Value of Coronal Scaling and Subgingival Debridement

TERMINOLOGY

Prophylaxis, Oral: The removal of plaque, calculus and stains from the exposed and unexposed surfaces of the teeth by scaling and polishing as a preventive measure for control of local irritational factors. In the clinic this procedure is selected in the treatment of gingivitis in the hope that the gingival will be returned to a state of health or at least will not develop into periodontitis.

Future preventive / recall cleaning will be termed prophylaxes as opposed to maintenance therapy.

Scaling: Instrumentation of the crown and root surfaces of the teeth to remove plaque, calculus and stains from the teeth.

Root Planing: A treatment procedure designed to remove cementum or surface dentin that is rough impregnated with calculus, or contaminated with toxins or microorganisms. The term is in common usage but is not favored at the UW because it is restrictive, referring only to the root surface and not the adjacent soft tissues.

Root Curettage: Scraping or cleaning the walls of a cavity or surface by mean if a curet.

The procedure not only addresses the root surfaces but also focuses on the soft tissue of the periodontal pocket, especially when sharp, double-edged curets are used. In the patient with periodontitis (as opposed to gingivitis), the student and supervising Periodontics instructor will design a treatment plan consisting of from between 1 to 4 quadrant- equivalents of root curettage depending on the severity of the case. Once this treatment of periodentitis has been selected, then future recall treatment will be termed maintenance as attempts are made to maintain the status quo and prevent further breakdown of the periodontal support. Unfortunately this term is not widely used because many people consider it a surgical procedure.

Subgingival Debridement (SD): The removal of inflamed, devitalized, or contaminated tissue or foreign material from or adjacent to a lesion. This descriptive term for  “ subgingival cleaning” is favored by the UW Department of Periodontics.

Note:  A prophylaxis and quadrants root curettage cannot both be treatment planned on the same patient at the same time.

Benefits and Limitations

During the 1960s, it was shown that supragingival plaque accumulation led to gingival inflammation. It also is generally accepted that pathogenic subgingival plaque cannot develop in the absence of supragingival plaque. Furthermore, changes in supragingival plaque can induce changes in subgingival plaque. Successful periodontal therefore depends on meticulous daily removal of supragingival plaque by the patient and removal of plaque (and probably calculus) by debridement og the crown and root surfaces of the tooth by dental personnel. Both are fraught with problems. Patient compliance usually is not ideal and access to deep periodontal pockets and furcation invasions is difficult, if not impossible. Waerhaug (J Periodontol 49:119,1978) and Rabbani et al (J Periodontol 52:119,1981) demonstrated that SD was fairly effective in removing subgingival deposits in shallow pockets. In pocket depths between 3-5 mm the chances of failure exceeded the chances for success. When pocket depth surpass 5 mm or if significant furcation invasion existed, the chances for failure dominated.

All is not lost! In spite of these limitations there is ample evidence of benefit – at least short-term benefit.

Clinical Studies:

In a 4-week study Morrison et al (J Clin Periodontol 7:199,1980) looked at the effects of OHI, S/SD and occlusal adjustment performed on 90 patients each of whom had at least 20 teeth. The treatment took 4-6 visits. Importat results are illustrated in the following figures.

Results do depend on the degree of inflammation in soft tissue. After 4 week there was a decrease in probing depth and a decrease in periodontal attachment loss in moderate to deep periodontal pockets.  Of equal importance was the slight loss of attachment after instrumentation in shallow pockets. Let the tissues do the talking. In the absence of gingival inflammation, increased probing depths, and calculus, the clinician should be cautious and avoid subgingival instrumentation. “If it ain’t broke, don’t fix it!”

Histologic Studies:

In a clinical / microscopic study in 22 patients, Tagge et al (J Periodontol 46:527,1975) gave OHI and per formed SD and in a site that displayed the same amount of gingival inflammation clinically as another area in the same mouth which was not treated – i.e., the control site. A third similar site was treated by OHI alone. Eight weeks later all 3 sites were assessed clinically for inflammation and 66 biopsy specimens were taken. Clinically and microscopically there was less evidence of inflammation in the SD + OHI sites than in the other two. The data are presented graphically below.

Stahl et al (J Periodontal 42:678,1971) conducted a study to ascertain how long it would take the histologic improvement seen in gingival inflammation as a result of SD to return pre-treatment levels. Eighty suprabony pockets averaging 4.6 mm depth were curetted and then biopsied at appearing specimens from the same patient. By 8 weeks the inflammatory infiltrate was similar in distribution and degree to the control specimens.

Microbiological Studies:

Subgingival debridement has been shown to alter the subgingival microflora purportedly associated with the development of periodontal disease. But for how long? Magnusson et al (J Clin Periodontal 11:193,1993) studied the recolonization of spirochetes and motile rods following SD. The total counts and percentage of these organisms dropped immediately after treatment. By 4 weeks a gradual increase was noted and by the examinations conducted at 8,12, and 16 weeks post- treatment the motile segment of the subgingival microbiota had approached baseline. In a similar study by Handleman and Hess (J Dent Res 49:340,1970) repeated bacterial samples were evaluated after SD at day 3, 10, 30 and 60. There was an immediate increase in Gm + cocci and a decrease in the more complex organisms. The various bacteria studied returned to baseline levels by day 60. Interestingly probing depth was not correlated to the degree of inflammation.

Extended Studies:

(Ⅰ)  Badersten et al (J Clin periodontal 8:57,1981 and 11:63,1984) investigated the effect of SD on moderately advanced (4-7mm) and severely advanced (>7mm) periodontitis. In both studies only single-rooted teeth were treated and assessed. The common format included repeated OHI for at least 3 months followed by aggressive SD (with either hand instruments or ultrasonics) every three months until 1 year. The advanced study continued for a second year during which time OHI was given and the teeth received a coronal polish every 3 months. Plaque index, bleeding on probing, pocket depth all improved during the first few months and then remained stable. The results for periodontal attachment level were mixed. In the moderate study there were 106 sites that initially measured at least 6 mm. At 7 months there were 11 such sites and at 13 months there were 13. The advanced study had 305 sites initially measuring at least 7 mm; there were 43 such sites by 24 months. Thus the investigators were able to improve and maintain the periodontal status for 13 to 24 months. It took careful and repeated OHI in a motivated group of people. It took several rounds of thorough SD during the first year and in the second study periodic OHI and coronal polishing for the next 12 mouths. Not to be overlooked is the fact that all teeth were single-rooted. Molars, especially those with furcation invasions, really complicate treatment. May require surgical access to cope with problems.

(Ⅱ)  In an excellent long-term clinical study by Kalkwarf et al (J Periodontol 59:794,1988) a variety of surgical and non-surgical modalities were compared in teeth with furcation invasions. Regardless of the method used all sites tended to breakdown in the second year of maintenance.

(Ⅲ)  Fleischer et al (J Periodontol 60:402,1989) demonstrated that in molars with furcation invasions and probing depths of at least 7 mm, the percent  of attachment loss in the furcations was over 3 times the percent of loss on external root surfaces. That’s ugly!

Summary:

In spite of the limitations of access, especially in the posterior of the mouth and in the presence of furcation invasions, careful SD will lead to clinical, histologic and microbiologic improvement in moderate to severe periodontal disease – at least over a 2-3 month period. The better the patient’s plaque control efforts, the better the results, and the longer they will last.

Subgingival debridement is not advised in healthy sulci.

Key Words : dental cleaning tooth cleaning teeth cleaning cleaning teeth periodontal disease periodontal periodontists periodontal treatment periodontal surgery gum disease gum disease treatment perio scaling and root planing periodontal dentistry root planing periodontist office periodontist treatment dental implants perio over denture endo perio perio-endo lesions perio grafting perio surgery

Disorders of Teeth other than Dental Caries

·         Eruption and Shedding

·         Non-Bacterial Loss of Tooth Substance  

·         Discoloration of Teeth

·         Transplantation and Reimplantation

·         Root Fracture

·         Age Changes     

Disorders of Eruption and Shedding

Premature eruption , Natal and Neonatal teeth :

Natal and Neonatal teeth:

·         Premature : before the proper time

·         Usually teeth start to erupt at the age of 6 months + or - , and sometimes as early as 3 months . It might be delayed as well, to the age of 9,12month.some neonate (new born) are born with teeth or start to erupt shortly after birth . these teeth are called :

·         Natal - if present at birth

·         Neonatal - if erupted shortly after birth

·         80% of these teeth are the mandibular incisors .

      Remember: the first teeth to erupt are the mandibular incisors, so common sense .

• Due to this premature eruption there is lack of root formation, and the mobility during eruption might lead to irregularities in its structure (it is still developing) leading to premature loss .
• we might extract them before they are lost if :
• we are scared that the infant might inhale them
• they are causing ulceration to the opposing oral mucosa
• they are causing injury to the mother while nursing
• If we feel that they are stable we can provide them with covering plate
• While nursing rather than extraction.

 Local Factors for Other Teeth:

Such as premature eruption of permanent teeth (which is widely seen in our population) as a result of :

Dental caries of deciduous teeth and lack of oral health education, which might lead to malocclusion as well - premature loss of deciduous teeth

Superficial location of tooth germs in the jaws

Endocrine abnormalities:

• lead to generalized premature eruption
• such as increase in GH and hyperthyroidism

 Remember:

             Increase in GH in children - gigantism

             Increase in GH in adults    - acromegaly

Retarded Eruption :

General causes:

·         Such as :

o   Hypothyroidism : leads to cretinism

o   Prematurity : born earlier

o   Nutritional deficiencies

o   Chromosomal abnormalities

 Local causes:

·         When permanent teeth (as well deciduous but less common) have got the eruptive force but there is sth preventing them .

·         it could be :

o   Idiopathic

o   Migration & traumatic displacement of tooth germs

                                                      

·         As if a child was exposed to a trauma that moved his tooth germs far in the jaw or to become impacted by other teeth

·         Abnormally large crowns : can’t find space for eruption

Delayed Eruption and Multiple Supernumerary Teeth:

• Any condition which have multiple or even single supernumerary teeth might obstruct the track of chronology , 
• Or the supernumerary teeth itself can’t erupt .

• Such in Cleidocranial Dysplasia : a condition associated with :
• Total or partial absence of the clavicles
• Cranial sutures abnormalities
• Hemifacial hypoplasia
• Depressed nasal bridge
• Multiple impacted supernumerary teeth

Premature Loss :

·         causes :

            1-dental cries and its sequelae^* - such as pulpitis 

            2- Chronic periodontitis ^*

            3- Aggressive periodontitis

·         Periodontitis is an inflammation that start with gingivitis and progress to the periodontal fibers and the alveolar bone .

·         There is a variant of periodontitis that isn’t related to poor oral hygiene - aggressive periodontitis

               

            4- Hypophosphatasia

            5- Papillion-lefèvre syndrome - also known as palmer planter Hyperkeratosis

                   * The most common causes dental caries + periodontitis
  

Persistence of Deciduous Teeth :

• it is also termed as : retained or submerged deciduous teeth
• the condition in which deciduous teeth don’t shed at the time they should
• A case for eg. is : when the development of the successor teeth is retarded, so it won’t erupt and the deciduous will persist in the mouth
• Another eg. is: when there is a congenitally missing permanent teeth the deciduous may remain in its position .

• so persistence of deciduous teeth result from failure of eruption of  permanent successor because it is missing , displaced or lack formation

A generalized condition is found in cleidocranial dysplasia  .

  e) Impaction of Teeth:

• A very common eg. is 3^rd molar impaction due to lack of space
• Other teeth might be affected such as : maxillary canine , mandibular 2ⁿ premolar .
• Impacted teeth : teeth which remain unerupted or partially erupted beyond the expected time 
• It might affect 1 or more teeth
• It might be symmetrical : on the Rt + Lf or in the upper + lower
• Is rare in deciduous
• When a tooth is partially erupted it might cause problems :

The gingiva is opened to the oral cavity - accumulation of food and debris

-          hard to clean - caries , periodontitis or any source of infection 

• it might cause resorption in the adjacent tooth

Local causes:

             1-Abnormal position of germ Æ too far in the jaw

             2-Lack of space Æ such for 3^rd molar and maxillary canine

             3-Supernumerary teeth Æ such in cleidocranial dysplasia

             4-Cysts (odontogenic tissues are capable of forming them)

             5-Tumors(odontogenic tissues are capable of forming them)

             6-Cleidocranial  dysplasia

Complications:

             e Resorption of impacted or adjacent teeth

             e Formation of dentigerous cyst

·       Dentigerous cyst :is a developmental cyst around the crown of impacted teeth that result from the accumulation of fluids between the enamel and residual enamel epithelium

             e Formation of odontogenic tumors

 f Another term is embedded teeth : teeth which remains unerupted due to 

Lack of eruptive force in the absence  of a physical barrier 

Remember: impacted - physical barrier 

But usually people use impacted for every thing.

      

f) Reimpaction of Teeth :

      

     f Occur when the alveolar process doesn’t grow enough and the tooth become ankylosis with adjacent bone.  

Ankylosis : the union of 2 bony structures .Cementum is similar to the bone structure.

Remember: the alveolar processes of the deciduous teeth grow to accommodate the size and length of the permanent teeth and to reach the correct occlusion.

  

•      As a result there is absent of PDL fibers in that aria 
•      Also known as infraocclusion  or submerged teeth
•      Called reimpaction because it is infraocclusal (impacted from the normal occlusion)  
•      In some situation neighboring teeth tilt over affected tooth, and it may be completely covered by mucosa
•      Mostly affects the deciduous mandibular 2^ed molar lacking a successor 2^ed premolar

Non Carious Tooth Substance loss

Attrition :

·         wearing away of tooth substance during tooth to tooth contact- during grinding of teeth against each other

·         it is a slow physiological process that appears more in elderly

·         might be accelerated by abrasive foods

·         pattern:

§  incisal edges of incisors,

§  occlusal surfaces of molars,

§  palatal cusps of maxillary teeth,

§  buccal cusps of mandibular teeth

You might be surprised of the presence of Approximal attrition on the proximal surface results from the movement of PDL fibers during eating ,talking,…etc so the contact points become flat as a result teeth tend to slightly move toward the mid line – mesial migration

   

     f More pronounced in males

     f Abrasive food property affects the rate 

     f Pathological attrition may result from

            1- Abnormal occlusal relationship

            2- Bruxism and habits such as tobacco and betel chewing

            3- Abrasive dust particles - consist of silica

            4- Abnormal tooth structure such as amelogenesis imperfecta and

                dentinogenesis imperfecta - weakness of the structure

 f Exposed dentin becomes discolored yellow to brown and it becomes attritic faster than enamel, cause it is softer, creating cup-shaped defects or wear facet

     f Formation of reactionary dentine protects pulp

     f And there is formation of dead tracks and translucent zones.

Abrasion :

• pathological wearing away of tooth structure due to repetitive friction of a foreign body

     f Examples:

           1- Nuts and million seed abrasion

           2- Toothbrush abrasion

• due to roughness and poor technique
• brushing motion should be vertical + circular with a smooth brush

           3- Habitual abrasion in pipe-smokers

           4- Occupational abrasion e.g. hair-grips, nails, musical instruments

           5- Ritual abrasion - related to certain tradition

Abfraction :

Loss of tooth structure that results from repeated tooth flexure caused by occlusal stresses

Flexure: blending

     f enamel tend to blend to some extant at stress then it will fracture

     f while dentin is able to withstand greater tensile stress than enamel

     f When eccentric occlusal forces are applied to a tooth, tensile stress is concentrated at cervical fulcrum, leading to flexure that may produce enamel cracks

     f Cracked enamel can be lost or more easily removed by erosion or abrasion

Erosion :

     f loss of tooth structure resulting from chemical action (acid action)

Dietary erosion :

     f Excessive intake of acidic beverages or sucking of citrus fruits- palatal surfaces of teeth and labial surfaces of maxillary incisors

Occupational erosion:

   

  f e.g. battery factories- labial surfaces of maxillary and mandibular incisors

Acid reflux or chronic vomiting:

  f e.g. anorexia, bulimia nervosa, chronic alcoholism as well in hernia

Idiopathic:

 Resorption :

   

    f Usually the root resorp but sometimes the crown resorp as well such in impacted teeth

Physiological resorption:

    f Is seen in the root of deciduous teeth prior to shedding

    f Sometimes it occurs as a result of permenant teeth movement and called transient resorption

    f Transient microscopic areas of superficial resorption of roots of permanent teeth, repaired by cementum or bone-like tissue apposition

  

Pathological resorption :

• External - start from the root surface
• Internal - start from the pulp

The cells of action are osteoclast or might call them odontoclast

    1- External resorption :

     f Might be associated with: Periapical inflammation

     e Results from the progression of dental caries , pulpitis , pulpal necrotic tissues through apical foramina

     e Inflammation might cause - bone resorptionroot resorption excessive mechanical force e.g. improper orthodontic treatment

     e Orthodontics is based on the movement of teeth resulted from the resorption and deposition of  bone

neoplasms or cysts transplanted or replanted teeth

     e Transplantation: the placement of a tooth in an another socket

     e Reimplantation : the placement of the lost tooth in its own socket idiopathic, burrowing type in cervical area - no known cause

Crowns of impacted teeth

    2- Internal resorption :

      f Occurs from the pulp chamber to the outside

      f The clasts originate from it and we call them dentinoclasts 

      f So a vital pulp is needed

      f May be:

Secondary to pulpitis

Idiopathic

      f Clinically we start to see the pulp through enamel - pink tooth or by a radiograph

                   Remember: pink because it is vascularised

Discoloration of Teeth

    By:

            a) Surface deposits - extrinsic staining such as smoking , coffee , tea

            b) Changes in the structure or thickness of the dental hard tissues

            c) Diffusion of pigments into the dental hard tissues after their formation

            d) Incorporation of pigments into the dental hard tissues during their formation

What is the difference between pigments and stains ?

• Pigments : produced by the body
• Stains : are extrinsic

Extrinsic Staining :

      f Causes:

              1- Foods and drinks - usually transient

              2- Chromogenic bacteria- pigment producing bacteria

                e Teeth apperes dark brown to black and they are usually caries resistance

                e But these stains are usually hard to remove

Topical medications and mouth rinses

Tobacco products

  

 b) Changes in Structure or Thickness of Dental Tissues :

      f Any abnormality in dental tissues

      f Causes:

              1-Dental caries

              2-Enamel hypoplasia: e.g. fluorosis (environmental), amelogenesis

                    imperfecta (hereditary) , enamel opacities

              3-Dentinogenesis imperfecta

              4-Dentinal dysplasia type II

              5-Age changes

c) Diffusion of Pigments into Dental Tissues After Formation :

   f At this stage the tooth isn’t vital and you can till from its appearance

   f Examples:

          1- take up of food & tobacco stains by exposed dentin

          2- restorative & endodontic materials : amalgam sometimes stains

          3- Pulp necrosis

Incorporation of Pigments into Dental Tissues During Formation :

  f Examples:

          1- Congenital hyperbilirubinemia - neonatal jaundice - green to yellowish brown

          2- Congenital porphyria - pinkish-brown - red fluorescence under UV light

          3- Tetracycline intake during pregnancy or childhood - yellowish changing into brown

                     eThe most important

                     eInfant deciduous and maybe first molars become stained

                     eSo it is contraindicated to prescribe this antibiotic in pregnancy and childhood conditions

Transplantation and Re-implantation

   

     f Reimplantation :

             eReturning a tooth to its socket after avulsion.

             eSupposing a child while running has lost his incisor if we try to re-implant it within an hour , and we’ve already preserved it in milk

               (Body temperature), then the process might success .

    f Transplantation:

             eTransfer of a tooth to another location in the jaw

             eIt is rarely done

             eSupposing that some one has lost his 1^st molar it could be replaced by for e.g. his 3^rd molar

    f Both are associated with resorption

    f Other complications:

          Loss of pulp vitality, failure of root completion, poor periodontal healing

Root Fracture

    f As a result of trauma

    f Occur at different levels of the root

    f The outcome depends on :

             1-presence or absence of infection - if the gingiva is opened or the tooth is carious there might be failure

             2-vitality of pulp

 Position of fragments - it is better when it is more toward the apex

 3-degree of comminution

 4-Location of fracture

 5-Mobility of coronal fragment

   f Pattern of healing:

                 1- Fragments become united totally or partly by calcified repair tissue - such as cements

                 2- Fractured surfaces become rounded off and clothed by cementum with formation of fibrous tissue in between

                 3- Fractured surfaces become rounded off and clothed by cementum with formation of fibrous tissue and bone in between

Age Changes

  a) Enamel become:

                  1- More brittle -more cracks

                  2- Less permeable

                  3- Darker

  b) Dentine:

                  1-Continued formation of secondary dentin with reduction or obliteration of pulp chamber

                  2-Continued formation of peritubular dentin results in transluce dentin

                               e The increase in thickness around the tubule results in this translucency

                  3-Roots become brittle

                                e So becoming thicker doesn’t mean becoming stronger

          

  c) Cementum :

                  1-Continued formation and increased root thickness

                  2-Hypercementosis in presence of other causes

In general if you look at an old tooth you’ll see:

• Narrowed pulp chambers and maybe some calcified portions
• Tertiary dentine
• Enamel cracks
• Gingival ressetion      

Migraine-Natural ways of treating migraine and Home Remedy for Migraine

Migraine

Causes & Symptoms of Migraine

Migraine is the name given to severe headaches, normally lasting from 4 to 72 hours. It is mainly felt s pulsing or throbbing in one area of the head. During migraine, there is contraction or dilation of the blood vessels. Some of the factors that can trigger a migraine attack anxiety, stress, lack of food or sleep, exposure to light and hormonal changes (in women). In women, menstruation can also result in migraine. The symptoms of migraine are pain on one side of the head, a short period of depression, irritability and loss of appetite, pounding pain, nausea and vomiting as well as numbness or weakness in an arm or leg or on one side of the face. This severe headache can, however, be cured, naturally using home remedies. Read onto know some of the natural ways of treating migraine.

Home Remedy for Migraine

 

• Migraine can be treated effectively with the help of fresh grape juice. Grind grapes to extract the juice. Consume the juice in the concentrated form, without adding water. 

 

• Increase the intake of niacin (vitamin B3), as it has been found to be helpful in alleviating migraine pain. Some of the foods rich in niacin are yeast, whole wheat, green leafy vegetables, tomatoes, nuts, sunflower seeds, liver and fish.

• Cabbage leaves are helpful in relieving the pain of a migraine headache. Squash cabbage leaves and place them in a cloth. Place the cloth on your forehead for sometime. Once the cabbage leaves become dry, remove the cloth and make a fresh one. 

 

• Lemon peel is helpful in solving migraine headache. Grind lemon peel to form a paste and apply it on the forehead. Let it dry and then rinse off with cool water.

 

• A mixture of carrot juice, either with spinach, beet or cucumber juice, works effectively in curing migraine. Combine 300 ml of carrot juice with 200 ml of any other juice and drink it.

 

• You can also mix 100 ml each of beet and cucumber juices, with 300 ml of carrot juice and drink it on a regular basis.
• Massaging the forehead with primrose oil is beneficial in curing migraine. It works as an excellent anti-inflammatory agent, preventing any kind of constriction in the blood vessels. 

 

• Taking lukewarm water enema is effective. It cleanses the bowels, thereby removing the toxins from the body and helping prevent migraine.
• Take some sandalwood powder and add a few drops of water to it, to form a paste. Apply this paste on the forehead and let it dry. Once dry, rub it off by hand and wash it. 

 

• It is advisable to avoid direct sunlight; smoking and drinking alcohol, as all these can aggravate migraine.

Menstrual Cycle-Gynecology Lecture

A.Series of rhythmic reproductive cycle

• From the onset of menstrual bleeding to the next period
• Characterized by changes in the ovaries and uterus
• Influenced by normal hormonal variation mediated by hypothalamus and anterior pituitary gland via feedback mechanis
• Recurring cyclically beginning at puberty with first menstruation called the  MENARCHE and ceasing at MENOPAUSE
• Mean cycle length  of 28 days; normal range 25-28 day per cycle

B.Function of the cycle

·         In preparation for the release of egg, fertilization and implantation 

3. Hormonal Control of Menstrual Cycle

 

1.      Follicle Stimulating Hormone (FSH)

• Secreted by the anterior pituitary gland during the first half of the menstrual cycle
• Stimulate the development of graafian follicle
• Thickens the endometrium

       

2.      Luteinizing Hormone (LH)

• Secreted by the pituitary gland
• Stimulates ovulation and development of corpus luteum
• Thickens the endometrium

3.      Estrogen

• Secreted primarily by the ovaries, by the adrenal cortex and by the placenta in pregnancy
• Stimulates thickening of the endometrium causes suppression  of FSH secretion
• Assist in maturation of  ovarian follicles
• Responsible for the development of secondary sex characteristics
• Stimulates uterine contractions
• Mildly accelerates sodium and water reabsorption by kidney tubules; increase water content of the uterus
• High estrogen contraction-inhibits secretion of FSH and prolactin but stimulates secretion of LH
•  Low estrogen concentration after pregnancy, stimulates secretion of prolactin
• Accelerates protein anabolism
• Responsible for the fertile cervical mucus; clear, stingy, stretchable, slippery, with fern patterns when dry

4.      Progesterone

• Secreted by corpus luteum and placenta during pregnancy
• Inhibits secretion of LH
• Has thermogenic effect (increases basal body temperature)
• Relaxes smooth muscles
• Responsible for infertile mucus, opaque, sticky, thick, non-stretchable, non-fern pattern when dry
• Maintain thickness of endometrium
• Allows pregnancy to be maintained

5.      Prostaglandin

·         Fatty acids categorized a hormone

·         Produced by many organs of the body, including the endometrium

·         Affects menstrual cycle

·         Influences the onset and maintenance of labor

Phases of Menstrual Cycle

       1.  Menstrual Phase (Day 1-5)

a.  Corpus luteum degenerates

b. There is cessation of progesterone and estrogen produced by corpus       luteum and blood level stops

c.   Endometrium degenerates and menstruation occurs

d. Drop in blood levels of estrogen and progesterone stimulate production of FSH and new cycle begins

2.      Proliferative Phase (Day 6-14)

• Follicle-stimulating hormone (FSH) released by the anterior pituitary stimulates the development 
• As graafian follicle develops, it produces increasing amounts of follicular fluid containing a hormone called estrogen
• Estrogen stimulates thickening of the endometrium
• As estrogen increasing in the bloodstream, it suppresses secretion of FSH and favors secretion of the luteinizing hormone (LH) 
•  LH stimulates ovulation and initiates development of corpus luteum

3.      Secretory Phase (Day 15-21)

• Follows ovulation, which is the release of mature ovum from the graafian follicle
• Cavity of the graafian follicle is replaced by the corpus luteum (secretes progesterone and some estrogen)
• Progesterone acts upon the endometrium to bring about secretory changes that prepare it for pregnancy. It also maintains the endometrium during the early phase of pregnancy, should a fertilized ovum be implanted

4.      Pre- Menstrual (Day 22-26)

a.    If fertilization does not occur the corpus luteum in the ovary begins to regress

b.      Production of progesterone and estrogen decreases

c.       Endometrium of uterus begins to degenerate and sloughs off

d.      Endometrium becomes thicker and vascular ready for implantation

Menstrual Disorders

Dysmenorrhea – pain with menses

Types:

Primary – begins 1-3 months after menarche in conjunction with ovulatory cycles

Secondary – suspected when pain is concentrated on a specific area or only on one side when its onset occurs after age 20

Etiology:

Ø  Due to unknown factors

Ø  Thought to be intrinsic to uterus; excessive production of prostaglandins

Ø  Sedentary occupation

Ø  Poor posture

Ø  Poor personal hygiene

Ø  Constitutional illness such as anemia

Ø  Daughter of women who have suffer or have suffered from dysmenorrhea are frequently dysmerrheic

Sign and Symptoms:

Ø  Cramps in the lower abdomen and occasionally into the groin, thigh, and vulva

Ø  Tension

Ø  Nausea and vomiting

Ø  Malaise

Ø  Chills and shivering

Ø  Diarrhea

Ø  Pallor

Ø  Hot and cold sensation

Ø  Fainting in some cases

Treatment and Management

Ø  Explanation or normal and anatomy and physiology of menstruation-serves to eradicate misconception and lessen fear and anxiety which may be associated with her periods

Nursing Management

Ø  Instruction  in menstrual hygiene-so that her period does not seem distasteful and restricting, encourage frequent bathing

Ø Encourage to get more good posture and exercise particularly aerobics (cycling, jogging, walking, and waist bending before the onset of the period)

Ø  Avoidance over fatigue and overexertion during the period

Ø  Apply heat (e.g. warm baths, putting a hot water bottle, or heating pads on the abdomen)

Ø  Focuses on education and psychosocial needs of the patient

Ø  Encourages to drink plenty of fluids, but avoid alcohol

Ø  Divert attention

Ø  Encourage rest and sleep

Ø  Apply relaxation technique; massage

Ø  Avoid aspirin or prostaglandin inhibitor such as ibuprofen, mefenamic acid-medication are to be taken with water, milk may be used if the medication causes an upset in the stomach

Ø   Usually eliminated by oral contraception which blocks ovulation