Download endocrine disorders and their effects in orthodontics

Sunil
Kumar Khare, Rajendra Gupta, Amit Prakash
Orthodontics
ENDOCRINE DISORDERS AND THEIR EFFECTS IN ORTHODONTICS
Sunil Kumar KHARE1, Rajendra GUPTA2, Amit PRAKASH3
1. Associate Professor, Dept. Physiology, LN Medical College and Research Centre, Bhopal
2. Associate Professor, Dept. Anatomy, Gaja Raja Medical College, Gwalior
3. Senior Lecturer, Dept. Orthodontics Dentofacial Orthopedics, Rishi-raj Dental College and Hospital, Bhopal
Contact person: Amit Prakash – [email protected]
Abstract
Orthodontic tooth movement results from the response
of the periodontal tissue to orthodontic forces, which leads
to modeling and remodeling of the surrounding alveolar
bone. The endocrine system is responsible for hormonal
secretion, being closely related to the central nervous sys‑
tem, as it diversifies its functions through the hypothala‑
mus and pituitary glands. It controls physiological
processes and maintains homeostasis. The neuroendocrine
system is responsible for adaptation to environmental
changes. Also, the nervous system may provide a correct
organic response, of primary type, with the release of neu‑
rotransmitters or, if the stimulus prevails, the endocrine
system secretes hormones. This is especially important in
dentistry because many of the patients attending dental
clinics face stressful situations. Awareness is therefore nec‑
essary on the risks and difficulties that may arise during
the dental and orthodontic management of patients with
endocrine disorders and most common oral manifesta‑
tions.
Keywords: endocrine, hormone, orthodontics
INTRODUCTION
The term ‘endocrine’ refers to endocrine or
ductless glands, because they secrete physiolog‑
ically-active substances (hormones) directly into
the blood stream. Hormones are secretory prod‑
ucts of the endocrine glands released directly
into the circulation in small amounts, in response
to a specific stimulus. On their delivery in circu‑
lation, they respond to the target cells or organs
[1].
Protein hormones and catecholamines act
through intracellular enzymes. The hormone,
which acts on a target cell, is called the first mes‑
senger. In combination with the receptor, it forms
the receptor-hormone complex. This, in turn acti‑
vates the enzymes of the cell and causes forma‑
tion of another substance, called the second
messenger or the intracellular hormonal
280
mediator, making the effects of the hormone to
be manifested inside the cells [2].
The most common second messenger is cyclic
AMP (cyclic adenosine 3’5’monophosphate or
cAMP). On the membrane of most of the target
cells, receptor proteins called G-proteins are pre‑
sent. The hormone binds with the receptor cou‑
pled with the G-protein, to form a receptor
hormone complex. This complex activates the
enzyme adenyl cyclase, which is also present in
the cell membrane. Most of the adenyl cyclase
protrudes into the cytoplasm of the cell from the
inner surface of the cell membrane. The activated
adenyl cyclase converts the ATP of the cytoplasm
into cAMP, called the second messenger, which
performs the hormonal actions inside the cell; by
stimulating some enzymes like protein kinase A,
it produces the response, as a function of the tar‑
get cells through these enzymes [1-2].
The thyroid and steroid hormones act on the
genes of the target cells. As soluble lipids, hor‑
mones can easily enter the target cells and bind
with the receptor in either cytoplasm (steroid
hormone) or nucleus (thyroid hormone), form‑
ing the hormone receptor complex. This complex
enters the nucleus and gets attached to chroma‑
tin. The complex reacts with DNA, stimulates
transcription (i.e., formation of mRNA), then it
enters the cytoplasm, where it directs the rhibo‑
somes to synthesize specific proteins (transla‑
tion). These proteins may be enzymes, structural
proteins and receptor proteins of secretory pro‑
teins.
Orthodontic tooth movement results from the
response of the periodontal tissue to the ortho‑
dontic force, which leads to modeling and
remodeling of the surrounding alveolar bone.
The response is considered to occur through the
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ENDOCRINE DISORDERS AND THEIR EFFECTS IN ORTHODONTICS
activation of specific signaling pathways, many
of which are known, all acting to ultimately
result in tooth movement. The rate at which
tooth movement occurs depends on the ability
of these pathways to realize bone metabolism by
the two main cell types responsible for tooth
movement: osteoblasts and osteoclasts [3-5].
GROWTH HORMONE (GH)
GH is a protein hormone, secreted by the aci‑
dophils of the anterior pituitary gland. GH secre‑
tion is pulsatile, secretory bursts occurring
especially at early hours of sleep and throughout
the night. GH has no specific target organ. It is
an anabolic hormone to which every organ sys‑
tem responds, considered in the present study
being craniofacial growth and its relation with
the orthodontic treatment. Apparently, it has no
direct action upon bones, acting through a sub‑
stance called somatomedin. GH stimulates the
liver to secrete somatomedin and is the main
regulator of childhood and adolescent growth.
Undersized children secrete less GH than the tall
ones. GH pulse amplitude is increased in growth
spurt, with simultaneous increase in plasma
IGF-I concentrations. These values often increase
to as high as 50ng/ml after depletion of the body
stores of proteins and carbohydrates during pro‑
longed starvation [1-5].
Dental development
Dental delay is always less pronounced than
height or bone delay. Dentition seems to be har‑
moniously delayed, so that all studied compo‑
nents of dental development (primary root
resorption, secondary tooth formation and erup‑
tive movement) display the same degree of retar‑
dation. GH influence on growth starts after 9
months of age, so that the effect on the growth
of primary teeth is very little known.
GH deficiency
Children show big skull with babyish face,
however their intelligence is normal for their
age. Cephalometric studies in such children have
shown small sizes of the anterior and posterior
International Journal of Medical Dentistry
cranial bases and smaller mandibular dimen‑
sions, small posterior facial height, and small
posterior mandibular height. Hypersecretion
leads to gigantism in the young ones and to acro‑
megaly in adults, which is usually caused by a
pituitary adenoma.
Gigantism
A cephalometric study was done on two
female patients suffering from gigantism, due to
GH excess. The anterior facial heights appeared
as the largest cephalometric dimensions, fol‑
lowed by posterior facial height. Acromegalyserum levels of IGF-I in these patients were very
high, the mean value being 10-fold higher than
in normal adults. Mandibular growth is gradual
and often noticed by the dentist when crossbite
was developed. The calvarium, hands and feet
grow by bone apposition. The tongue grows, and
a general visceral growth has been also docu‑
mented. The cartilaginous tissue gets larger, the
ribs are thicker and the costochondral cartilage
appears hypertrophic. The hypertrophic articu‑
lar cartilage and the growth of chondrocytes in
the articular cartilage may cause acromegalic
arthropathy. Mandibular growth in acromegaly
results from both appositional growth and
hypertrophic changes in the condylar cartilage.
[6-9]
INSULIN
Insulin is a polypeptide hormone secreted by
the beta cells of the Langerhans islets of the pan‑
creas. A normal non-obese man secretes approx‑
imately 50U/day, with a basal plasma insulin
concentration of 10-50 microns/ml. Its main
function is to maintain the blood glucose level.
Insulin deficiency produces a clinical state called
diabetes mellitus, while its excess leads to hypo‑
glycemia. Diabetes mellitus is diagnosed in 3-4%
of the population treated in our day-to-day
orthodontic practice. The orthodontic practi‑
tioner should have a basic knowledge and under‑
standing of this disease and of its impact on the
oral cavity, as well as of its consequences upon
the dental treatment. [1,10]
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Sunil Kumar Khare, Rajendra Gupta, Amit Prakash
Orthodontic considerations
Informed on the oral complications induced
by diabetes mellitus, the dental practitioner
should consider them when treating a DM
patient; the key to any orthodontic treatment is
a good medical control. No orthodontic treat‑
ment should be performed in a patient with
uncontrolled diabetes. There is no treatment ref‑
erence with regard to fixed or removable appli‑
ances. A good oral hygiene is especially important
when fixed appliances are used, as they may
increase plaque retention, which could more eas‑
ily cause tooth decay and periodontal break‑
down. Daily rinses with fluoride-rich mouthwash
can provide further preventive benefits. Candida
infections may also occur in the oral cavity, so
that they should be well monitored. Diabetesrelated microangiopathy can occasionally appear
in the periapical vascular supply, resulting in
unexplained odontalgia, percussion sensitivity,
pulpitis, or even loss of vitality in sound teeth.
Especially in orthodontic treatments involving
force application for moving teeth over a consid‑
erable distance, the practitioner should regularly
check the vitality of the teeth involved. It is
advisable to apply light forces and not to over‑
load the teeth [11].
Holtgrave and Donath, who studied the peri‑
odontal reaction to orthodontic forces, evidenced
retarded osseous regeneration, weakening of the
periodontal fibers and microangiopathies in the
gingival areas. In adults, before starting the
orthodontic treatment, the orthodontist should
obtain a full-mouth (periodontal) examination
and evaluation of the need for periodontal treat‑
ment. The periodontal condition should be
improved before staring the treatment and
should be monitored regularly. Maintaining a
strict oral hygiene is important, by a proper use
of toothbrush, interdental toothbrush and chlo‑
rhexidine mouthwash. To minimize the neutral‑
izing effect of toothpaste on the chlorhexidine
molecule, an at least 30-min interval should be
left between tooth brushing and chlorhexidine
rinse.
As no upper age limit for orthodontic treat‑
ments is any longer valid today, the practitioner
will see both type1 and type2 DM patients. Type2
patients can be considered more stable than
282
type1 ones, as hypoglycemic reactions are more
frequent in these patients. If a patient is sched‑
uled for a long treatment session, he or she
should be advised to eat a usual meal and take
the medication as usual. At each appointment,
the orthodontist should confirm the meal and
medication, to avoid a hypoglycemic reaction in
the office. DM patients with good metabolic con‑
trol, without local factors, such as calculus, and
with a good oral hygiene, have a similar gingival
status as the healthy ones, consequently they can
be treated orthodontically [12-14].
THYROXIN HORMONES (TH)
TH lack in a specific target organ may affect
every organ and system and every biologic pro‑
cess. Thyroid disorders are common and affect
craniofacial and dental structures. The dental
and craniofacial retardation manifested under
prolongued hypothyroid conditions differs from
the isolated lack of GH. The main difference is
the cranial vault, which shows growth retarda‑
tion in hypothyroidism, and reduced facial
height in children with prolongued untreated
hypothyroidism. Thyroxin administration seems
to lead to increased bone remodeling, increased
bone resorptive activity and reduced bone den‑
sity. Thyroid hormones increase osteoclastic
bone resorption in neonatal mouse calvarium by
stimulation of prostaglandin synthesis [14].
PARATHORMONE (PTH)
It is a polypeptide hormone secreted by the
parathyroid glands, which increases serum cal‑
cium by releasing calcium from the bone. Pos‑
sibly, it may enhance orthodontic tooth movement
by the local use of PTH. The discrete removal of
the alveolar bone prior to force application may
reduce resistance to tooth movement, permitting
a selective tooth movement [15].
CALCITONIN
It is a peptide hormone secreted by the inter‑
follicular or C-cells in the thyroid gland, also
called thyrocalcitonin. Thyrocalcitonin flows
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ENDOCRINE DISORDERS AND THEIR EFFECTS IN ORTHODONTICS
into the bloodstream and attracts calcium to the
bone, thus reducing serum calcium. It also inhib‑
its bone resorption by reducing the number of
osteoclasts. Calcitonin is used in the treatment of
hypercalcemia and in osteoporosis; because of its
physiological role, it is considered as inhibiting
tooth movement. consequently, a delay in the
orthodontic treatment can be expected [1,15].
VITAMIN-D3
Vitamin-D and its most active metabolite,
vitamin-D3, together with parathyroid hormone
and Calcitonin, regulate the amount of calcium
and phosphorus in the human organism. It pro‑
motes intestinal Ca+2 and PO4-3 absorption. Vita‑
min-D3 increases bone mass and thus reduce
fractures in osteoporosis patients. Considering
its beneficial effects on bone tissue, it may be
assumed that it inhibits tooth movement [16,17].
SEX-STEROIDS
A slight increase in the growth rate is seen at
the age of 6-8 years in most children, possibly
due to an increased GH and IGF-I production,
which is stimulated by adrenal androgens. Dur‑
ing puberty, an increase in GH production is
seen in boys and girls. Several lines of evidence
indicate that this increase is sex-steroid depend‑
ent. The sex-steroids here involved are adrenal
and ovarian androgens and ovarian and testicu‑
lar estrogens. Plasma concentration of IGF-I
shows a similar increase [18].
Estrogen directly stimulates the bone-forming
activity of osteoblasts, so it is reasonably to
expect a slower rate of orthodontic tooth move‑
ment. Androgens also inhibit bone resorption
and modulate the growth of the muscular sys‑
tem. Thus, the excessive use of these drugs by
athletes, in an attempt to achieve better athletic
scores, may affect the duration and results of the
orthodontic treatment.
CORTICOSTEROIDS
Hyperglucocorticoidism causes short stature
and bone maturation, while increasing relative
International Journal of Medical Dentistry
weight. Very small amounts of medication can
decrease the growth rate. Skeletal IGF-I synthesis
is decreased by cortisol, which has an inhibitory
effect on bone collagen synthesis. In the process
of tooth eruption, however, cortisone has a spe‑
cial effect, the eruption rate being accelerated
[19-20].
PROSTAGLANDINS (PGS)
The precursor of PGs is the arachidonic acid,
which is metabolized by cyclaseoxygenase (cox)
enzymes. Experiments have shown that PGs may
act as important mediators of mechanical stress
during orthodontic tooth movement. They stim‑
ulate bone resorption by increasing the number
of osteoclasts and by activating the already exist‑
ing osteoclasts [21].
LEUKOTRIENES
These also exist metabolites of the arachidonic
acid, produced when metabolized by the lipoxy‑
genase enzyme. Leukotrienes may be also impor‑
tant mediators of orthodontic tooth movement.
A study of Mohammed, Takikis and Dziak
devoted to the role of inhibitors of leukotrienes
synthesis in orthodontic tooth movement showed
a significant reduction of orthodontic tooth
movement. Consequently, the use of leukotriene
inhibitors can delay the orthodontic treatment,
whereas leukotrienes and PGs can have future
clinical applications, causing enhanced tooth
movements [22-23].
BIPHOSPHONATES
This class of pharmacological agents is char‑
acterized by their high affinity for calcified tis‑
sues. Biphosphonates are potent blockers of bone
resorption, successfully used in the treatment of
hypercalcemia, osteoporosis and, generally, in
the treatment of metabolic bone diseases involv‑
ing increased bone resorption. Inhibition of the
osteoclastic metabolism is caused by a decrease
in the number of osteoclasts, which may recom‑
mend it for anchoring and retaining teeth under
orthodontic treatment. However, further studies
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Sunil Kumar Khare, Rajendra Gupta, Amit Prakash
are required before any clinical application in
orthodontics, for avoiding any possible systemic
effects [24].
FLUORIDE
It is one of the several trace elements that
affect hard tissue metabolism. It stimulates the
growth and synthesis activity of osteoblasts and
bone formation, and increases bone mass and
mineral density. At clinical level, the mentioned
findings suggest that the use of fluoride can
influence the rate of orthodontic tooth move‑
ment. Even a very active preventive caries treat‑
ment with sodium fluoride (NaF) during
orthodontic tooth movement can affect the dura‑
tion of orthodontic therapy [22-24].
NSAIDS (SALICYLATES)
These non-steroidal anti-inflammatory drugs
inhibit the cyclase -oxygenase (cox) activity.
Salicylates’ action can be attributed to their inhi‑
bition of PG synthesis, which seems to play a
significant role in bone resorption during ortho‑
dontic therapy. Therefore, it is not recommended
to patients undergoing orthodontic treatment to
take salicylates for long periods, as this might
possibly prolongue the treatment [25].
CONCLUSIONS
Most of the studies on hormones have been
done on rats, squirrels and monkeys and not on
human beings; consequently, very little is still
known on the effects of hormones on the devel‑
opment of face and craniofacial skeletal and on
the rate of orthodontic tooth movement in
humans. The role of endocrine disorders in
orthodontics is still a great mystery for an ortho‑
dontic practitioner and further research is
required to understand it better.
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