bone that then become non-vital; they're called sequestra which are non-vital pieces of bone "swimming" or floating inside the puss. It may lead to the formation of sinuses, and they may open and become exposed to the skin exteriorly or inside the oral cavity and secrete puss. Again it's inside the bone and then spreads through the cortical bone to the periosteum so all the parts of bone are inflamed.

Sclerosing osteomyelitis:

Some consider it to be cemento-ossifying dysplasia that underwent infection therefore some are suspicious of the existence of Sclerosing osteomyelitis, however you may find Sclerosing osteomyelitis in some textbooks with a few chapters devoted to it. Nonetheless there are some types of chronic sclerosing osteomyelitis such as Garre’s osteomyelitis aka Chronic osteomyelitis with productive periostitis, this exists and is well recognized.

Chronic osteomyelitis w productive periostitis (Garre’s osteomyelitis):

It is uncommon, it’s a response of the bone to a low grade infection. It's when a non-vital tooth especially the first molar has an infection beneath it, then the infection spreads through the cortical bone to the periosteum, as a result the periosteum induces bone formation underneath it; in a form of layers. The patient suffers from swelling in the area adjacent to the affected tooth which is in most cases the first molar, and the tooth has to be non-vital.

So it is reactive sub-periosteal new bone formation.


When you take a radiograph you see that next to the first molar; which is non-vital, a bony swelling is visible. The occlusal radiograph provides the best view of the swelling of bone beneath the periosteum. It resembles an "onion skin" appearance because it's formed in layers.

Again the first molar and the area around it is the mostly likely tooth to be affected by Garre's osteomyelitis, but the tooth has to be non-vital. Usually young patients are affected because they have a better healing capacity. The pain is not severe, since it’s a chronic type of infection/inflammation so the pain is mild. It's in the form of a non-tender hard swelling around the lateral border of the mandible.

Chronic periostitis associated with hyaline bodies:

Aka “Pulse granuloma” or “Vegetable granuloma”

˜™ The doctor said that we should read this topic on our own, here's what's written in the handout:

Ó Vegetable material via socket, flap, RC, breach in mucosa


Ó Thickening of periosteum

Ó Hyaline ring-shaped bodies

Ó FB giant Cs

Pulse granuloma is an uncommonly reported oral finding with undefined etiology. [1] They appear as spherical, ovoid, or irregular bodies surrounded by fibroblasts and appear as homogeneous, eosinophilic material in Hematoxylin and Eosin stained section surrounded by acute and chronic inflammatory cells and foreign body giant cells. Occasionally, there may be presence of small round calcified basophilic bodies within the amorphous hyaline material. [3]

Many authors believe this hyaline material to be a vegetable matter embedded within the edentulous portion of jaw bones, periapical lesions, and extraction sockets or in the wall of the odontogenic cysts, etc.

Radiographically, intraosseous pulse granuloma is an irregular radiolucent lesion with well formed trabeculae of bone, an appearance that can be confused with that of other jaw lesions

Histologically, the oral pulse granuloma contains starch granules, with cellulose envelopes that appear as hyaline rings surrounded by foreign body giant cells and concentrically arranged delicate connective tissue.

_ http://www.amsjournal.com/article.asp?issn=2231-0746;year=2011;volume=1;issue=1;spage=83;epage=86;aulast=Kotrashetti


It is normal bone in a patient who has cancer and was exposed to radiotherapy, then ischemia to the bone ensued, so it's necrosis to the bone of the mandible due to ischemia. There is no inflammation unless bacteria appears in the picture. This bone is susceptible to inflammation and infection, because when there's no blood (due to ischemia) there's no immunity. As a result a patient who has Osteoradionecrosis is more susceptible to osteomyelitis. Again Osteoradionecrosis is NOT osteomyelitis; it's just that a patient suffering from Osteoradionecrosis is more susceptible to osteomyelitis if the bacteria started to spread extensively in the area which is likely to happen because of the compromised blood supply and consequently compromised immunity. Such patients; it's dangerous for them to be exposed to infections, which is why usually cancer patients that receive radiotherapy should be dentally treated before undergoing radiotherapy; if any tooth needs to be extracted or needs RCT, or if scaling needs to be done, so that before radiotherapy he has good oral hygiene and all his/her teeth have a good prognosis. This is necessary in order to ensure no procedures are done after the patient's radiotherapy, because any procedure that's done after radiotherapy may result in extensive osteomyelitis.

A question was asked about an image that was shown, in this radiograph the bony plate (which is used to splint the mandible in the case of fracture) is exposed.

This patient suffering from Osteoradionecrosis if he is exposed to an infection or if he suffered from trauma from a denture for example which enabled the bacteria to enter into the area this will lead to as we mentioned above an extensive inflammation that may result in necrosis of the soft tissues which will lead to exposure of the bone, pathological fractures may result from this that need splinting and the entire healing process is quite difficult and this may lead to infection all over again and the bony plates will be exposed this time around….all this may result if a patient suffering from Osteoradionecrosis was exposed to an infection.

The time span that such patients are most likely to be affected by infections is the time during radiotherapy and immediately after the radiotherapy is over, because after a while the vascularity may start to go back to normal.

As we said all dental procedures should be done before the patient undergoes radiotherapy to avoid infections, even partial dentures and such, to avoid the exposure of bone if a cut or wound was inflicted by it which may lead to an infection. However, there are some ways to treat the mandible by placing the patients in chambers full of oxygen for certain amounts of time to increase the vascularity.

Endarteritis oblitrans ® non-vital bone

**The dr. didn't mention this point in the lecture, but I searched it all the same, apparently the teeth are non-vital due to Endarteritis oblitrans (as a result of the ischemia that takes place).

Endarteritis Obliterans

This is not an independent disease, but is frequently of considerable importance as a part of the phenomena of other conditions. It affects the finer vessels of certain organs, and consists, like atheroma, in a thickening of the internal coat which, in these fine arteries, frequently leads to complete.obliteration.

_ http://chestofbooks.com/health/disease/Pathology-2/5-Endarteritis-Obliterans.html

Metabolic & Endocrine disorders of bone:


The image to the left shows both normal bone and bone affected by osteoporosis, notice in the image of the bone affected by osteoporosis the thinning of the bone trabeculae, so the amount of bone is reduced. Bone formation

It usually affects elderly people, the bone density and the amount of bone is reduced.

The areas most affected by osteoporosis are the areas that are under the most pressure and carry the most weight; so the legs and the vertebral column are mostly affected.

The people most susceptible to become affected by osteoporosis if they have no medical problems are post-menopausal females. However certain diseases, regardless of whether the person is male or female, may lead to osteoporosis such as hyperthyroidism, hyperparathyroidism because it removes the calcium from the bone, and Cushing’s syndrome because it opposes the formation of collagen which leads to osteoporosis.

What are the dental aspects?

What matters to us is that osteoporosis affects the alveolar bone, it reduces the amount and density of it so such patients are more likely to have periodontal diseases, because the bone density around the teeth is reduced which eases the progression of periodontal disease. The periodontal disease with mobility in the teeth may lead to an early loss of the teeth.

Patients with osteoporosis present a difficulty in their construction of dentures because they don’t have an alveolar ridge so it's difficult to obtain retention especially in the mandible, and this results in rocking in the denture and trauma to the soft tissues. Surgery may easily result in fractures in the mandible. Implants are also difficult to be inserted since the amount of bone is reduced so retention is difficult to obtain. In the maxilla since there is no alveolar bone; it was all resorbed; it's easy to communicate with the sinus, so any maxillary tooth that you extract may result in an oro-antral fistula or a communication with the sinus. Thus before you attempt to extract you should carefully evaluate your case with the aid of radiographs and make sure you have enough bone in order to avoid this communication from taking place.

(Known in older patients as Osteomalacia)

It is a vitamin D deficiency or a resistance to its action, it may occur in patients who have renal failure due to the loss of calcium from their body, or a malabsorption of calcium, basically the patient has a reduced amount of calcium which affects the bones and teeth. Failure of mineralization of osteoid and cartilage, so the bones are weak and may bend, especially the bones under a high amount of pressure such as the bones of the legs.

The biochemistry is normal because of an increase in the parathyroid hormone which returns the calcium back to its normal level, however the phosphate level is decreased, and the ALKP (alkaline phosphatase) is increased.

Dental aspects:

Ó Enamel hypoplasia

Ó Dentine hypocalcification

Ó Large pulp chambers which is expected because of the reduced amount of dentine, so early exposure of the pulp may occur if attrition took place for example, so such patients have more periapical lesions, infections, and pain than others.

Ó Short roots

Ó Poorly defined lamina dura

Ó Hypoplastic alveolar ridge

Ó Delayed eruption because the roots have problems

Ó The Condyle is smaller


It is an increase in the growth hormone in the adult stage; after the growth of bones stopped. So they grow in width, especially certain bones such as the bones of the face and hands, as a result their mandible is longer and wider which leads to Prognathism. The hands and feet grow and become very large. Not just the bones increase in size but the soft tissues as well, such as the lips, nose, and tongue (as we know it's one of the causes of macroglossia).

To confirm you evaluate the levels of growth hormone and find them increased, and if you take a lateral skull radiograph; since the growth hormone is from the pituitary gland; you find the sella tursica is enlarged, it usually has a tumor.


It is an increase in the parathyroid hormone resulting from an adenoma, or carcinoma, or hyperplasia in the gland. Mostly affects postmenopausal females. It ultimately results in hypercalcaemia, an increase in calcium levels in the blood and urine, which leads to calcification especially in the kidneys; the calcium is deposited in them resulting in the formation of renal stones that may lead to renal failure.

What matters to us is the bone pathology that affects the mandible and maxilla of people who have hyperparathyroidism. The parathyroid hormone removes the calcium from the jaws, as a result there's an increase in the osteoclastic activity which leads to a reduction in the density of the bone, the trabeculae become weakened and thin, sometimes you find a certain limited space in the maxilla or mandible suffered from a great amount of bone loss and was then replaced by granulation tissue filled with giant cells and osteoclasts; this is termed "brown tumor of hyperparathyroidism" it is NOT a neoplasm, but it is a reaction to the increase in the parathyroid hormone hence if you treat the problem, healing takes place which proves it's not an actual tumor/neoplasm. What we mean by treating the problem is to remove the for example adenoma that’s in the parathyroid gland or whatever it is that’s causing the hyperparathyroidism, and then replacement with calcium and vitamin D.


In the beginning the bone density is reduced, so it’s the same image as osteoporosis, the bone density is decreased and the bone marrow spaces are increased, so the radiolucency is increased. Mottled areas of radiolucency and thinning of the cortical plates, this is more apparent in the skull. You may see what's referred to as a "salt and pepper" appearance, areas that are in black and white due to the loss of calcium in some areas. This is seen in both the skull and jaws. In the jaws, there is a loss of the normal trabeculae pattern, and the lamina dura may no longer be visible. Therefore if you take a radiograph for a patient and the lamina dura is not visible you should suspect hyperparathyroidism. You may also see the "brown tumor" which results in multilocular radiolucency .

To confirm:

If you suspect hyperparathyroidism; and in these cases the patient suffers from its symptoms which are: weakness, constipation, renal stones, pain in kidneys, hypertension, peptic ulcer etc. in order to confirm you order a blood biochemistry test, there should be an increase in the calcium levels, a decrease in the phosphate levels, an increase in the parathyroid hormone level, an increase in the alkaline phosphatase enzyme since the osteoclasts are active, and if you did a urine analysis test you find an increase in the urinary calcium levels and an increase in the urinary phosphate levels, because all the calcium and phosphate thats removed from bone is lost in the urine (wasting of bone).

Secondary hyperparathyroidism:

If a patient has renal failure the calcium is reduced so stimulation of the parathyroid gland results and consequently hyperplasia of the gland occurs. Secondary hyperparathyroidism may also be seen in patients who have Ricketts and osteomalasia; people who have a problem in their vitamin D, so hypocalcaemia results and then stimulation of the parathyroid gland.

Success means doing the best we can with what we have. Success is the doing, not the getting; in the trying, not the triumph. Success is a personal standard, reaching for the highest that is in us, becoming all that we can be.
Best WishesJ
Done by: Hanan Musleh

Shadi Jarrar
مشرف عام

عدد المساهمات : 997
النشاط : 12
تاريخ التسجيل : 2009-08-28
العمر : 26
الموقع : Amman-Jordan


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